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��ࡱ�>��	�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������q`��0�#bjbjqPqP	:(::��%�������```````t|||8���<t�5����"���   �4�4�4�4�4�4�4$n6h�8��4�`&  &&�4``���r5�.�.�.&�`�`��4�.&�4�.�.1``S1��0yJ�u�|�,�14��50�5'1,�9�-��9S1�9`S1� r�!�.�"��#G   �4�4r.X   �5&&&&ttt�dtttttt``````����Mesenchymal Stem Cells and Molecular Mechanisms, Feasible Candidates for Neuroprotection and Regeneration
Fatemeh Pourrajaba, c, (PhD), Seyed Hosain Hekmatimoghadama, b, d,*, (MD), Seyed Khalil Forouzanniab,(MD)

  aYazd Research Center of Sciences and Molecular Biothecnology, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
bYazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
cDepartment of Clinical Biochemistry and Molecular Biology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
d Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran



Corresponding authors: Yazd Research Center of Sciences and Molecular Biothecnology, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Tel: +98 351 8203410 ; fax: +98 351 8203414.
E-mail address: mina_poorrajab@yahoo.com (F. Pourrajab), 

Disclosure statement for authors: On behalf of the authors, I (Fatemeh Pourrajab) should to insure that there are no potential conflicts of interest to disclose.






Abstract
Cell therapy is an attractive strategy for protection or restoration of degenerative diseases. Human bone marrow-derived mesenchymal stem cells (BMSCs) reservoirs of the reparative mechanisms, exhibit a beneficial population for treatment of neurodegenerative diseases. The key players involved in BMSC tropism are up-regulated signals after ischemia/reperfusion or inflammation. Molecular signals also induced by injuries, trigger BMSC migration, homing and invasion. Cytokines and chemoattractant in particular VEGF, G-CSF, PDGF, FGF, CCRs and matrix proteases imply pivotal roles in reparative pathways. Under homing, BMSCs induce immunomodulatory and regenerative mechanisms as well as milieu-dependent differentiation to express phenotypes of the local microenvironment, great potentials for treatment of neurodegenerative and ischemic diseases.

Keywords: Neuroprotective; immunomodulator; genetic reprogramming; modulating hypoxia.

Beneficial Features of Bone Marrow Mesenchymal Stem Cells
Human bone marrow-derived mesenchymal stem cells (BMSCs) are of therapeutic interest in a variety of neurological diseases, a population which can differentiate into multiple cellular lineages. The autologous origin of BMSCs avoids the risk of immune rejection and being adult cells weaken the possibility of tumor development. Furthermore, they also have anti-tumor, immunomodulatory and anti-inflammatory effects  ADDIN REFMGR.CITE <Refman><Cite><Author>Karussis</Author><Year>2008</Year><RecNum>6</RecNum><IDText>Immunomodulation and neuroprotection with mesenchymal bone marrow stem cells (MSCs): a proposed treatment for multiple sclerosis and other neuroimmunological/neurodegenerative diseases</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>6</Ref_ID><Title_Primary>Immunomodulation and neuroprotection with mesenchymal bone marrow stem cells (MSCs): a proposed treatment for multiple sclerosis and other neuroimmunological/neurodegenerative diseases</Title_Primary><Authors_Primary>Karussis,D.</Authors_Primary><Authors_Primary>Kassis,I.</Authors_Primary><Authors_Primary>Kurkalli,B.G.</Authors_Primary><Authors_Primary>Slavin,S.</Authors_Primary><Date_Primary>2008/2/15</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Clinical Trials as Topic</Keywords><Keywords>Humans</Keywords><Keywords>Immunologic Factors</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Multiple Sclerosis</Keywords><Keywords>Neurodegenerative Diseases</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>131</Start_Page><End_Page>135</End_Page><Periodical>J.Neurol.Sci.</Periodical><Volume>265</Volume><Issue>1-2</Issue><Misc_3>S0022-510X(07)00325-5 [pii];10.1016/j.jns.2007.05.005 [doi]</Misc_3><Address>Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Hospital, Ein-Karem, Jerusalem, IL-91120, Israel. karus@cc.huji.ac.il</Address><Web_URL>PM:17610906</Web_URL><ZZ_JournalFull><f name="System">J.Neurol.Sci.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">J.Neurol.Sci.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(1). Although the mechanisms underlying the immunosuppressive effect of MSCs has not been clearly defined, but their immunosuppressive properties have already been exploited in the clinical settings. Beside, BMSCs in human body represent reservoirs of reparative cells and capable of homing to the site of diseases. They include a high quality for provoking the regeneration pathways in the injured tissue without fibrous tissue formation  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (2).
When, BMSCs are co-cultured rescue dorsal root ganglia from dying and allow the long-lasting survival and maturation, otherwise neurons are committed to die. The BMSC rescue effects on the neurons is achieved only by direct contact  ADDIN REFMGR.CITE <Refman><Cite><Author>Scuteri</Author><Year>2006</Year><RecNum>5</RecNum><IDText>Adult mesenchymal stem cells rescue dorsal root ganglia neurons from dying</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>5</Ref_ID><Title_Primary>Adult mesenchymal stem cells rescue dorsal root ganglia neurons from dying</Title_Primary><Authors_Primary>Scuteri,A.</Authors_Primary><Authors_Primary>Cassetti,A.</Authors_Primary><Authors_Primary>Tredici,G.</Authors_Primary><Date_Primary>2006/10/20</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Death</Keywords><Keywords>Cell Survival</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Ganglia,Spinal</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Microscopy,Confocal</Keywords><Keywords>Mitosis</Keywords><Keywords>Neurons</Keywords><Keywords>Neurons,Afferent</Keywords><Keywords>physiology</Keywords><Keywords>Pregnancy</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>75</Start_Page><End_Page>81</End_Page><Periodical>Brain Res.</Periodical><Volume>1116</Volume><Issue>1</Issue><Address>Dipartimento di Neuroscienze e Tecnologie Biomediche, Facolta di Medicina e Chirurgia, Universita degli Studi di Milano-Bicocca, Via Cadore 48, 20052 Monza, Italy. arianna.scuteri@unimib.it</Address><Web_URL>PM:16959225</Web_URL><ZZ_JournalFull><f name="System">Brain Res.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Brain Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(3, 4). In experimental models of ischemia, tumors, and neurodegenerative diseases, many studies have imply that BMSCs migrate to site of lesions in the brain to ameliorate functional deficits  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (5,6). BMSCs can also be used as vehicles to deliver therapeutic compounds or genes to site of prions  ADDIN REFMGR.CITE <Refman><Cite><Author>Song</Author><Year>2009</Year><RecNum>45</RecNum><IDText>Effect of transplantation of bone marrow-derived mesenchymal stem cells on mice infected with prions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>45</Ref_ID><Title_Primary>Effect of transplantation of bone marrow-derived mesenchymal stem cells on mice infected with prions</Title_Primary><Authors_Primary>Song,C.H.</Authors_Primary><Authors_Primary>Honmou,O.</Authors_Primary><Authors_Primary>Ohsawa,N.</Authors_Primary><Authors_Primary>Nakamura,K.</Authors_Primary><Authors_Primary>Hamada,H.</Authors_Primary><Authors_Primary>Furuoka,H.</Authors_Primary><Authors_Primary>Hasebe,R.</Authors_Primary><Authors_Primary>Horiuchi,M.</Authors_Primary><Date_Primary>2009/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Brain</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>cytology</Keywords><Keywords>Female</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mice</Keywords><Keywords>Neurodegenerative Diseases</Keywords><Keywords>pathology</Keywords><Keywords>Prion Diseases</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Survival Rate</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>5918</Start_Page><End_Page>5927</End_Page><Periodical>J.Virol.</Periodical><Volume>83</Volume><Issue>11</Issue><User_Def_5>PMC2681942</User_Def_5><Misc_3>JVI.00165-09 [pii];10.1128/JVI.00165-09 [doi]</Misc_3><Address>Laboratory of Prion Diseases, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan</Address><Web_URL>PM:19297502</Web_URL><ZZ_JournalFull><f name="System">J.Virol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">J.Virol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(7). 
Under adequate stimuli and contact stimulation, BMSCs express typical markers of specific cell lines including glial cells and neurons. The neuronal differentiation seems to be increased by the auto-release of specific molecules such as bone morphogenetic proteins or chemicals such as Dimethyl Sulfoxide and b-mercaptoethanol or by experimental conditions that increase the cyclic-AMP level. BMSCs arrange in elongated cells to form a flattened layer among which the neuronal processes can be done  ADDIN REFMGR.CITE <Refman><Cite><Author>Woodbury</Author><Year>2000</Year><RecNum>205</RecNum><IDText>Adult rat and human bone marrow stromal cells differentiate into neurons</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>205</Ref_ID><Title_Primary>Adult rat and human bone marrow stromal cells differentiate into neurons</Title_Primary><Authors_Primary>Woodbury,D.</Authors_Primary><Authors_Primary>Schwarz,E.J.</Authors_Primary><Authors_Primary>Prockop,D.J.</Authors_Primary><Authors_Primary>Black,I.B.</Authors_Primary><Date_Primary>2000/8/15</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Line</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Humans</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>Nerve Growth Factor</Keywords><Keywords>Neurofilament Proteins</Keywords><Keywords>Neurons</Keywords><Keywords>pharmacology</Keywords><Keywords>Phenotype</Keywords><Keywords>Phosphopyruvate Hydratase</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Rats</Keywords><Keywords>Receptor,trkA</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stromal Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>364</Start_Page><End_Page>370</End_Page><Periodical>J.Neurosci.Res.</Periodical><Volume>61</Volume><Issue>4</Issue><Misc_3>10.1002/1097-4547(20000815)61:4&lt;364::AID-JNR2&gt;3.0.CO;2-C [pii]</Misc_3><Address>Department of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA. woodburydl@aol.com</Address><Web_URL>PM:10931522</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Neurosci.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(8, 9). Beside neurotrophic factors released by BMSCs, contribution of cell-cell interaction is also essential to prevent neuron dying and survival. Direct cellular interactions promote a proteomic change or a genetic switching in BMSCs, which enables them to mediate different functions  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (10).

Trophic Factors by BMSCs to modulate the microenvironment
Originally thought, BMSCs mediate their therapeutic action by stemness multi-potency now, it has become clear that the secretion of multiple growth factors and cytokines (trophic action) is primarily responsible for therapeutic benefits  ADDIN REFMGR.CITE <Refman><Cite><Author>Prockop</Author><Year>2007</Year><RecNum>120</RecNum><IDText>&quot;Stemness&quot; does not explain the repair of many tissues by mesenchymal stem/multipotent stromal cells (MSCs)</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>120</Ref_ID><Title_Primary>&quot;Stemness&quot; does not explain the repair of many tissues by mesenchymal stem/multipotent stromal cells (MSCs)</Title_Primary><Authors_Primary>Prockop,D.J.</Authors_Primary><Date_Primary>2007/9</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>Gene Therapy</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Multipotent Stem Cells</Keywords><Keywords>physiology</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>241</Start_Page><End_Page>243</End_Page><Periodical>Clin.Pharmacol.Ther.</Periodical><Volume>82</Volume><Issue>3</Issue><Misc_3>6100313 [pii];10.1038/sj.clpt.6100313 [doi]</Misc_3><Address>Tulane Center for Gene Therapy, Tulane University Health Sciences Center, New Orleans, Louisiana, USA. dprocko@tulane.edu</Address><Web_URL>PM:17700588</Web_URL><ZZ_JournalFull><f name="System">Clin.Pharmacol.Ther.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Clin.Pharmacol.Ther.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(11). In addition to replace lost cells, BMSCs provide a source of trophic factors to modulate the immune system and to prevent further neuron-degeneration  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (12). In experimental autoimmune encephalomyelitis (EAE), BMSCs improve clinical outcomes via immunomodulation and reduction in central nervous system inflammation  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (15). Particularly, secreted cytokines play pivotal roles in modulating the microenvironment and inducing morphological changes  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (11,13,14). The studies detected the expression of IL-1�, IL-6, IL-8, MCP-1, VEGF, G-CSF, SCF and IL-11  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (14,16) . Of these cytokines, IL-6 plays an important role in the differentiation and regeneration of various stem cells, inhibits osteoblast development and promotes cell survival and proliferation. While IL-1�, a major intermediary of inflammation and immunological reactions, regulate the expression of IL-6  ADDIN REFMGR.CITE <Refman><Cite><Author>Mracek</Author><Year>2004</Year><RecNum>383</RecNum><IDText>IL-1 and LPS but not IL-6 inhibit differentiation and downregulate PPAR gamma in brown adipocytes</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>383</Ref_ID><Title_Primary>IL-1 and LPS but not IL-6 inhibit differentiation and downregulate PPAR gamma in brown adipocytes</Title_Primary><Authors_Primary>Mracek,T.</Authors_Primary><Authors_Primary>Cannon,B.</Authors_Primary><Authors_Primary>Houstek,J.</Authors_Primary><Date_Primary>2004/4/7</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adipose Tissue</Keywords><Keywords>Adipose Tissue,Brown</Keywords><Keywords>Animals</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Down-Regulation</Keywords><Keywords>drug effects</Keywords><Keywords>genetics</Keywords><Keywords>Genomics</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mammals</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Norepinephrine</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>PPAR gamma</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Time</Keywords><Reprint>Not in File</Reprint><Start_Page>9</Start_Page><End_Page>15</End_Page><Periodical>Cytokine</Periodical><Volume>26</Volume><Issue>1</Issue><Address>Institute of Physiology and Center for Integrated Genomics, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague, Czech Republic</Address><Web_URL>PM:15016406</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cytokine</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(17). Additionally, TSG-6 is another anti-inflammatory factor secreted by BMSCs to mediate disruption  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (18,19). One of the most important cytokines, the vascular endothelial growth factor (VEGF) induces both BMSCs and endothelials for recovery of microvascular injury  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (16,18,20). VEGF is well known for its ability to mobilize bone marrow progenitor cells for participate in myogenesis and angiogenesis  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (21). VEGF can per se be secreted by BMSCs and boost the regenerative activity of progenitor cells to differentiate into myocytes and endothelial cells  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (18,22,23). VEGF well known for its participating in angiogenesis promotes also differentiation of stem cells into neuronal and endothelial cells  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (18, 34). VEGF contributing to progenitor cell mobilization also evokes pronounced trophic factors with angiogenic, cytoprotective and anti-inflammatory properties  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (32). In other side, high levels of VEGF stimulate PDGFR which regulate cell migration and proliferation  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (18,24). 
Even more, MSC-secreted matrix metalloproteinases (MMPs) display crucial roles for beneficial matrix remodeling and BMSC homing at the site of injury. Under hypoxic conditions, the interactions between brain microvascular and BMSCs are enhanced  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (18,20,25,26).
BMSCs are able to elaborate various potentially neuroprotective growth factors such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), glial cell line-derived neurotrophic factor (GDNF), fibroblast growth factor-2, and insulin-like growth factor type 1 ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (28,29). Neuroprotective factors then inhibit death-inducing pathways and also activate a variety of cell survival pathways. For example, BDNF is a member of the neurotrophin family of growth factors that is widely expressed in the adult and developing nervous system. BDNF activates a number of signaling pathways in neurons specially, PI3kinase/Akt pathways. The PI3kinase/Akt signaling pathway is a critical cellular survival. This pathway can be activated by a variety of trophic factors  ADDIN REFMGR.CITE <Refman><Cite><Author>Wilkins</Author><Year>2009</Year><RecNum>472</RecNum><IDText>Human bone marrow-derived mesenchymal stem cells secrete brain-derived neurotrophic factor which promotes neuronal survival in vitro</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>472</Ref_ID><Title_Primary>Human bone marrow-derived mesenchymal stem cells secrete brain-derived neurotrophic factor which promotes neuronal survival in vitro</Title_Primary><Authors_Primary>Wilkins,A.</Authors_Primary><Authors_Primary>Kemp,K.</Authors_Primary><Authors_Primary>Ginty,M.</Authors_Primary><Authors_Primary>Hares,K.</Authors_Primary><Authors_Primary>Mallam,E.</Authors_Primary><Authors_Primary>Scolding,N.</Authors_Primary><Date_Primary>2009/3/27</Date_Primary><Keywords>Antibodies</Keywords><Keywords>Brain-Derived Neurotrophic Factor</Keywords><Keywords>culture</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Neurons</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Periodical>Stem Cell Res.</Periodical><Address>Department of Neurology, Institute of Clinical Neurosciences, Clinical Sciences North Bristol, University of Bristol, Bristol BS16 1LE, UK</Address><Web_URL>PM:19411199</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(27).
Intracellular signaling underlying processes of neuronal cell death is complex, but evidence points to a critical role for both MAPkinase and PI3kinase/Akt signaling pathways. Members of MAPkinase pathways are known to be activated by a variety of signals in neurons and specifically p38 has been implicated in neuronal cell death pathways. Several reports have shown p38 MAPkinase activation during nitric oxide mediated neuronal death vs. trophic factors inhibit the p38 activation and promote survival in this context  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (30).

BMSC mechanisms to attenuate stress condition and inflammatory reactions 
BMSCs are multipotent stem cells express endothelial phenotypes and further increase capillary density and decrease the disrupt size  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (31) , but also by their ability to supply large amounts of angiogenic, anti-apoptotic and mitogenic factors ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA  (32).
The trophic mediators secreted by BMSCs improve organ function by a combination of multiple mechanisms such as attenuating tissue injury, inhibiting fibrotic remodeling, promoting angiogenesis, mobilizing host tissue stem cells, and reducing inflammation  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (20,25,33).
For example, EAE are associated with elevated levels of nitric oxide (NO) within the central nervous system, combined with reductions in trophic support from surrounding glia  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (15). BMSCs protect neurons from NO-mediated damage or trophic deprivation, a process which depend on survival signaling and PI3kinase/Akt pathway. Immune activators cause NO exposure which inhibit PI3kinase/Akt signaling and activate p38 MAPkinase pathway in neurons. Whereas, BMSCs exposure significantly activate the PI3kinase/Akt pathway, while reduce p38 signaling in NO-exposed neurons  ADDIN REFMGR.CITE <Refman><Cite><Author>Wilkins</Author><Year>2009</Year><RecNum>472</RecNum><IDText>Human bone marrow-derived mesenchymal stem cells secrete brain-derived neurotrophic factor which promotes neuronal survival in vitro</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>472</Ref_ID><Title_Primary>Human bone marrow-derived mesenchymal stem cells secrete brain-derived neurotrophic factor which promotes neuronal survival in vitro</Title_Primary><Authors_Primary>Wilkins,A.</Authors_Primary><Authors_Primary>Kemp,K.</Authors_Primary><Authors_Primary>Ginty,M.</Authors_Primary><Authors_Primary>Hares,K.</Authors_Primary><Authors_Primary>Mallam,E.</Authors_Primary><Authors_Primary>Scolding,N.</Authors_Primary><Date_Primary>2009/3/27</Date_Primary><Keywords>Antibodies</Keywords><Keywords>Brain-Derived Neurotrophic Factor</Keywords><Keywords>culture</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Neurons</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Periodical>Stem Cell Res.</Periodical><Address>Department of Neurology, Institute of Clinical Neurosciences, Clinical Sciences North Bristol, University of Bristol, Bristol BS16 1LE, UK</Address><Web_URL>PM:19411199</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(27).
Intravenous injection of autologenic or allogeneic BMSCs strongly suppresses T-lymphocyte proliferation. More recently, the immunosuppressive effects of BMSCs have been found to target T cell proliferation but not its effector function. BMSCs show immunoregulatory function at different phases of T cell responses, the ability to inhibit mitogen-activated CD4+ and CD8+ subpopulations of T cells. For this reason, they have the potential to be exploited in the control of unwanted immune responses, in particular graft versus host disease (GVHD) and autoimmunity ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (39-41). 
Clinical trials of BMSCs have demonstrated no significant adverse side effects even with multiple cell administrations  ADDIN REFMGR.CITE <Refman><Cite><Author>Giordano</Author><Year>2007</Year><RecNum>30</RecNum><IDText>From the laboratory bench to the patient&apos;s bedside: an update on clinical trials with mesenchymal stem cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>30</Ref_ID><Title_Primary>From the laboratory bench to the patient&apos;s bedside: an update on clinical trials with mesenchymal stem cells</Title_Primary><Authors_Primary>Giordano,A.</Authors_Primary><Authors_Primary>Galderisi,U.</Authors_Primary><Authors_Primary>Marino,I.R.</Authors_Primary><Date_Primary>2007/4</Date_Primary><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cardiovascular Diseases</Keywords><Keywords>Clinical Trials as Topic</Keywords><Keywords>cytology</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Therapy</Keywords><Keywords>trends</Keywords><Reprint>Not in File</Reprint><Start_Page>27</Start_Page><End_Page>35</End_Page><Periodical>J.Cell Physiol</Periodical><Volume>211</Volume><Issue>1</Issue><Misc_3>10.1002/jcp.20959 [doi]</Misc_3><Address>Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USA. giordano@temple.edu</Address><Web_URL>PM:17226788</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Cell Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(36). In non-ischemic inflammatory and edema disease, BMSC transplantation attenuates the infiltration of CD68-positive inflammatory cells and MCP-1 expression in milieu, and improves organ function. Hence, MCP-1 is a chemoattractant protein and results in monocyte/macrophage infiltration into the injured tissue and provokes inflammation. In disrupted organ and in response to MCP-1, BMSCs act in a paracrine manner to secret large amounts of angiogenic and anti-apoptotic signals such as VEGF, HGF, insulin-like growth factor-1 and adrenomedullin  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (32, 37-39). Beside anti-inflammatory response, the cells express CCR2 the receptor for MCP-1 which promotes the migration of BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (32,37,39).
Further, capillary density is increased by BMSC transplantation associated with improved organ function and decreased lesion size. 24 h after transplantation, at least 3% of the intravenously administered MSCs will be homed at the damaged site  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (32). 

Molecular Reprogramming of the Injured Tissue, Novel Cellular Mechanisms 
Understanding of how MSCs evoke neuron improvement is ever more controversial. While preventing progressive inflammatory and apoptosis reaction, BMSCs also elicit reparative effects through genetic reprogramming of the microenvironment manifest by alterations in the pattern of cytokine release and attenuation of the activation of proinflammatory transcription factor, NF-�B  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (42,43). Proinflammatory cytokines that are downstream products of the receptor-stimulated NF-�B signaling cascade, such as TNF�, can be the ultimate harmful agents  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (43). Reportedly, the well characterized LPS-evoked release of TNF-� is completely blunted in co-cultures while the spontaneous release of a beneficial cytokine, IL-10 is unaltered. In consistency, MSCs block the activation of NF-�B signaling cascade in cardiac myocytes  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (42). BMSC-derived factors act as powerful benefactors for restoring and maintain Ca2+ signaling to the damaged site  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (44). 
Evidence has emerged a long list of potential soluble factors underlying beneficial action of BMSCs, including stromal derived factor-1�, secreted frizzled-related protein 2 (sfrp-2), IL-10, TNF�- induced protein 6 (TSG-6), and VEGF  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (45). Different protocols have revealed that BMSC conditioned medium could repair stress induced abnormal Ca2+ signaling both in long term (24 h) and acute (3 h) incubations  ADDIN REFMGR.CITE <Refman><Cite><Author>Caplan</Author><Year>2009</Year><RecNum>16</RecNum><IDText>Why are MSCs therapeutic? New data: new insight</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>16</Ref_ID><Title_Primary>Why are MSCs therapeutic? New data: new insight</Title_Primary><Authors_Primary>Caplan,A.I.</Authors_Primary><Date_Primary>2009/1</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Apoptosis</Keywords><Keywords>Autoimmunity</Keywords><Keywords>Cartilage</Keywords><Keywords>Humans</Keywords><Keywords>Immune System</Keywords><Keywords>immunology</Keywords><Keywords>Immunomodulation</Keywords><Keywords>injuries</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mitosis</Keywords><Keywords>pathology</Keywords><Keywords>Pericytes</Keywords><Keywords>physiology</Keywords><Keywords>Stem Cell Niche</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>318</Start_Page><End_Page>324</End_Page><Periodical>J.Pathol.</Periodical><Volume>217</Volume><Issue>2</Issue><Address>Skeletal Research Center, Department of Biology, Case Western Reserve University, Cleveland, OH 44106, USA. arnold.caplan@case.edu</Address><Web_URL>PM:19023885</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Pathol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(46). 
MSCs have direct action on cardiac myocyte responses to stress at the gene transcriptional level that are consistent with their beneficial effects on the organ function. BMSCs exploit the stressors; endotoxin LPS and a downstream signaling proinflammatory cytokine IL-1� implicated in damages associated with sepsis and ischemia/reperfusion  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (46). LPS and pro-inflammatory cytokine IL-1� has proposed to act directly through their cognate receptors TLR4 and ILR, respectively. It has been shown that BMSCs, microglial and myocardial cells also express TLRs. Toll-like receptors (TLRs) are a group of transmembrane proteins which play critical roles in immune responses. The ligand-mediated stimulation of TLRs family can induce apoptosis of microglial, myocardial and endothelial cells  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (47). Alternatively, other studies have observed that LPS, an agonist of TLR4, protects myocytes and human dendritic cells from apoptosis through a NF-kB-dependent PI3K/Akt pathway  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (48). Reports reveal that LPS protect MSCs from oxidative stress-induced apoptosis and enhance proliferation of MSCs via TLR4 and PI3K/Akt pathway  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (48). 
Conclusively, stress-stimulated secretion of a variety of growth factors and cytokines by BMSCs, markedly change the pattern of microinviroment cytokine release, all of which accompanied by a genetic reprogramming and molecular switching. 

BMSCs behavior for Reconstitution of Hypoxic Micro-Vascular 
In ischemic cerebrovascular disease, the injury of brain microvascular endothelial cells (BMEC) induces the opening of the brain barrier border (BBB), which leads to a brain edema and nerve damage. Then, the recovery and neogenesis of ischemic penumbral microvasculature is a key point in the retrieval of injured cells  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (49). BMSCs have become the recent focus of intense research in the treatment of ischemic disease due to their ability to repair and rebuilt of injured microvasculature. Data indicate that under hypoxia BMECs induce BMSCs to differentiate into endothelial cells, whereas BMSCs enhance proliferation and migration of BMECs, and simultaneously increasing the permeability of the BMEC monolayer, presumably through paracrine function  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (50).
Following an injury, there are significantly increased numbers of BMSCs in peripheral blood and at the disrupted site of the injured subjects  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (51), this trend correlates with significantly increased concentrations of the cytokines VEGF and G-CSF, suggestive of a molecular mechanism for BMSCs mobilization, recruitment and homing  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (20). BMSC homing to the site of injury involves the arrest within the vasculature and transendothelial migration followed by chemotaxis at the injured tissue. While arresting in the proper vascular position, BMSCs secrete proteases such as MMPs, and be capable of breaking down the endothelial basement membrane and journeying presumably toward chemotactic agents  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (20, 26).
In terms of the second, however, the collagen matrix is essential for the efficient homing. The putative proteases released into collagen I or collagen IV matrices produce proteolytic fragments for attracting more BMSCs toward the site of injury where the medium is a result of stress  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (25, 26, 52).
MMPs are a family of zinc-dependent proteases and classically described in the context of extracellular matrix remodeling under physiological and pathophysiological conditions. They are very important for BMSCs recruitment, migration and differentiation. High-levels of MMPs can enhance angiogenesis in hypoxic conditions. MMP-9 known as Gelatinase B, for example plays an important role in the migration of BMSCs and capable of degrading type IV collagen (a key component of basement membranes) and gelatin. Both, VEGF and MMP-9 can increase vascular permeability  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (20).
Under hypoxic condition, VEGF and MMPs have been secreted by both BMECs and BMSCs. Hypoxia induces hypoxia-inducible factor-1 (HIF-1), to autocrine more VEGF, the over activity of HIF-1 and stimulate MMP expression in BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (53, 54). 
BMECs are able to induce Flk-1 expression in BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (20). The Flk-1 is one of the earliest markers for endothelial cells, followed in sequence by Tie-2, VE-cadherin, Tie-1, CD34, and vWF expression  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (55). 
Hypoxia results in HIF-1 stabilization, nuclear translocation and transcription of genes containing hypoxia response elements (HRE). HIF-1 interacts with the co-activator protein p300 that results in transactivating of hypoxia responsive genes, which exemplifies the promoter of VEGF gene  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (56). HIF-1 taking a positive role in vascularization, is also considered important in the process of wound repair  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (53, 54). 
Interestingly, NF-�B inflammatory mediators and HIF-1 act at the same target genes, identifying inflammatory signals antagonize the HIF-1. For example, NF-�B interferes with VEGF expression, while causes the iNOS gene activation, in the presence of LPS and TNF-�. Since both transcription factors are essential for wound healing thereby, depending on condition, inflammation and hypoxia behave in synergism or counterpart to influence out come  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (57, 58) . The high HIF-1 activity causes to survive hypoxic/ ischemic stress more successfully by mediating cellular adaptive response to hypoxia. Elevated HIF-1 level also up-regulates MMP1 and MMP3 expression in BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (41). So, it is reasonable to speculate that BMSCs with high HIF-1 level will be less affected by low oxygen level associated with aging. Since the vascular function and blood flow are reduced with age, which lowers oxygen level in tissues and represents a risk factor of age-related diseases ADDIN REFMGR.CITE <Refman><Cite><Author>Dinenno</Author><Year>1999</Year><RecNum>640</RecNum><IDText>Limb blood flow and vascular conductance are reduced with age in healthy humans: relation to elevations in sympathetic nerve activity and declines in oxygen demand</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>640</Ref_ID><Title_Primary>Limb blood flow and vascular conductance are reduced with age in healthy humans: relation to elevations in sympathetic nerve activity and declines in oxygen demand</Title_Primary><Authors_Primary>Dinenno,F.A.</Authors_Primary><Authors_Primary>Jones,P.P.</Authors_Primary><Authors_Primary>Seals,D.R.</Authors_Primary><Authors_Primary>Tanaka,H.</Authors_Primary><Date_Primary>1999/7/13</Date_Primary><Keywords>Adult</Keywords><Keywords>Aging</Keywords><Keywords>blood</Keywords><Keywords>Blood Pressure</Keywords><Keywords>blood supply</Keywords><Keywords>Cardiac Output</Keywords><Keywords>Femoral Artery</Keywords><Keywords>Humans</Keywords><Keywords>innervation</Keywords><Keywords>Leg</Keywords><Keywords>Male</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Muscle,Skeletal</Keywords><Keywords>Oxygen</Keywords><Keywords>Oxygen Consumption</Keywords><Keywords>physiology</Keywords><Keywords>Pressure</Keywords><Keywords>Reference Values</Keywords><Keywords>Regional Blood Flow</Keywords><Keywords>Research</Keywords><Keywords>Sympathetic Nervous System</Keywords><Keywords>Vascular Resistance</Keywords><Reprint>Not in File</Reprint><Start_Page>164</Start_Page><End_Page>170</End_Page><Periodical>Circulation</Periodical><Volume>100</Volume><Issue>2</Issue><Address>Human Cardiovascular Research Laboratory, Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Colorado, USA</Address><Web_URL>PM:10402446</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(59). In addition, high HIF-1 levels promote the migratory activity in the collagen-rich microenvironments, during the recruitment of BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (60). These findings suggest that in spite of being a cell survival signal, higher level of HIF-1 may participate in remodeling and reconstitution for healthy tissue. 

Conclusion
Stem cell-based therapies to repair and replace lost neural cells are a highly promising treatment for CNS degenerative diseases. BMSCs are great promise as therapeutic agents against neurological maladies. They have the ability to differentiate into neural phenotypes and can be readily isolated and auto-transplanted with no risk of immun reaction/rejection. Although multi-lineage differentiation, BMSCs therapeutic benefits have now become attributed to secretion of multiple growth factors and cytokines (trophic action). The cells have direct action on microenvironment cell responses and the pattern of cytokine release.  BMCSs induce genetic reprogramming of milieu gene expression manifest by alterations in the pattern of cytokines and attenuation of pro-inflammatory transcription factors. The change of cytokine pattern is fallowed by prevention of stress-induced apoptosis, appropriate differentiation and immunomodulatory regulation, an important protective outcome. 


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h1q0Jjh1q0JU81�h:p�p&��. ��A!�"�#��$��%�������(2*2�	D<Refman><Cite><Author>Asanuma</Author><Year>2011</Year><RecNum>208</RecNum><IDText>Arterially delivered mesenchymal stem cells prevent obstruction-induced renal fibrosis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>208</Ref_ID><Title_Primary>Arterially delivered mesenchymal stem cells prevent obstruction-induced renal fibrosis</Title_Primary><Authors_Primary>Asanuma,H.</Authors_Primary><Authors_Primary>Vanderbrink,B.A.</Authors_Primary><Authors_Primary>Campbell,M.T.</Authors_Primary><Authors_Primary>Hile,K.L.</Authors_Primary><Authors_Primary>Zhang,H.</Authors_Primary><Authors_Primary>Meldrum,D.R.</Authors_Primary><Authors_Primary>Meldrum,K.K.</Authors_Primary><Date_Primary>2011/6/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Cytokines</Keywords><Keywords>Epithelial-Mesenchymal Transition</Keywords><Keywords>Fibrosis</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Humans</Keywords><Keywords>Intercellular Signaling Peptides and Proteins</Keywords><Keywords>Interleukin-10</Keywords><Keywords>Kidney</Keywords><Keywords>Kidney Diseases</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Models,Animal</Keywords><Keywords>Necrosis</Keywords><Keywords>pathology</Keywords><Keywords>Peptides</Keywords><Keywords>prevention &amp; control</Keywords><Keywords>Proteins</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time</Keywords><Keywords>Transforming Growth Factor beta1</Keywords><Keywords>Transplantation,Heterologous</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Keywords>Ureteral Obstruction</Keywords><Reprint>Not in File</Reprint><Start_Page>e51</Start_Page><End_Page>e59</End_Page><Periodical>J.Surg.Res.</Periodical><Volume>168</Volume><Issue>1</Issue><Address>Department of Urology, Indiana University School of Medicine, Indianapolis, Indianapolis, Indiana 46202, USA</Address><Web_URL>PM:20850784</Web_URL><ZZ_JournalFull><f name="System">J.Surg.Res.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">J.Surg.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Chen</Author><Year>2003</Year><RecNum>10</RecNum><IDText>Intravenous bone marrow stromal cell therapy reduces apoptosis and promotes endogenous cell proliferation after stroke in female rat</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>10</Ref_ID><Title_Primary>Intravenous bone marrow stromal cell therapy reduces apoptosis and promotes endogenous cell proliferation after stroke in female rat</Title_Primary><Authors_Primary>Chen,J.</Authors_Primary><Authors_Primary>Li,Y.</Authors_Primary><Authors_Primary>Katakowski,M.</Authors_Primary><Authors_Primary>Chen,X.</Authors_Primary><Authors_Primary>Wang,L.</Authors_Primary><Authors_Primary>Lu,D.</Authors_Primary><Authors_Primary>Lu,M.</Authors_Primary><Authors_Primary>Gautam,S.C.</Authors_Primary><Authors_Primary>Chopp,M.</Authors_Primary><Date_Primary>2003/9/15</Date_Primary><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Behavior,Animal</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Brain</Keywords><Keywords>Bromodeoxyuridine</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Division</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Dna</Keywords><Keywords>Female</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Glial Fibrillary Acidic Protein</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>In Situ Hybridization</Keywords><Keywords>In Situ Nick-End Labeling</Keywords><Keywords>Infarction,Middle Cerebral Artery</Keywords><Keywords>Ischemia</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Motor Activity</Keywords><Keywords>Nerve Tissue</Keywords><Keywords>Nerve Tissue Proteins</Keywords><Keywords>Neurogenesis</Keywords><Keywords>Nuclear Proteins</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proteins</Keywords><Keywords>Psychomotor Performance</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Wistar</Keywords><Keywords>Reaction Time</Keywords><Keywords>Recovery of Function</Keywords><Keywords>Stroke</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time</Keywords><Keywords>Time Factors</Keywords><Keywords>transplantation</Keywords><Keywords>Tubulin</Keywords><Keywords>von Willebrand Factor</Keywords><Keywords>Y Chromosome</Keywords><Reprint>Not in File</Reprint><Start_Page>778</Start_Page><End_Page>786</End_Page><Periodical>J.Neurosci.Res.</Periodical><Volume>73</Volume><Issue>6</Issue><Address>Department of Neurology, Henry Ford Health Sciences Center, Detroit, Michigan 48202, USA</Address><Web_URL>PM:12949903</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Neurosci.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Nakamizo</Author><Year>2005</Year><RecNum>269</RecNum><IDText>Human bone marrow-derived mesenchymal stem cells in the treatment of gliomas</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>269</Ref_ID><Title_Primary>Human bone marrow-derived mesenchymal stem cells in the treatment of gliomas</Title_Primary><Authors_Primary>Nakamizo,A.</Authors_Primary><Authors_Primary>Marini,F.</Authors_Primary><Authors_Primary>Amano,T.</Authors_Primary><Authors_Primary>Khan,A.</Authors_Primary><Authors_Primary>Studeny,M.</Authors_Primary><Authors_Primary>Gumin,J.</Authors_Primary><Authors_Primary>Chen,J.</Authors_Primary><Authors_Primary>Hentschel,S.</Authors_Primary><Authors_Primary>Vecil,G.</Authors_Primary><Authors_Primary>Dembinski,J.</Authors_Primary><Authors_Primary>Andreeff,M.</Authors_Primary><Authors_Primary>Lang,F.F.</Authors_Primary><Date_Primary>2005/4/15</Date_Primary><Keywords>Animals</Keywords><Keywords>Astrocytes</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Brain</Keywords><Keywords>Brain Neoplasms</Keywords><Keywords>Carotid Arteries</Keywords><Keywords>Cell Movement</Keywords><Keywords>cytology</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Genetic Engineering</Keywords><Keywords>genetics</Keywords><Keywords>Glioblastoma</Keywords><Keywords>Glioma</Keywords><Keywords>Humans</Keywords><Keywords>Injections</Keywords><Keywords>Interferon-beta</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Nude</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Platelet-Derived Growth Factor</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Xenograft Model Antitumor Assays</Keywords><Reprint>Not in File</Reprint><Start_Page>3307</Start_Page><End_Page>3318</End_Page><Periodical>Cancer Res.</Periodical><Volume>65</Volume><Issue>8</Issue><Misc_3>65/8/3307 [pii];10.1158/0008-5472.CAN-04-1874 [doi]</Misc_3><Address>Department of Neurosurgery, Brain Tumor Center, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA</Address><Web_URL>PM:15833864</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cancer Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Ball</Author><Year>2004</Year><RecNum>615</RecNum><IDText>Direct cell contact influences bone marrow mesenchymal stem cell fate</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>615</Ref_ID><Title_Primary>Direct cell contact influences bone marrow mesenchymal stem cell fate</Title_Primary><Authors_Primary>Ball,S.G.</Authors_Primary><Authors_Primary>Shuttleworth,A.C.</Authors_Primary><Authors_Primary>Kielty,C.M.</Authors_Primary><Date_Primary>2004/4</Date_Primary><Keywords>Actins</Keywords><Keywords>Adolescent</Keywords><Keywords>Adult</Keywords><Keywords>analysis</Keywords><Keywords>Biological Markers</Keywords><Keywords>blood</Keywords><Keywords>Blood Vessels</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Communication</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Female</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microfilaments</Keywords><Keywords>Middle Aged</Keywords><Keywords>Muscle Cells</Keywords><Keywords>Myoblasts,Smooth Muscle</Keywords><Keywords>physiology</Keywords><Keywords>Research</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tissue Engineering</Keywords><Reprint>Not in File</Reprint><Start_Page>714</Start_Page><End_Page>727</End_Page><Periodical>Int.J.Biochem.Cell Biol.</Periodical><Volume>36</Volume><Issue>4</Issue><Address>UK Centre for Tissue Engineering, University of Manchester, 2.205 Stopford Building, Oxford Road, Manchester M13 9PT, UK</Address><Web_URL>PM:15010334</Web_URL><ZZ_JournalFull><f name="System">Int.J.Biochem.Cell Biol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Int.J.Biochem.Cell Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�	D<Refman><Cite><Author>Barhum</Author><Year>2010</Year><RecNum>253</RecNum><IDText>Intracerebroventricular transplantation of human mesenchymal stem cells induced to secrete neurotrophic factors attenuates clinical symptoms in a mouse model of multiple sclerosis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>253</Ref_ID><Title_Primary>Intracerebroventricular transplantation of human mesenchymal stem cells induced to secrete neurotrophic factors attenuates clinical symptoms in a mouse model of multiple sclerosis</Title_Primary><Authors_Primary>Barhum,Y.</Authors_Primary><Authors_Primary>Gai-Castro,S.</Authors_Primary><Authors_Primary>Bahat-Stromza,M.</Authors_Primary><Authors_Primary>Barzilay,R.</Authors_Primary><Authors_Primary>Melamed,E.</Authors_Primary><Authors_Primary>Offen,D.</Authors_Primary><Date_Primary>2010/5</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cell Survival</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Multiple Sclerosis</Keywords><Keywords>Nerve Growth Factor</Keywords><Keywords>Nerve Growth Factors</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>T-Lymphocytes</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>129</Start_Page><End_Page>137</End_Page><Periodical>J.Mol.Neurosci.</Periodical><Volume>41</Volume><Issue>1</Issue><Misc_3>10.1007/s12031-009-9302-8 [doi]</Misc_3><Address>Felsenstein Medical Research Center, Tel Aviv University, Sackler School of Medicine, Petach Tikva, 49100, Israel</Address><Web_URL>PM:19902385</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Neurosci.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>X
D<Refman><Cite><Author>Kassis</Author><Year>2008</Year><RecNum>382</RecNum><IDText>Neuroprotection and immunomodulation with mesenchymal stem cells in chronic experimental autoimmune encephalomyelitis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>382</Ref_ID><Title_Primary>Neuroprotection and immunomodulation with mesenchymal stem cells in chronic experimental autoimmune encephalomyelitis</Title_Primary><Authors_Primary>Kassis,I.</Authors_Primary><Authors_Primary>Grigoriadis,N.</Authors_Primary><Authors_Primary>Gowda-Kurkalli,B.</Authors_Primary><Authors_Primary>Mizrachi-Kol,R.</Authors_Primary><Authors_Primary>Ben-Hur,T.</Authors_Primary><Authors_Primary>Slavin,S.</Authors_Primary><Authors_Primary>Abramsky,O.</Authors_Primary><Authors_Primary>Karussis,D.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Axons</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Brain-Derived Neurotrophic Factor</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Central Nervous System</Keywords><Keywords>Chronic Disease</Keywords><Keywords>cytology</Keywords><Keywords>Encephalomyelitis,Autoimmune,Experimental</Keywords><Keywords>genetics</Keywords><Keywords>Glial Fibrillary Acidic Protein</Keywords><Keywords>immunology</Keywords><Keywords>Immunomodulation</Keywords><Keywords>Inflammation</Keywords><Keywords>Lymph Nodes</Keywords><Keywords>Lymphocytes</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Mitogens</Keywords><Keywords>mortality</Keywords><Keywords>Multiple Sclerosis</Keywords><Keywords>Myelin Sheath</Keywords><Keywords>Nerve 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[doi]</Misc_3><Address>Tulane Center for Gene Therapy, Tulane University Health Sciences Center, New Orleans, Louisiana, USA. dprocko@tulane.edu</Address><Web_URL>PM:17700588</Web_URL><ZZ_JournalFull><f name="System">Clin.Pharmacol.Ther.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Clin.Pharmacol.Ther.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Haynesworth</Author><Year>1996</Year><RecNum>616</RecNum><IDText>Cytokine expression by human marrow-derived mesenchymal progenitor cells in vitro: effects of dexamethasone and IL-1 alpha</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>616</Ref_ID><Title_Primary>Cytokine expression by human marrow-derived mesenchymal progenitor cells in vitro: effects of dexamethasone and IL-1 alpha</Title_Primary><Authors_Primary>Haynesworth,S.E.</Authors_Primary><Authors_Primary>Baber,M.A.</Authors_Primary><Authors_Primary>Caplan,A.I.</Authors_Primary><Date_Primary>1996/3</Date_Primary><Keywords>Adult</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Child,Preschool</Keywords><Keywords>Cytokines</Keywords><Keywords>Dexamethasone</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Hematopoiesis</Keywords><Keywords>Humans</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Male</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>pharmacology</Keywords><Keywords>Phenotype</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>585</Start_Page><End_Page>592</End_Page><Periodical>J.Cell Physiol</Periodical><Volume>166</Volume><Issue>3</Issue><Address>Department of Biology, Skeletal Research Center, Case Western Reserve University, Cleveland, Ohio, 44106-7080, USA</Address><Web_URL>PM:8600162</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Cell Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Liu</Author><Year>2005</Year><RecNum>617</RecNum><IDText>Cytokine interactions in mesenchymal stem cells from cord blood</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>617</Ref_ID><Title_Primary>Cytokine interactions in mesenchymal stem cells from cord blood</Title_Primary><Authors_Primary>Liu,C.H.</Authors_Primary><Authors_Primary>Hwang,S.M.</Authors_Primary><Date_Primary>2005/12/21</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>analysis</Keywords><Keywords>Angiogenesis Inducing Agents</Keywords><Keywords>Antigens</Keywords><Keywords>Antigens,Surface</Keywords><Keywords>blood</Keywords><Keywords>CCAAT-Enhancer-Binding Protein-beta</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>chemistry</Keywords><Keywords>Chemokines</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>drug effects</Keywords><Keywords>Fetal Blood</Keywords><Keywords>Flavonoids</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Growth Substances</Keywords><Keywords>Humans</Keywords><Keywords>Imidazoles</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Leptin</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinases</Keywords><Keywords>Osteoprotegerin</Keywords><Keywords>p38 Mitogen-Activated Protein Kinases</Keywords><Keywords>pharmacology</Keywords><Keywords>PPAR gamma</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Protein Array Analysis</Keywords><Keywords>Protein Kinase Inhibitors</Keywords><Keywords>Protein Kinases</Keywords><Keywords>Pyridines</Keywords><Keywords>Receptors,Growth Factor</Keywords><Keywords>Research</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>secretion</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>270</Start_Page><End_Page>279</End_Page><Periodical>Cytokine</Periodical><Volume>32</Volume><Issue>6</Issue><Address>Graduate Institute of Biochemical and Biomedical Engineering, Chang Gung University, Taoyuan, Taiwan. chl@mail.cgu.edu.tw</Address><Web_URL>PM:16377203</Web_URL><ZZ_JournalFull><f name="System">Cytokine</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Cytokine</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>
D<Refman><Cite><Author>Liu</Author><Year>2005</Year><RecNum>617</RecNum><IDText>Cytokine interactions in mesenchymal stem cells from cord blood</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>617</Ref_ID><Title_Primary>Cytokine interactions in mesenchymal stem cells from cord blood</Title_Primary><Authors_Primary>Liu,C.H.</Authors_Primary><Authors_Primary>Hwang,S.M.</Authors_Primary><Date_Primary>2005/12/21</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>analysis</Keywords><Keywords>Angiogenesis Inducing Agents</Keywords><Keywords>Antigens</Keywords><Keywords>Antigens,Surface</Keywords><Keywords>blood</Keywords><Keywords>CCAAT-Enhancer-Binding Protein-beta</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>chemistry</Keywords><Keywords>Chemokines</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>drug effects</Keywords><Keywords>Fetal Blood</Keywords><Keywords>Flavonoids</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Growth Substances</Keywords><Keywords>Humans</Keywords><Keywords>Imidazoles</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Leptin</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinases</Keywords><Keywords>Osteoprotegerin</Keywords><Keywords>p38 Mitogen-Activated Protein Kinases</Keywords><Keywords>pharmacology</Keywords><Keywords>PPAR gamma</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Protein Array Analysis</Keywords><Keywords>Protein Kinase Inhibitors</Keywords><Keywords>Protein Kinases</Keywords><Keywords>Pyridines</Keywords><Keywords>Receptors,Growth Factor</Keywords><Keywords>Research</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>secretion</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>270</Start_Page><End_Page>279</End_Page><Periodical>Cytokine</Periodical><Volume>32</Volume><Issue>6</Issue><Address>Graduate Institute of Biochemical and Biomedical Engineering, Chang Gung University, Taoyuan, Taiwan. chl@mail.cgu.edu.tw</Address><Web_URL>PM:16377203</Web_URL><ZZ_JournalFull><f name="System">Cytokine</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Cytokine</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Choi</Author><Year>2010</Year><RecNum>8</RecNum><IDText>Selection of optimal passage of bone marrow-derived mesenchymal stem cells for stem cell therapy in patients with amyotrophic lateral sclerosis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>8</Ref_ID><Title_Primary>Selection of optimal passage of bone marrow-derived mesenchymal stem cells for stem cell therapy in patients with amyotrophic lateral sclerosis</Title_Primary><Authors_Primary>Choi,M.R.</Authors_Primary><Authors_Primary>Kim,H.Y.</Authors_Primary><Authors_Primary>Park,J.Y.</Authors_Primary><Authors_Primary>Lee,T.Y.</Authors_Primary><Authors_Primary>Baik,C.S.</Authors_Primary><Authors_Primary>Chai,Y.G.</Authors_Primary><Authors_Primary>Jung,K.H.</Authors_Primary><Authors_Primary>Park,K.S.</Authors_Primary><Authors_Primary>Roh,W.</Authors_Primary><Authors_Primary>Kim,K.S.</Authors_Primary><Authors_Primary>Kim,S.H.</Authors_Primary><Date_Primary>2010/3/19</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Amyotrophic Lateral Sclerosis</Keywords><Keywords>Antigens</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Culture Techniques</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Chondrocytes</Keywords><Keywords>culture</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Humans</Keywords><Keywords>Kinetics</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Osteocytes</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>94</Start_Page><End_Page>98</End_Page><Periodical>Neurosci.Lett.</Periodical><Volume>472</Volume><Issue>2</Issue><Address>Division of Molecular and Life Sciences, Hanyang University, Ansan, 426-791, Republic of Korea</Address><Web_URL>PM:20117176</Web_URL><ZZ_JournalStdAbbrev><f name="System">Neurosci.Lett.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>>D<Refman><Cite><Author>Zisa</Author><Year>2009</Year><RecNum>43</RecNum><IDText>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>43</Ref_ID><Title_Primary>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</Title_Primary><Authors_Primary>Zisa,D.</Authors_Primary><Authors_Primary>Shabbir,A.</Authors_Primary><Authors_Primary>Suzuki,G.</Authors_Primary><Authors_Primary>Lee,T.</Authors_Primary><Date_Primary>2009/12/18</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cricetinae</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Swine</Keywords><Keywords>therapy</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>834</Start_Page><End_Page>838</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>390</Volume><Issue>3</Issue><User_Def_5>PMC2788008</User_Def_5><Misc_3>S0006-291X(09)02036-1 [pii];10.1016/j.bbrc.2009.10.058 [doi]</Misc_3><Address>Department of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA</Address><Web_URL>PM:19836359</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Lee</Author><Year>2009</Year><RecNum>625</RecNum><IDText>Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>625</Ref_ID><Title_Primary>Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6</Title_Primary><Authors_Primary>Lee,R.H.</Authors_Primary><Authors_Primary>Pulin,A.A.</Authors_Primary><Authors_Primary>Seo,M.J.</Authors_Primary><Authors_Primary>Kota,D.J.</Authors_Primary><Authors_Primary>Ylostalo,J.</Authors_Primary><Authors_Primary>Larson,B.L.</Authors_Primary><Authors_Primary>Semprun-Prieto,L.</Authors_Primary><Authors_Primary>Delafontaine,P.</Authors_Primary><Authors_Primary>Prockop,D.J.</Authors_Primary><Date_Primary>2009/7/2</Date_Primary><Keywords>Animals</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Adhesion Molecules</Keywords><Keywords>Cell Migration Assays</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>Gene Therapy</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Inflammation</Keywords><Keywords>Inflammation Mediators</Keywords><Keywords>Infusions,Intravenous</Keywords><Keywords>Lung</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Multipotent Stem Cells</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>pathology</Keywords><Keywords>physiopathology</Keywords><Keywords>Pulmonary Embolism</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>54</Start_Page><End_Page>63</End_Page><Periodical>Cell Stem Cell</Periodical><Volume>5</Volume><Issue>1</Issue><Address>Center for Gene Therapy, Tulane University Health Sciences Center, New Orleans, LA 70112, USA</Address><Web_URL>PM:19570514</Web_URL><ZZ_JournalFull><f name="System">Cell Stem Cell</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Cell Stem Cell</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Choi</Author><Year>2010</Year><RecNum>8</RecNum><IDText>Selection of optimal passage of bone marrow-derived mesenchymal stem cells for stem cell therapy in patients with amyotrophic lateral sclerosis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>8</Ref_ID><Title_Primary>Selection of optimal passage of bone marrow-derived mesenchymal stem cells for stem cell therapy in patients with amyotrophic lateral sclerosis</Title_Primary><Authors_Primary>Choi,M.R.</Authors_Primary><Authors_Primary>Kim,H.Y.</Authors_Primary><Authors_Primary>Park,J.Y.</Authors_Primary><Authors_Primary>Lee,T.Y.</Authors_Primary><Authors_Primary>Baik,C.S.</Authors_Primary><Authors_Primary>Chai,Y.G.</Authors_Primary><Authors_Primary>Jung,K.H.</Authors_Primary><Authors_Primary>Park,K.S.</Authors_Primary><Authors_Primary>Roh,W.</Authors_Primary><Authors_Primary>Kim,K.S.</Authors_Primary><Authors_Primary>Kim,S.H.</Authors_Primary><Date_Primary>2010/3/19</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Amyotrophic Lateral Sclerosis</Keywords><Keywords>Antigens</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Culture Techniques</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Chondrocytes</Keywords><Keywords>culture</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Humans</Keywords><Keywords>Kinetics</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Osteocytes</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>94</Start_Page><End_Page>98</End_Page><Periodical>Neurosci.Lett.</Periodical><Volume>472</Volume><Issue>2</Issue><Address>Division of Molecular and Life Sciences, Hanyang University, Ansan, 426-791, Republic of Korea</Address><Web_URL>PM:20117176</Web_URL><ZZ_JournalStdAbbrev><f name="System">Neurosci.Lett.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Zisa</Author><Year>2009</Year><RecNum>43</RecNum><IDText>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>43</Ref_ID><Title_Primary>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</Title_Primary><Authors_Primary>Zisa,D.</Authors_Primary><Authors_Primary>Shabbir,A.</Authors_Primary><Authors_Primary>Suzuki,G.</Authors_Primary><Authors_Primary>Lee,T.</Authors_Primary><Date_Primary>2009/12/18</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cricetinae</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Swine</Keywords><Keywords>therapy</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>834</Start_Page><End_Page>838</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>390</Volume><Issue>3</Issue><User_Def_5>PMC2788008</User_Def_5><Misc_3>S0006-291X(09)02036-1 [pii];10.1016/j.bbrc.2009.10.058 [doi]</Misc_3><Address>Department of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA</Address><Web_URL>PM:19836359</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Liu</Author><Year>2008</Year><RecNum>15</RecNum><IDText>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>15</Ref_ID><Title_Primary>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</Title_Primary><Authors_Primary>Liu,K.</Authors_Primary><Authors_Primary>Chi,L.</Authors_Primary><Authors_Primary>Guo,L.</Authors_Primary><Authors_Primary>Liu,X.</Authors_Primary><Authors_Primary>Luo,C.</Authors_Primary><Authors_Primary>Zhang,S.</Authors_Primary><Authors_Primary>He,G.</Authors_Primary><Date_Primary>2008/1</Date_Primary><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Antibodies</Keywords><Keywords>Antibodies,Blocking</Keywords><Keywords>blood supply</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Brain</Keywords><Keywords>Brain Ischemia</Keywords><Keywords>Capillary Permeability</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>59</Start_Page><End_Page>67</End_Page><Periodical>Microvasc.Res.</Periodical><Volume>75</Volume><Issue>1</Issue><Address>Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China</Address><Web_URL>PM:17662311</Web_URL><ZZ_JournalStdAbbrev><f name="System">Microvasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�	D<Refman><Cite><Author>Asahara</Author><Year>1999</Year><RecNum>20</RecNum><IDText>VEGF contributes to postnatal neovascularization by mobilizing bone marrow-derived endothelial progenitor cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>20</Ref_ID><Title_Primary>VEGF contributes to postnatal neovascularization by mobilizing bone marrow-derived endothelial progenitor cells</Title_Primary><Authors_Primary>Asahara,T.</Authors_Primary><Authors_Primary>Takahashi,T.</Authors_Primary><Authors_Primary>Masuda,H.</Authors_Primary><Authors_Primary>Kalka,C.</Authors_Primary><Authors_Primary>Chen,D.</Authors_Primary><Authors_Primary>Iwaguro,H.</Authors_Primary><Authors_Primary>Inai,Y.</Authors_Primary><Authors_Primary>Silver,M.</Authors_Primary><Authors_Primary>Isner,J.M.</Authors_Primary><Date_Primary>1999/7/15</Date_Primary><Keywords>Animals</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Cornea</Keywords><Keywords>Corneal Neovascularization</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelial Growth Factors</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Kinetics</Keywords><Keywords>Leukocytes,Mononuclear</Keywords><Keywords>Lymphokines</Keywords><Keywords>Male</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>pharmacology</Keywords><Keywords>Stem Cells</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>3964</Start_Page><End_Page>3972</End_Page><Periodical>EMBO J.</Periodical><Volume>18</Volume><Issue>14</Issue><Address>Departments of Medicine (Cardiology) and Biomedical Research, St Elizabeth&apos;s Medical Center, Tufts University School of Medicine, 736 Cambridge Street, Boston, MA 02135, USA</Address><Web_URL>PM:10406801</Web_URL><ZZ_JournalStdAbbrev><f name="System">EMBO 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Cells</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chondrocytes</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Osteocytes</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Stem Cells</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-1</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>377</Start_Page><End_Page>384</End_Page><Periodical>Stem Cells</Periodical><Volume>22</Volume><Issue>3</Issue><Address>Institute of Polymer Research Dresden and The Max Bergmann Center of Biomaterials Dresden, Dresden, Germany. oswald@ipfdd.de</Address><Web_URL>PM:15153614</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cells</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Song</Author><Year>2007</Year><RecNum>608</RecNum><IDText>VEGF is critical for spontaneous differentiation of stem cells into cardiomyocytes</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>608</Ref_ID><Title_Primary>VEGF is critical for spontaneous differentiation of stem cells into cardiomyocytes</Title_Primary><Authors_Primary>Song,Y.H.</Authors_Primary><Authors_Primary>Gehmert,S.</Authors_Primary><Authors_Primary>Sadat,S.</Authors_Primary><Authors_Primary>Pinkernell,K.</Authors_Primary><Authors_Primary>Bai,X.</Authors_Primary><Authors_Primary>Matthias,N.</Authors_Primary><Authors_Primary>Alt,E.</Authors_Primary><Date_Primary>2007/3/23</Date_Primary><Keywords>Adipose Tissue</Keywords><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>Cardiac Myosins</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>GATA4 Transcription Factor</Keywords><Keywords>Homeodomain Proteins</Keywords><Keywords>Humans</Keywords><Keywords>Light</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Myosin Light Chains</Keywords><Keywords>Myosins</Keywords><Keywords>pathology</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Rats</Keywords><Keywords>Regeneration</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Subcutaneous Fat</Keywords><Keywords>therapy</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Troponin T</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>999</Start_Page><End_Page>1003</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>354</Volume><Issue>4</Issue><Address>Department of Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA</Address><Web_URL>PM:17276389</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Zisa</Author><Year>2009</Year><RecNum>43</RecNum><IDText>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>43</Ref_ID><Title_Primary>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</Title_Primary><Authors_Primary>Zisa,D.</Authors_Primary><Authors_Primary>Shabbir,A.</Authors_Primary><Authors_Primary>Suzuki,G.</Authors_Primary><Authors_Primary>Lee,T.</Authors_Primary><Date_Primary>2009/12/18</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cricetinae</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Swine</Keywords><Keywords>therapy</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>834</Start_Page><End_Page>838</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>390</Volume><Issue>3</Issue><User_Def_5>PMC2788008</User_Def_5><Misc_3>S0006-291X(09)02036-1 [pii];10.1016/j.bbrc.2009.10.058 [doi]</Misc_3><Address>Department of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA</Address><Web_URL>PM:19836359</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Iwaguro</Author><Year>2002</Year><RecNum>29</RecNum><IDText>Endothelial progenitor cell vascular endothelial growth factor gene transfer for vascular regeneration</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>29</Ref_ID><Title_Primary>Endothelial progenitor cell vascular endothelial growth factor gene transfer for vascular regeneration</Title_Primary><Authors_Primary>Iwaguro,H.</Authors_Primary><Authors_Primary>Yamaguchi,J.</Authors_Primary><Authors_Primary>Kalka,C.</Authors_Primary><Authors_Primary>Murasawa,S.</Authors_Primary><Authors_Primary>Masuda,H.</Authors_Primary><Authors_Primary>Hayashi,S.</Authors_Primary><Authors_Primary>Silver,M.</Authors_Primary><Authors_Primary>Li,T.</Authors_Primary><Authors_Primary>Isner,J.M.</Authors_Primary><Authors_Primary>Asahara,T.</Authors_Primary><Date_Primary>2002/2/12</Date_Primary><Keywords>Adenoviridae</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Blood</Keywords><Keywords>blood supply</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Division</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Dendritic Cells</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Endothelial Growth Factors</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Female</Keywords><Keywords>Gene Therapy</Keywords><Keywords>Gene Transfer,Horizontal</Keywords><Keywords>Genetic Vectors</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Ischemia</Keywords><Keywords>Lymphokines</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Nude</Keywords><Keywords>Microcirculation</Keywords><Keywords>Muscle,Skeletal</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time</Keywords><Keywords>Transgenes</Keywords><Keywords>transplantation</Keywords><Keywords>Treatment Outcome</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>732</Start_Page><End_Page>738</End_Page><Periodical>Circulation</Periodical><Volume>105</Volume><Issue>6</Issue><Address>Division of Cardiovascular Research and Medicine, St Elizabeth&apos;s Medical Center, Tufts University School of Medicine, Boston, Mass 02135, USA</Address><Web_URL>PM:11839630</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Nagaya</Author><Year>2005</Year><RecNum>3</RecNum><IDText>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>3</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</Title_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Itoh,T.</Authors_Primary><Authors_Primary>Iwase,T.</Authors_Primary><Authors_Primary>Murakami,S.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Fujii,T.</Authors_Primary><Authors_Primary>Uematsu,M.</Authors_Primary><Authors_Primary>Ohgushi,H.</Authors_Primary><Authors_Primary>Yamagishi,M.</Authors_Primary><Authors_Primary>Tokudome,T.</Authors_Primary><Authors_Primary>Mori,H.</Authors_Primary><Authors_Primary>Miyatake,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Date_Primary>2005/8/23</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cardiomyopathy,Dilated</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Connexin 43</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Fibrosis</Keywords><Keywords>Growth Substances</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Immunization</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Myocardial Contraction</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Pluripotent Stem Cells</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Keywords>Troponin T</Keywords><Keywords>ultrasonography</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>1128</Start_Page><End_Page>1135</End_Page><Periodical>Circulation</Periodical><Volume>112</Volume><Issue>8</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan. nnagaya@ri.ncvc.go.jp</Address><Web_URL>PM:16103243</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Zisa</Author><Year>2009</Year><RecNum>43</RecNum><IDText>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>43</Ref_ID><Title_Primary>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</Title_Primary><Authors_Primary>Zisa,D.</Authors_Primary><Authors_Primary>Shabbir,A.</Authors_Primary><Authors_Primary>Suzuki,G.</Authors_Primary><Authors_Primary>Lee,T.</Authors_Primary><Date_Primary>2009/12/18</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cricetinae</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Swine</Keywords><Keywords>therapy</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>834</Start_Page><End_Page>838</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>390</Volume><Issue>3</Issue><User_Def_5>PMC2788008</User_Def_5><Misc_3>S0006-291X(09)02036-1 [pii];10.1016/j.bbrc.2009.10.058 [doi]</Misc_3><Address>Department of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA</Address><Web_URL>PM:19836359</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ball</Author><Year>2007</Year><RecNum>619</RecNum><IDText>Vascular endothelial growth factor can signal through platelet-derived growth factor receptors</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>619</Ref_ID><Title_Primary>Vascular endothelial growth factor can signal through platelet-derived growth factor receptors</Title_Primary><Authors_Primary>Ball,S.G.</Authors_Primary><Authors_Primary>Shuttleworth,C.A.</Authors_Primary><Authors_Primary>Kielty,C.M.</Authors_Primary><Date_Primary>2007/5/7</Date_Primary><Keywords>Adolescent</Keywords><Keywords>Adult</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Dermis</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Humans</Keywords><Keywords>Infant,Newborn</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Platelet-Derived Growth Factor</Keywords><Keywords>Protein Binding</Keywords><Keywords>Receptor,Platelet-Derived Growth Factor alpha</Keywords><Keywords>Receptor,Platelet-Derived Growth Factor beta</Keywords><Keywords>Regeneration</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>Tyrosine</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>489</Start_Page><End_Page>500</End_Page><Periodical>J.Cell Biol.</Periodical><Volume>177</Volume><Issue>3</Issue><Address>UK Centre for Tissue Engineering and 2Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, The University of Manchester, Manchester, England, UK</Address><Web_URL>PM:17470632</Web_URL><ZZ_JournalFull><f name="System">J.Cell Biol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">J.Cell Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�%D<Refman><Cite><Author>Mauney</Author><Year>2010</Year><RecNum>127</RecNum><IDText>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen matrix</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>127</Ref_ID><Title_Primary>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen matrix</Title_Primary><Authors_Primary>Mauney,J.</Authors_Primary><Authors_Primary>Olsen,B.R.</Authors_Primary><Authors_Primary>Volloch,V.</Authors_Primary><Date_Primary>2010/10</Date_Primary><Keywords>Adipose Tissue</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Antibodies</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Collagen</Keywords><Keywords>Collagen Type I</Keywords><Keywords>Collagen Type IV</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cysteine Proteinase Inhibitors</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Extracellular Matrix</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Heat-Shock Response</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Immunoprecipitation</Keywords><Keywords>injuries</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Serine Endopeptidases</Keywords><Keywords>Serine Proteinase Inhibitors</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stromal Cells</Keywords><Keywords>Wounds and Injuries</Keywords><Reprint>Not in File</Reprint><Start_Page>657</Start_Page><End_Page>663</End_Page><Periodical>Matrix Biol.</Periodical><Volume>29</Volume><Issue>8</Issue><Misc_3>S0945-053X(10)00133-2 [pii];10.1016/j.matbio.2010.08.008 [doi]</Misc_3><Address>Children&apos;s Hospital, Boston, United States</Address><Web_URL>PM:20828613</Web_URL><ZZ_JournalFull><f name="System">Matrix Biol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Matrix Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Steingen</Author><Year>2008</Year><RecNum>405</RecNum><IDText>Characterization of key mechanisms in transmigration and invasion of mesenchymal stem cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>405</Ref_ID><Title_Primary>Characterization of key mechanisms in transmigration and invasion of mesenchymal stem cells</Title_Primary><Authors_Primary>Steingen,C.</Authors_Primary><Authors_Primary>Brenig,F.</Authors_Primary><Authors_Primary>Baumgartner,L.</Authors_Primary><Authors_Primary>Schmidt,J.</Authors_Primary><Authors_Primary>Schmidt,A.</Authors_Primary><Authors_Primary>Bloch,W.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>Aged</Keywords><Keywords>Aged,80 and over</Keywords><Keywords>Antigens,CD29</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Female</Keywords><Keywords>Gelatinases</Keywords><Keywords>Humans</Keywords><Keywords>Integrin alpha4beta1</Keywords><Keywords>Integrins</Keywords><Keywords>Male</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardium</Keywords><Keywords>Organ Specificity</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Pseudopodia</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time</Keywords><Keywords>Vascular Cell Adhesion Molecule-1</Keywords><Keywords>Veins</Keywords><Reprint>Not in File</Reprint><Start_Page>1072</Start_Page><End_Page>1084</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>44</Volume><Issue>6</Issue><Address>German Sport University Cologne, Institute for Cardiovascular Research and Sport Medicine, Department for Molecular and Cellular Sport Medicine, Cologne, Germany</Address><Web_URL>PM:18462748</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Liu</Author><Year>2008</Year><RecNum>15</RecNum><IDText>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>15</Ref_ID><Title_Primary>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic 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Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>59</Start_Page><End_Page>67</End_Page><Periodical>Microvasc.Res.</Periodical><Volume>75</Volume><Issue>1</Issue><Address>Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China</Address><Web_URL>PM:17662311</Web_URL><ZZ_JournalStdAbbrev><f name="System">Microvasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Zisa</Author><Year>2009</Year><RecNum>43</RecNum><IDText>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>43</Ref_ID><Title_Primary>Vascular endothelial growth factor (VEGF) as a key therapeutic trophic factor in bone marrow mesenchymal stem cell-mediated cardiac repair</Title_Primary><Authors_Primary>Zisa,D.</Authors_Primary><Authors_Primary>Shabbir,A.</Authors_Primary><Authors_Primary>Suzuki,G.</Authors_Primary><Authors_Primary>Lee,T.</Authors_Primary><Date_Primary>2009/12/18</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cricetinae</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Swine</Keywords><Keywords>therapy</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>834</Start_Page><End_Page>838</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>390</Volume><Issue>3</Issue><User_Def_5>PMC2788008</User_Def_5><Misc_3>S0006-291X(09)02036-1 [pii];10.1016/j.bbrc.2009.10.058 [doi]</Misc_3><Address>Department of Biochemistry and Center for Research in Cardiovascular Medicine, University at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA</Address><Web_URL>PM:19836359</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Boucherie</Author><Year>2008</Year><RecNum>473</RecNum><IDText>In vitro evidence for impaired neuroprotective capacities of adult mesenchymal stem cells derived from a rat model of familial amyotrophic lateral sclerosis (hSOD1(G93A))</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>473</Ref_ID><Title_Primary>In vitro evidence for impaired neuroprotective capacities of adult mesenchymal stem cells derived from a rat model of familial amyotrophic lateral sclerosis (hSOD1(G93A))</Title_Primary><Authors_Primary>Boucherie,C.</Authors_Primary><Authors_Primary>Caumont,A.S.</Authors_Primary><Authors_Primary>Maloteaux,J.M.</Authors_Primary><Authors_Primary>Hermans,E.</Authors_Primary><Date_Primary>2008/8</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Amino Acid Transport System X-AG</Keywords><Keywords>Amyotrophic Lateral Sclerosis</Keywords><Keywords>Animals</Keywords><Keywords>Animals,Genetically Modified</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>drug effects</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>genetics</Keywords><Keywords>Glial Cell Line-Derived Neurotrophic Factor</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Neural Stem Cells</Keywords><Keywords>Neurodegenerative Diseases</Keywords><Keywords>Neurons</Keywords><Keywords>Neuroprotective Agents</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Research</Keywords><Keywords>Riluzole</Keywords><Keywords>Stem Cells</Keywords><Keywords>Superoxide Dismutase</Keywords><Keywords>therapy</Keywords><Keywords>Up-Regulation</Keywords><Reprint>Not in File</Reprint><Start_Page>557</Start_Page><End_Page>561</End_Page><Periodical>Exp.Neurol.</Periodical><Volume>212</Volume><Issue>2</Issue><Address>Laboratoire de Pharmacologie Experimentale, Universite catholique de Louvain, 54.10, Av. Hippocrate 54, 1200 Brussels, Belgium</Address><Web_URL>PM:18539273</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Neurol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Crisostomo</Author><Year>2008</Year><RecNum>195</RecNum><IDText>Human mesenchymal stem cells stimulated by TNF-alpha, LPS, or hypoxia produce growth factors by an NF kappa B- but not JNK-dependent mechanism</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>195</Ref_ID><Title_Primary>Human mesenchymal stem cells stimulated by TNF-alpha, LPS, or hypoxia produce growth factors by an NF kappa B- but not JNK-dependent mechanism</Title_Primary><Authors_Primary>Crisostomo,P.R.</Authors_Primary><Authors_Primary>Wang,Y.</Authors_Primary><Authors_Primary>Markel,T.A.</Authors_Primary><Authors_Primary>Wang,M.</Authors_Primary><Authors_Primary>Lahm,T.</Authors_Primary><Authors_Primary>Meldrum,D.R.</Authors_Primary><Date_Primary>2008/3</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Shape</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>drug effects</Keywords><Keywords>Enzyme Activation</Keywords><Keywords>enzymology</Keywords><Keywords>Extracellular Signal-Regulated MAP Kinases</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Insulin-Like Growth Factor I</Keywords><Keywords>Intercellular Signaling Peptides and Proteins</Keywords><Keywords>JNK Mitogen-Activated Protein Kinases</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>Peptide Fragments</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>Protein Kinase Inhibitors</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>C675</Start_Page><End_Page>C682</End_Page><Periodical>Am.J.Physiol Cell Physiol</Periodical><Volume>294</Volume><Issue>3</Issue><Misc_3>00437.2007 [pii];10.1152/ajpcell.00437.2007 [doi]</Misc_3><Address>Departments of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA</Address><Web_URL>PM:18234850</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Cell Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Cell Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>"
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Media,Conditioned</Keywords><Keywords>Cytoprotection</Keywords><Keywords>Demyelinating Diseases</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>drug effects</Keywords><Keywords>Encephalitis</Keywords><Keywords>Glial Cell Line-Derived Neurotrophic Factor</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Insulin-Like Growth Factor I</Keywords><Keywords>MAP Kinase Signaling System</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinases</Keywords><Keywords>Models,Neurological</Keywords><Keywords>Multiple Sclerosis</Keywords><Keywords>Nerve Growth Factors</Keywords><Keywords>Neurons</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Donors</Keywords><Keywords>p38 Mitogen-Activated Protein Kinases</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Protein Kinases</Keywords><Keywords>Rats</Keywords><Keywords>toxicity</Keywords><Keywords>Wallerian Degeneration</Keywords><Reprint>Not in File</Reprint><Start_Page>1487</Start_Page><End_Page>1496</End_Page><Periodical>J.Neurochem.</Periodical><Volume>92</Volume><Issue>6</Issue><Address>Department of Clinical Neurosciences and Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK. aw255@cam.ac.uk</Address><Web_URL>PM:15748166</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Neurochem.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Nagaya</Author><Year>2004</Year><RecNum>661</RecNum><IDText>Intravenous administration of mesenchymal stem cells improves cardiac function in rats with acute myocardial infarction through angiogenesis and myogenesis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>661</Ref_ID><Title_Primary>Intravenous administration of mesenchymal stem cells improves cardiac function in rats with acute myocardial infarction through angiogenesis and myogenesis</Title_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Authors_Primary>Fujii,T.</Authors_Primary><Authors_Primary>Iwase,T.</Authors_Primary><Authors_Primary>Ohgushi,H.</Authors_Primary><Authors_Primary>Itoh,T.</Authors_Primary><Authors_Primary>Uematsu,M.</Authors_Primary><Authors_Primary>Yamagishi,M.</Authors_Primary><Authors_Primary>Mori,H.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Date_Primary>2004/12</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Capillaries</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Diastole</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Hand</Keywords><Keywords>Injections,Intravenous</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mesoderm</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Keywords>Troponin T</Keywords><Keywords>Ventricular Pressure</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>H2670</Start_Page><End_Page>H2676</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>287</Volume><Issue>6</Issue><Address>Dept. of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan. nnagaya@ri.ncvc.go.jp</Address><Web_URL>PM:15284059</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Nagaya</Author><Year>2005</Year><RecNum>3</RecNum><IDText>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>3</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</Title_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Itoh,T.</Authors_Primary><Authors_Primary>Iwase,T.</Authors_Primary><Authors_Primary>Murakami,S.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Fujii,T.</Authors_Primary><Authors_Primary>Uematsu,M.</Authors_Primary><Authors_Primary>Ohgushi,H.</Authors_Primary><Authors_Primary>Yamagishi,M.</Authors_Primary><Authors_Primary>Tokudome,T.</Authors_Primary><Authors_Primary>Mori,H.</Authors_Primary><Authors_Primary>Miyatake,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Date_Primary>2005/8/23</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cardiomyopathy,Dilated</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Connexin 43</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Fibrosis</Keywords><Keywords>Growth Substances</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Immunization</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Myocardial Contraction</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Pluripotent Stem Cells</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Keywords>Troponin T</Keywords><Keywords>ultrasonography</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>1128</Start_Page><End_Page>1135</End_Page><Periodical>Circulation</Periodical><Volume>112</Volume><Issue>8</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan. nnagaya@ri.ncvc.go.jp</Address><Web_URL>PM:16103243</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>$D<Refman><Cite><Author>Mauney</Author><Year>2010</Year><RecNum>127</RecNum><IDText>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen matrix</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>127</Ref_ID><Title_Primary>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen matrix</Title_Primary><Authors_Primary>Mauney,J.</Authors_Primary><Authors_Primary>Olsen,B.R.</Authors_Primary><Authors_Primary>Volloch,V.</Authors_Primary><Date_Primary>2010/10</Date_Primary><Keywords>Adipose Tissue</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Antibodies</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Collagen</Keywords><Keywords>Collagen Type I</Keywords><Keywords>Collagen Type IV</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cysteine Proteinase Inhibitors</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Extracellular Matrix</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Heat-Shock Response</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Immunoprecipitation</Keywords><Keywords>injuries</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Serine Endopeptidases</Keywords><Keywords>Serine Proteinase Inhibitors</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stromal Cells</Keywords><Keywords>Wounds and Injuries</Keywords><Reprint>Not in File</Reprint><Start_Page>657</Start_Page><End_Page>663</End_Page><Periodical>Matrix Biol.</Periodical><Volume>29</Volume><Issue>8</Issue><Misc_3>S0945-053X(10)00133-2 [pii];10.1016/j.matbio.2010.08.008 [doi]</Misc_3><Address>Children&apos;s Hospital, Boston, United States</Address><Web_URL>PM:20828613</Web_URL><ZZ_JournalFull><f name="System">Matrix Biol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Matrix Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Eggenhofer</Author><Year>2011</Year><RecNum>385</RecNum><IDText>Features of synergism between mesenchymal stem cells and immunosuppressive drugs in a murine heart transplantation model</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>385</Ref_ID><Title_Primary>Features of synergism between mesenchymal stem cells and immunosuppressive drugs in a murine heart transplantation model</Title_Primary><Authors_Primary>Eggenhofer,E.</Authors_Primary><Authors_Primary>Renner,P.</Authors_Primary><Authors_Primary>Soeder,Y.</Authors_Primary><Authors_Primary>Popp,F.C.</Authors_Primary><Authors_Primary>Hoogduijn,M.J.</Authors_Primary><Authors_Primary>Geissler,E.K.</Authors_Primary><Authors_Primary>Schlitt,H.J.</Authors_Primary><Authors_Primary>Dahlke,M.H.</Authors_Primary><Date_Primary>2011/9</Date_Primary><Keywords>analysis</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Graft Survival</Keywords><Keywords>Heart</Keywords><Keywords>Heart Transplantation</Keywords><Keywords>Immunomodulation</Keywords><Keywords>Lymphocytes</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>methods</Keywords><Keywords>Organ Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>T-Lymphocytes</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>141</Start_Page><End_Page>147</End_Page><Periodical>Transpl.Immunol.</Periodical><Volume>25</Volume><Issue>2-3</Issue><Address>Department of Surgery, University Medical Center Regensburg, Regensburg, Germany</Address><Web_URL>PM:21704160</Web_URL><ZZ_JournalStdAbbrev><f name="System">Transpl.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Liu</Author><Year>2008</Year><RecNum>15</RecNum><IDText>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>15</Ref_ID><Title_Primary>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic 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Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>59</Start_Page><End_Page>67</End_Page><Periodical>Microvasc.Res.</Periodical><Volume>75</Volume><Issue>1</Issue><Address>Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China</Address><Web_URL>PM:17662311</Web_URL><ZZ_JournalStdAbbrev><f name="System">Microvasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>X
D<Refman><Cite><Author>Kassis</Author><Year>2008</Year><RecNum>382</RecNum><IDText>Neuroprotection and immunomodulation with mesenchymal stem cells in chronic experimental autoimmune encephalomyelitis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>382</Ref_ID><Title_Primary>Neuroprotection and immunomodulation with mesenchymal stem cells in chronic experimental autoimmune encephalomyelitis</Title_Primary><Authors_Primary>Kassis,I.</Authors_Primary><Authors_Primary>Grigoriadis,N.</Authors_Primary><Authors_Primary>Gowda-Kurkalli,B.</Authors_Primary><Authors_Primary>Mizrachi-Kol,R.</Authors_Primary><Authors_Primary>Ben-Hur,T.</Authors_Primary><Authors_Primary>Slavin,S.</Authors_Primary><Authors_Primary>Abramsky,O.</Authors_Primary><Authors_Primary>Karussis,D.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Axons</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Brain-Derived Neurotrophic Factor</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Central Nervous System</Keywords><Keywords>Chronic Disease</Keywords><Keywords>cytology</Keywords><Keywords>Encephalomyelitis,Autoimmune,Experimental</Keywords><Keywords>genetics</Keywords><Keywords>Glial Fibrillary Acidic Protein</Keywords><Keywords>immunology</Keywords><Keywords>Immunomodulation</Keywords><Keywords>Inflammation</Keywords><Keywords>Lymph Nodes</Keywords><Keywords>Lymphocytes</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Mitogens</Keywords><Keywords>mortality</Keywords><Keywords>Multiple Sclerosis</Keywords><Keywords>Myelin Sheath</Keywords><Keywords>Nerve Regeneration</Keywords><Keywords>Neuroimmunomodulation</Keywords><Keywords>Oligodendroglia</Keywords><Keywords>pathology</Keywords><Keywords>prevention &amp; control</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stromal Cells</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>753</Start_Page><End_Page>761</End_Page><Periodical>Arch.Neurol.</Periodical><Volume>65</Volume><Issue>6</Issue><Address>Department of Neurology and Agnes-Ginges Center for Neurogenetics, Jerusalem, Israel</Address><Web_URL>PM:18541795</Web_URL><ZZ_JournalStdAbbrev><f name="System">Arch.Neurol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Xu</Author><Year>2007</Year><RecNum>663</RecNum><IDText>Immunosuppressive properties of cloned bone marrow mesenchymal stem cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>663</Ref_ID><Title_Primary>Immunosuppressive properties of cloned bone marrow mesenchymal stem cells</Title_Primary><Authors_Primary>Xu,G.</Authors_Primary><Authors_Primary>Zhang,L.</Authors_Primary><Authors_Primary>Ren,G.</Authors_Primary><Authors_Primary>Yuan,Z.</Authors_Primary><Authors_Primary>Zhang,Y.</Authors_Primary><Authors_Primary>Zhao,R.C.</Authors_Primary><Authors_Primary>Shi,Y.</Authors_Primary><Date_Primary>2007/3</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Communication</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Clone Cells</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>genetics</Keywords><Keywords>Graft Survival</Keywords><Keywords>Humans</Keywords><Keywords>Immune Tolerance</Keywords><Keywords>immunology</Keywords><Keywords>Ionomycin</Keywords><Keywords>Lymphocyte Activation</Keywords><Keywords>Lymphocytes</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred BALB C</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>microbiology</Keywords><Keywords>pharmacology</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Skin</Keywords><Keywords>Skin Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tetradecanoylphorbol Acetate</Keywords><Keywords>Transplantation,Homologous</Keywords><Reprint>Not in File</Reprint><Start_Page>240</Start_Page><End_Page>248</End_Page><Periodical>Cell Res.</Periodical><Volume>17</Volume><Issue>3</Issue><Address>Department of Molecular Genetics, Microbiology and Immunology, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854, USA</Address><Web_URL>PM:17325691</Web_URL><ZZ_JournalFull><f name="System">Cell Res.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Dai</Author><Year>2007</Year><RecNum>388</RecNum><IDText>HIF-1alpha induced-VEGF overexpression in bone marrow stem cells protects cardiomyocytes against ischemia</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>388</Ref_ID><Title_Primary>HIF-1alpha induced-VEGF overexpression in bone marrow stem cells protects cardiomyocytes against ischemia</Title_Primary><Authors_Primary>Dai,Y.</Authors_Primary><Authors_Primary>Xu,M.</Authors_Primary><Authors_Primary>Wang,Y.</Authors_Primary><Authors_Primary>Pasha,Z.</Authors_Primary><Authors_Primary>Li,T.</Authors_Primary><Authors_Primary>Ashraf,M.</Authors_Primary><Date_Primary>2007/6</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>Antibodies</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>DNA Fragmentation</Keywords><Keywords>drug effects</Keywords><Keywords>Enzyme-Linked Immunosorbent Assay</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>injuries</Keywords><Keywords>Ischemia</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Proteins</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>Up-Regulation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>1036</Start_Page><End_Page>1044</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>42</Volume><Issue>6</Issue><Address>Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA</Address><Web_URL>PM:17498737</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ramasamy</Author><Year>2008</Year><RecNum>622</RecNum><IDText>The immunosuppressive effects of human bone marrow-derived mesenchymal stem cells target T cell proliferation but not its effector function</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>622</Ref_ID><Title_Primary>The immunosuppressive effects of human bone marrow-derived mesenchymal stem cells target T cell proliferation but not its effector function</Title_Primary><Authors_Primary>Ramasamy,R.</Authors_Primary><Authors_Primary>Tong,C.K.</Authors_Primary><Authors_Primary>Seow,H.F.</Authors_Primary><Authors_Primary>Vidyadaran,S.</Authors_Primary><Authors_Primary>Dazzi,F.</Authors_Primary><Date_Primary>2008/2</Date_Primary><Keywords>Adult</Keywords><Keywords>Autoimmunity</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>CD4-Positive T-Lymphocytes</Keywords><Keywords>CD8-Positive T-Lymphocytes</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>cytology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Fluoresceins</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Immunosuppression</Keywords><Keywords>Lymphocyte Activation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>pathology</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Succinimides</Keywords><Keywords>Thymidine</Keywords><Reprint>Not in File</Reprint><Start_Page>131</Start_Page><End_Page>136</End_Page><Periodical>Cell Immunol.</Periodical><Volume>251</Volume><Issue>2</Issue><Address>Department of Pathology, Immunology Unit, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor, Malaysia. r.rajesh@medic.upm.edu.my</Address><Web_URL>PM:18502411</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cell Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>
D<Refman><Cite><Author>Ohnishi</Author><Year>2007</Year><RecNum>682</RecNum><IDText>Transplantation of mesenchymal stem cells attenuates myocardial injury and dysfunction in a rat model of acute myocarditis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>682</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells attenuates myocardial injury and dysfunction in a rat model of acute myocarditis</Title_Primary><Authors_Primary>Ohnishi,S.</Authors_Primary><Authors_Primary>Yanagawa,B.</Authors_Primary><Authors_Primary>Tanaka,K.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Obata,H.</Authors_Primary><Authors_Primary>Kataoka,M.</Authors_Primary><Authors_Primary>Kodama,M.</Authors_Primary><Authors_Primary>Ishibashi-Ueda,H.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Date_Primary>2007/1</Date_Primary><Keywords>Acute Disease</Keywords><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Creatine Kinase</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Heart</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Ischemia</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Myocarditis</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiopathology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>88</Start_Page><End_Page>97</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>42</Volume><Issue>1</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Fujishirodai 5-7-1, Osaka 565-8565, Japan</Address><Web_URL>PM:17101147</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>2D<Refman><Cite><Author>Ohnishi</Author><Year>2007</Year><RecNum>682</RecNum><IDText>Transplantation of mesenchymal stem cells attenuates myocardial injury and dysfunction in a rat model of acute myocarditis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>682</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells attenuates myocardial injury and dysfunction in a rat model of acute myocarditis</Title_Primary><Authors_Primary>Ohnishi,S.</Authors_Primary><Authors_Primary>Yanagawa,B.</Authors_Primary><Authors_Primary>Tanaka,K.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Obata,H.</Authors_Primary><Authors_Primary>Kataoka,M.</Authors_Primary><Authors_Primary>Kodama,M.</Authors_Primary><Authors_Primary>Ishibashi-Ueda,H.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Date_Primary>2007/1</Date_Primary><Keywords>Acute Disease</Keywords><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Creatine Kinase</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Heart</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Ischemia</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Myocarditis</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiopathology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>88</Start_Page><End_Page>97</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>42</Volume><Issue>1</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Fujishirodai 5-7-1, Osaka 565-8565, Japan</Address><Web_URL>PM:17101147</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Nagaya</Author><Year>2005</Year><RecNum>3</RecNum><IDText>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>3</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</Title_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Itoh,T.</Authors_Primary><Authors_Primary>Iwase,T.</Authors_Primary><Authors_Primary>Murakami,S.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Fujii,T.</Authors_Primary><Authors_Primary>Uematsu,M.</Authors_Primary><Authors_Primary>Ohgushi,H.</Authors_Primary><Authors_Primary>Yamagishi,M.</Authors_Primary><Authors_Primary>Tokudome,T.</Authors_Primary><Authors_Primary>Mori,H.</Authors_Primary><Authors_Primary>Miyatake,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Date_Primary>2005/8/23</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cardiomyopathy,Dilated</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Connexin 43</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Fibrosis</Keywords><Keywords>Growth Substances</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Immunization</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Myocardial Contraction</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Pluripotent Stem Cells</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Keywords>Troponin T</Keywords><Keywords>ultrasonography</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>1128</Start_Page><End_Page>1135</End_Page><Periodical>Circulation</Periodical><Volume>112</Volume><Issue>8</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan. nnagaya@ri.ncvc.go.jp</Address><Web_URL>PM:16103243</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ramasamy</Author><Year>2008</Year><RecNum>622</RecNum><IDText>The immunosuppressive effects of human bone marrow-derived mesenchymal stem cells target T cell proliferation but not its effector function</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>622</Ref_ID><Title_Primary>The immunosuppressive effects of human bone marrow-derived mesenchymal stem cells target T cell proliferation but not its effector function</Title_Primary><Authors_Primary>Ramasamy,R.</Authors_Primary><Authors_Primary>Tong,C.K.</Authors_Primary><Authors_Primary>Seow,H.F.</Authors_Primary><Authors_Primary>Vidyadaran,S.</Authors_Primary><Authors_Primary>Dazzi,F.</Authors_Primary><Date_Primary>2008/2</Date_Primary><Keywords>Adult</Keywords><Keywords>Autoimmunity</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>CD4-Positive T-Lymphocytes</Keywords><Keywords>CD8-Positive T-Lymphocytes</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>cytology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Fluoresceins</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Immunosuppression</Keywords><Keywords>Lymphocyte Activation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>pathology</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Succinimides</Keywords><Keywords>Thymidine</Keywords><Reprint>Not in File</Reprint><Start_Page>131</Start_Page><End_Page>136</End_Page><Periodical>Cell Immunol.</Periodical><Volume>251</Volume><Issue>2</Issue><Address>Department of Pathology, Immunology Unit, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor, Malaysia. r.rajesh@medic.upm.edu.my</Address><Web_URL>PM:18502411</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cell Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Nagaya</Author><Year>2005</Year><RecNum>3</RecNum><IDText>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>3</Ref_ID><Title_Primary>Transplantation of mesenchymal stem cells improves cardiac function in a rat model of dilated cardiomyopathy</Title_Primary><Authors_Primary>Nagaya,N.</Authors_Primary><Authors_Primary>Kangawa,K.</Authors_Primary><Authors_Primary>Itoh,T.</Authors_Primary><Authors_Primary>Iwase,T.</Authors_Primary><Authors_Primary>Murakami,S.</Authors_Primary><Authors_Primary>Miyahara,Y.</Authors_Primary><Authors_Primary>Fujii,T.</Authors_Primary><Authors_Primary>Uematsu,M.</Authors_Primary><Authors_Primary>Ohgushi,H.</Authors_Primary><Authors_Primary>Yamagishi,M.</Authors_Primary><Authors_Primary>Tokudome,T.</Authors_Primary><Authors_Primary>Mori,H.</Authors_Primary><Authors_Primary>Miyatake,K.</Authors_Primary><Authors_Primary>Kitamura,S.</Authors_Primary><Date_Primary>2005/8/23</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Capillaries</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cardiomyopathy,Dilated</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Connexin 43</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Fibrosis</Keywords><Keywords>Growth Substances</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Immunization</Keywords><Keywords>Japan</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>Mesoderm</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Myocardial Contraction</Keywords><Keywords>Myocardium</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Pluripotent Stem Cells</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Regenerative Medicine</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Tissue Engineering</Keywords><Keywords>transplantation</Keywords><Keywords>Troponin T</Keywords><Keywords>ultrasonography</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>1128</Start_Page><End_Page>1135</End_Page><Periodical>Circulation</Periodical><Volume>112</Volume><Issue>8</Issue><Address>Department of Regenerative Medicine and Tissue Engineering, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan. nnagaya@ri.ncvc.go.jp</Address><Web_URL>PM:16103243</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Hall</Author><Year>2006</Year><RecNum>623</RecNum><IDText>Regulating the regulator: NF-kappaB signaling in heart</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>623</Ref_ID><Title_Primary>Regulating the regulator: NF-kappaB signaling in heart</Title_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>Hasday,J.D.</Authors_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Date_Primary>2006/10</Date_Primary><Keywords>Acetylation</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cytosol</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>Heart</Keywords><Keywords>Heart Diseases</Keywords><Keywords>Humans</Keywords><Keywords>I-kappa B Proteins</Keywords><Keywords>injuries</Keywords><Keywords>metabolism</Keywords><Keywords>Models,Biological</Keywords><Keywords>Myocardium</Keywords><Keywords>NF-kappa B</Keywords><Keywords>pathology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Protein Processing,Post-Translational</Keywords><Keywords>Proteins</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Transcription,Genetic</Keywords><Reprint>Not in File</Reprint><Start_Page>580</Start_Page><End_Page>591</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>41</Volume><Issue>4</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA</Address><Web_URL>PM:16949095</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Rogers</Author><Year>2011</Year><RecNum>609</RecNum><IDText>Mesenchymal stem cells stimulate protective genetic reprogramming of injured cardiac ventricular myocytes</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>609</Ref_ID><Title_Primary>Mesenchymal stem cells stimulate protective genetic reprogramming of injured cardiac ventricular myocytes</Title_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Authors_Primary>Pati,S.</Authors_Primary><Authors_Primary>Gaa,S.</Authors_Primary><Authors_Primary>Riley,D.</Authors_Primary><Authors_Primary>Khakoo,A.Y.</Authors_Primary><Authors_Primary>Patel,S.</Authors_Primary><Authors_Primary>Wardlow,R.D.</Authors_Primary><Authors_Primary>Frederick,C.A.</Authors_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>He,L.P.</Authors_Primary><Authors_Primary>Lederer,W.J.</Authors_Primary><Date_Primary>2011/2</Date_Primary><Keywords>Adjuvants,Immunologic</Keywords><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Antibodies</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Heart Ventricles</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Interleukin-18</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Models,Biological</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nuclear Reprogramming</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Reprint>Not in File</Reprint><Start_Page>346</Start_Page><End_Page>356</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>50</Volume><Issue>2</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. trogers@som.umaryland.edu</Address><Web_URL>PM:20837021</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Hall</Author><Year>2006</Year><RecNum>623</RecNum><IDText>Regulating the regulator: NF-kappaB signaling in heart</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>623</Ref_ID><Title_Primary>Regulating the regulator: NF-kappaB signaling in heart</Title_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>Hasday,J.D.</Authors_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Date_Primary>2006/10</Date_Primary><Keywords>Acetylation</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cytosol</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>Heart</Keywords><Keywords>Heart Diseases</Keywords><Keywords>Humans</Keywords><Keywords>I-kappa B Proteins</Keywords><Keywords>injuries</Keywords><Keywords>metabolism</Keywords><Keywords>Models,Biological</Keywords><Keywords>Myocardium</Keywords><Keywords>NF-kappa B</Keywords><Keywords>pathology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Protein Processing,Post-Translational</Keywords><Keywords>Proteins</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Transcription,Genetic</Keywords><Reprint>Not in File</Reprint><Start_Page>580</Start_Page><End_Page>591</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>41</Volume><Issue>4</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA</Address><Web_URL>PM:16949095</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Wright</Author><Year>2002</Year><RecNum>624</RecNum><IDText>Endotoxin stress-response in cardiomyocytes: NF-kappaB activation and tumor necrosis factor-alpha expression</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>624</Ref_ID><Title_Primary>Endotoxin stress-response in cardiomyocytes: NF-kappaB activation and tumor necrosis factor-alpha expression</Title_Primary><Authors_Primary>Wright,G.</Authors_Primary><Authors_Primary>Singh,I.S.</Authors_Primary><Authors_Primary>Hasday,J.D.</Authors_Primary><Authors_Primary>Farrance,I.K.</Authors_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>Cross,A.S.</Authors_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Date_Primary>2002/3</Date_Primary><Keywords>Acetylcysteine</Keywords><Keywords>analogs &amp; derivatives</Keywords><Keywords>Animals</Keywords><Keywords>Animals,Newborn</Keywords><Keywords>Antioxidants</Keywords><Keywords>Blotting,Western</Keywords><Keywords>Cell Nucleus</Keywords><Keywords>Cysteine Endopeptidases</Keywords><Keywords>Cysteine Proteinase Inhibitors</Keywords><Keywords>cytology</Keywords><Keywords>Cytoplasm</Keywords><Keywords>drug effects</Keywords><Keywords>Endotoxins</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Multienzyme Complexes</Keywords><Keywords>Myeloid Cells</Keywords><Keywords>Myocardium</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Proteasome Endopeptidase Complex</Keywords><Keywords>Pyrrolidines</Keywords><Keywords>Research</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Stress,Physiological</Keywords><Keywords>Thiocarbamates</Keywords><Keywords>toxicity</Keywords><Keywords>Transcription,Genetic</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Reprint>Not in File</Reprint><Start_Page>H872</Start_Page><End_Page>H879</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>282</Volume><Issue>3</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA</Address><Web_URL>PM:11834481</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Wright</Author><Year>2002</Year><RecNum>624</RecNum><IDText>Endotoxin stress-response in cardiomyocytes: NF-kappaB activation and tumor necrosis factor-alpha expression</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>624</Ref_ID><Title_Primary>Endotoxin stress-response in cardiomyocytes: NF-kappaB activation and tumor necrosis factor-alpha expression</Title_Primary><Authors_Primary>Wright,G.</Authors_Primary><Authors_Primary>Singh,I.S.</Authors_Primary><Authors_Primary>Hasday,J.D.</Authors_Primary><Authors_Primary>Farrance,I.K.</Authors_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>Cross,A.S.</Authors_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Date_Primary>2002/3</Date_Primary><Keywords>Acetylcysteine</Keywords><Keywords>analogs &amp; derivatives</Keywords><Keywords>Animals</Keywords><Keywords>Animals,Newborn</Keywords><Keywords>Antioxidants</Keywords><Keywords>Blotting,Western</Keywords><Keywords>Cell Nucleus</Keywords><Keywords>Cysteine Endopeptidases</Keywords><Keywords>Cysteine Proteinase Inhibitors</Keywords><Keywords>cytology</Keywords><Keywords>Cytoplasm</Keywords><Keywords>drug effects</Keywords><Keywords>Endotoxins</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Multienzyme Complexes</Keywords><Keywords>Myeloid Cells</Keywords><Keywords>Myocardium</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Proteasome Endopeptidase Complex</Keywords><Keywords>Pyrrolidines</Keywords><Keywords>Research</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Stress,Physiological</Keywords><Keywords>Thiocarbamates</Keywords><Keywords>toxicity</Keywords><Keywords>Transcription,Genetic</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Reprint>Not in File</Reprint><Start_Page>H872</Start_Page><End_Page>H879</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>282</Volume><Issue>3</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA</Address><Web_URL>PM:11834481</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Burchfield</Author><Year>2008</Year><RecNum>123</RecNum><IDText>Interleukin-10 from transplanted bone marrow mononuclear cells contributes to cardiac protection after myocardial infarction</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>123</Ref_ID><Title_Primary>Interleukin-10 from transplanted bone marrow mononuclear cells contributes to cardiac protection after myocardial infarction</Title_Primary><Authors_Primary>Burchfield,J.S.</Authors_Primary><Authors_Primary>Iwasaki,M.</Authors_Primary><Authors_Primary>Koyanagi,M.</Authors_Primary><Authors_Primary>Urbich,C.</Authors_Primary><Authors_Primary>Rosenthal,N.</Authors_Primary><Authors_Primary>Zeiher,A.M.</Authors_Primary><Authors_Primary>Dimmeler,S.</Authors_Primary><Date_Primary>2008/7/18</Date_Primary><Keywords>Adult</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Collagen</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Female</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Interleukin-10</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Knockout</Keywords><Keywords>Microarray Analysis</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>Neutrophils</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>prevention &amp; control</Keywords><Keywords>Stroke</Keywords><Keywords>T-Lymphocytes</Keywords><Keywords>therapy</Keywords><Keywords>Ventricular Function,Left</Keywords><Keywords>Ventricular Remodeling</Keywords><Reprint>Not in File</Reprint><Start_Page>203</Start_Page><End_Page>211</End_Page><Periodical>Circ.Res.</Periodical><Volume>103</Volume><Issue>2</Issue><Misc_3>CIRCRESAHA.108.178475 [pii];10.1161/CIRCRESAHA.108.178475 [doi]</Misc_3><Address>Department of Molecular Cardiology, Internal Medicine III, University of Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany</Address><Web_URL>PM:18566343</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circ.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Rogers</Author><Year>2011</Year><RecNum>609</RecNum><IDText>Mesenchymal stem cells stimulate protective genetic reprogramming of injured cardiac ventricular myocytes</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>609</Ref_ID><Title_Primary>Mesenchymal stem cells stimulate protective genetic reprogramming of injured cardiac ventricular myocytes</Title_Primary><Authors_Primary>Rogers,T.B.</Authors_Primary><Authors_Primary>Pati,S.</Authors_Primary><Authors_Primary>Gaa,S.</Authors_Primary><Authors_Primary>Riley,D.</Authors_Primary><Authors_Primary>Khakoo,A.Y.</Authors_Primary><Authors_Primary>Patel,S.</Authors_Primary><Authors_Primary>Wardlow,R.D.</Authors_Primary><Authors_Primary>Frederick,C.A.</Authors_Primary><Authors_Primary>Hall,G.</Authors_Primary><Authors_Primary>He,L.P.</Authors_Primary><Authors_Primary>Lederer,W.J.</Authors_Primary><Date_Primary>2011/2</Date_Primary><Keywords>Adjuvants,Immunologic</Keywords><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Antibodies</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>Heart Ventricles</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Interleukin-18</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Models,Biological</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nuclear Reprogramming</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Reprint>Not in File</Reprint><Start_Page>346</Start_Page><End_Page>356</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>50</Volume><Issue>2</Issue><Address>Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. trogers@som.umaryland.edu</Address><Web_URL>PM:20837021</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Bujak</Author><Year>2009</Year><RecNum>213</RecNum><IDText>The role of IL-1 in the pathogenesis of heart disease</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>213</Ref_ID><Title_Primary>The role of IL-1 in the pathogenesis of heart disease</Title_Primary><Authors_Primary>Bujak,M.</Authors_Primary><Authors_Primary>Frangogiannis,N.G.</Authors_Primary><Date_Primary>2009/5</Date_Primary><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Apoptosis</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Heart</Keywords><Keywords>Heart Diseases</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Inflammation</Keywords><Keywords>Interleukin 1 Receptor Antagonist Protein</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Interleukin-1alpha</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Matrix Metalloproteinases</Keywords><Keywords>metabolism</Keywords><Keywords>Metalloproteases</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Receptors,Interleukin-1 Type I</Keywords><Keywords>Signal Transduction</Keywords><Keywords>therapeutic use</Keywords><Reprint>Not in File</Reprint><Start_Page>165</Start_Page><End_Page>176</End_Page><Periodical>Arch.Immunol.Ther.Exp.(Warsz.)</Periodical><Volume>57</Volume><Issue>3</Issue><User_Def_5>PMC2788964</User_Def_5><Misc_3>10.1007/s00005-009-0024-y [doi]</Misc_3><Address>Section of Cardiovascular Sciences, Baylor College of Medicine, Houston, TX 77030, USA</Address><Web_URL>PM:19479203</Web_URL><ZZ_JournalFull><f name="System">Arch.Immunol.Ther.Exp.(Warsz.)</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Arch.Immunol.Ther.Exp.(Warsz.)</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Chao</Author><Year>2009</Year><RecNum>687</RecNum><IDText>Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>687</Ref_ID><Title_Primary>Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart</Title_Primary><Authors_Primary>Chao,W.</Authors_Primary><Date_Primary>2009/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cell Survival</Keywords><Keywords>deficiency</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Immunity,Innate</Keywords><Keywords>Infection</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Ischemic Preconditioning,Myocardial</Keywords><Keywords>Ligands</Keywords><Keywords>Myeloid Differentiation Factor 88</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Toll-Like Receptors</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Ventricular Function</Keywords><Keywords>Ventricular Remodeling</Keywords><Reprint>Not in File</Reprint><Start_Page>H1</Start_Page><End_Page>12</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>296</Volume><Issue>1</Issue><Address>Dept. of Anesthesia &amp; Critical Care, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114, USA. wchao@partners.org</Address><Web_URL>PM:19011041</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Crisostomo</Author><Year>2008</Year><RecNum>195</RecNum><IDText>Human mesenchymal stem cells stimulated by TNF-alpha, LPS, or hypoxia produce growth factors by an NF kappa B- but not JNK-dependent mechanism</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>195</Ref_ID><Title_Primary>Human mesenchymal stem cells stimulated by TNF-alpha, LPS, or hypoxia produce growth factors by an NF kappa B- but not JNK-dependent mechanism</Title_Primary><Authors_Primary>Crisostomo,P.R.</Authors_Primary><Authors_Primary>Wang,Y.</Authors_Primary><Authors_Primary>Markel,T.A.</Authors_Primary><Authors_Primary>Wang,M.</Authors_Primary><Authors_Primary>Lahm,T.</Authors_Primary><Authors_Primary>Meldrum,D.R.</Authors_Primary><Date_Primary>2008/3</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Shape</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>drug effects</Keywords><Keywords>Enzyme Activation</Keywords><Keywords>enzymology</Keywords><Keywords>Extracellular Signal-Regulated MAP Kinases</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Insulin-Like Growth Factor I</Keywords><Keywords>Intercellular Signaling Peptides and Proteins</Keywords><Keywords>JNK Mitogen-Activated Protein Kinases</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>Peptide Fragments</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>Protein Kinase Inhibitors</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Stem Cells</Keywords><Keywords>surgery</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>C675</Start_Page><End_Page>C682</End_Page><Periodical>Am.J.Physiol Cell Physiol</Periodical><Volume>294</Volume><Issue>3</Issue><Misc_3>00437.2007 [pii];10.1152/ajpcell.00437.2007 [doi]</Misc_3><Address>Departments of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA</Address><Web_URL>PM:18234850</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Cell Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Cell Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Gnecchi</Author><Year>2006</Year><RecNum>222</RecNum><IDText>Evidence supporting paracrine hypothesis for Akt-modified mesenchymal stem cell-mediated cardiac protection and functional improvement</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>222</Ref_ID><Title_Primary>Evidence supporting paracrine hypothesis for Akt-modified mesenchymal stem cell-mediated cardiac protection and functional improvement</Title_Primary><Authors_Primary>Gnecchi,M.</Authors_Primary><Authors_Primary>He,H.</Authors_Primary><Authors_Primary>Noiseux,N.</Authors_Primary><Authors_Primary>Liang,O.D.</Authors_Primary><Authors_Primary>Zhang,L.</Authors_Primary><Authors_Primary>Morello,F.</Authors_Primary><Authors_Primary>Mu,H.</Authors_Primary><Authors_Primary>Melo,L.G.</Authors_Primary><Authors_Primary>Pratt,R.E.</Authors_Primary><Authors_Primary>Ingwall,J.S.</Authors_Primary><Authors_Primary>Dzau,V.J.</Authors_Primary><Date_Primary>2006/4</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cytoprotection</Keywords><Keywords>Female</Keywords><Keywords>Fibroblast Growth Factors</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Hepatocyte Growth Factor</Keywords><Keywords>Insulin-Like Growth Factor I</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proto-Oncogene Proteins c-akt</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Thymosin</Keywords><Keywords>Up-Regulation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Ventricular Remodeling</Keywords><Reprint>Not in File</Reprint><Start_Page>661</Start_Page><End_Page>669</End_Page><Periodical>FASEB J.</Periodical><Volume>20</Volume><Issue>6</Issue><Misc_3>20/6/661 [pii];10.1096/fj.05-5211com [doi]</Misc_3><Address>Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA</Address><Web_URL>PM:16581974</Web_URL><ZZ_JournalFull><f name="System">FASEB J.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">FASEB J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Lee</Author><Year>2009</Year><RecNum>625</RecNum><IDText>Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>625</Ref_ID><Title_Primary>Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6</Title_Primary><Authors_Primary>Lee,R.H.</Authors_Primary><Authors_Primary>Pulin,A.A.</Authors_Primary><Authors_Primary>Seo,M.J.</Authors_Primary><Authors_Primary>Kota,D.J.</Authors_Primary><Authors_Primary>Ylostalo,J.</Authors_Primary><Authors_Primary>Larson,B.L.</Authors_Primary><Authors_Primary>Semprun-Prieto,L.</Authors_Primary><Authors_Primary>Delafontaine,P.</Authors_Primary><Authors_Primary>Prockop,D.J.</Authors_Primary><Date_Primary>2009/7/2</Date_Primary><Keywords>Animals</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Adhesion Molecules</Keywords><Keywords>Cell Migration Assays</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>Gene Therapy</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Inflammation</Keywords><Keywords>Inflammation Mediators</Keywords><Keywords>Infusions,Intravenous</Keywords><Keywords>Lung</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Multipotent Stem Cells</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>pathology</Keywords><Keywords>physiopathology</Keywords><Keywords>Pulmonary Embolism</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>54</Start_Page><End_Page>63</End_Page><Periodical>Cell Stem Cell</Periodical><Volume>5</Volume><Issue>1</Issue><Address>Center for Gene Therapy, Tulane University Health Sciences Center, New Orleans, LA 70112, USA</Address><Web_URL>PM:19570514</Web_URL><ZZ_JournalFull><f name="System">Cell Stem Cell</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Cell Stem Cell</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Bujak</Author><Year>2009</Year><RecNum>213</RecNum><IDText>The role of IL-1 in the pathogenesis of heart disease</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>213</Ref_ID><Title_Primary>The role of IL-1 in the pathogenesis of heart disease</Title_Primary><Authors_Primary>Bujak,M.</Authors_Primary><Authors_Primary>Frangogiannis,N.G.</Authors_Primary><Date_Primary>2009/5</Date_Primary><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Apoptosis</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Heart</Keywords><Keywords>Heart Diseases</Keywords><Keywords>Heart Failure</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Inflammation</Keywords><Keywords>Interleukin 1 Receptor Antagonist Protein</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Interleukin-1alpha</Keywords><Keywords>Interleukin-1beta</Keywords><Keywords>Matrix Metalloproteinases</Keywords><Keywords>metabolism</Keywords><Keywords>Metalloproteases</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Receptors,Interleukin-1 Type I</Keywords><Keywords>Signal Transduction</Keywords><Keywords>therapeutic use</Keywords><Reprint>Not in File</Reprint><Start_Page>165</Start_Page><End_Page>176</End_Page><Periodical>Arch.Immunol.Ther.Exp.(Warsz.)</Periodical><Volume>57</Volume><Issue>3</Issue><User_Def_5>PMC2788964</User_Def_5><Misc_3>10.1007/s00005-009-0024-y [doi]</Misc_3><Address>Section of Cardiovascular Sciences, Baylor College of Medicine, Houston, TX 77030, USA</Address><Web_URL>PM:19479203</Web_URL><ZZ_JournalFull><f name="System">Arch.Immunol.Ther.Exp.(Warsz.)</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Arch.Immunol.Ther.Exp.(Warsz.)</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Chao</Author><Year>2009</Year><RecNum>687</RecNum><IDText>Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>687</Ref_ID><Title_Primary>Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart</Title_Primary><Authors_Primary>Chao,W.</Authors_Primary><Date_Primary>2009/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cell Survival</Keywords><Keywords>deficiency</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Immunity,Innate</Keywords><Keywords>Infection</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Ischemic Preconditioning,Myocardial</Keywords><Keywords>Ligands</Keywords><Keywords>Myeloid Differentiation Factor 88</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Toll-Like Receptors</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Ventricular Function</Keywords><Keywords>Ventricular Remodeling</Keywords><Reprint>Not in File</Reprint><Start_Page>H1</Start_Page><End_Page>12</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>296</Volume><Issue>1</Issue><Address>Dept. of Anesthesia &amp; Critical Care, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114, USA. wchao@partners.org</Address><Web_URL>PM:19011041</Web_URL><ZZ_JournalFull><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Am.J.Physiol Heart Circ.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Jung</Author><Year>2005</Year><RecNum>393</RecNum><IDText>TLR4, but not TLR2, signals autoregulatory apoptosis of cultured microglia: a critical role of IFN-beta as a decision maker</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>393</Ref_ID><Title_Primary>TLR4, but not TLR2, signals autoregulatory apoptosis of cultured microglia: a critical role of IFN-beta as a decision maker</Title_Primary><Authors_Primary>Jung,D.Y.</Authors_Primary><Authors_Primary>Lee,H.</Authors_Primary><Authors_Primary>Jung,B.Y.</Authors_Primary><Authors_Primary>Ock,J.</Authors_Primary><Authors_Primary>Lee,M.S.</Authors_Primary><Authors_Primary>Lee,W.H.</Authors_Primary><Authors_Primary>Suk,K.</Authors_Primary><Date_Primary>2005/5/15</Date_Primary><Keywords>Adaptor Proteins,Signal Transducing</Keywords><Keywords>agonists</Keywords><Keywords>Animals</Keywords><Keywords>Antigens,CD14</Keywords><Keywords>Antigens,Differentiation</Keywords><Keywords>Antigens,Ly</Keywords><Keywords>Apoptosis</Keywords><Keywords>biosynthesis</Keywords><Keywords>Brain</Keywords><Keywords>Caspase 3</Keywords><Keywords>Caspases</Keywords><Keywords>Cell Death</Keywords><Keywords>Cell Line</Keywords><Keywords>cytology</Keywords><Keywords>DNA-Binding Proteins</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Interferon Regulatory Factor-3</Keywords><Keywords>Interferon-beta</Keywords><Keywords>Jurkat Cells</Keywords><Keywords>Ligands</Keywords><Keywords>Lymphocyte Antigen 96</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C3H</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Knockout</Keywords><Keywords>Microglia</Keywords><Keywords>Myeloid Differentiation Factor 88</Keywords><Keywords>Peptidoglycan</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Receptors,Immunologic</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Toll-Like Receptor 2</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>6467</Start_Page><End_Page>6476</End_Page><Periodical>J.Immunol.</Periodical><Volume>174</Volume><Issue>10</Issue><Address>Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Korea</Address><Web_URL>PM:15879150</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Niu</Author><Year>2008</Year><RecNum>392</RecNum><IDText>Protection against lipopolysaccharide-induced myocardial dysfunction in mice by cardiac-specific expression of soluble Fas</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>392</Ref_ID><Title_Primary>Protection against lipopolysaccharide-induced myocardial dysfunction in mice by cardiac-specific expression of soluble Fas</Title_Primary><Authors_Primary>Niu,J.</Authors_Primary><Authors_Primary>Azfer,A.</Authors_Primary><Authors_Primary>Kolattukudy,P.E.</Authors_Primary><Date_Primary>2008/1</Date_Primary><Keywords>analogs &amp; derivatives</Keywords><Keywords>Animals</Keywords><Keywords>Antigens,CD95</Keywords><Keywords>Apoptosis</Keywords><Keywords>biosynthesis</Keywords><Keywords>Caspase 3</Keywords><Keywords>Caspase 7</Keywords><Keywords>Cell Death</Keywords><Keywords>chemically induced</Keywords><Keywords>complications</Keywords><Keywords>Cytokines</Keywords><Keywords>drug effects</Keywords><Keywords>Echocardiography</Keywords><Keywords>Enzyme Activation</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Inflammation</Keywords><Keywords>injuries</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Lung</Keywords><Keywords>Lung Injury</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Myocardium</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Synthase Type II</Keywords><Keywords>Organ Specificity</Keywords><Keywords>pharmacology</Keywords><Keywords>physiopathology</Keywords><Keywords>Sepsis</Keywords><Keywords>Solubility</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Tyrosine</Keywords><Reprint>Not in File</Reprint><Start_Page>160</Start_Page><End_Page>169</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>44</Volume><Issue>1</Issue><Address>Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA. jniu@mail.ucf.edu</Address><Web_URL>PM:17996250</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Bannerman</Author><Year>2002</Year><RecNum>686</RecNum><IDText>TIRAP mediates endotoxin-induced NF-kappaB activation and apoptosis in endothelial cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>686</Ref_ID><Title_Primary>TIRAP mediates endotoxin-induced NF-kappaB activation and apoptosis in endothelial cells</Title_Primary><Authors_Primary>Bannerman,D.D.</Authors_Primary><Authors_Primary>Erwert,R.D.</Authors_Primary><Authors_Primary>Winn,R.K.</Authors_Primary><Authors_Primary>Harlan,J.M.</Authors_Primary><Date_Primary>2002/7/5</Date_Primary><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cell Death</Keywords><Keywords>Cell Line</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>genetics</Keywords><Keywords>Glycoproteins</Keywords><Keywords>Humans</Keywords><Keywords>Interleukin-1</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Macrophages</Keywords><Keywords>Membrane Glycoproteins</Keywords><Keywords>metabolism</Keywords><Keywords>Monocytes</Keywords><Keywords>Mutation</Keywords><Keywords>NF-kappa B</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Receptors,Interleukin-1</Keywords><Keywords>Research</Keywords><Keywords>surgery</Keywords><Reprint>Not in File</Reprint><Start_Page>157</Start_Page><End_Page>162</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>295</Volume><Issue>1</Issue><Address>Department of Surgery, University of Washington School of Medicine, Seattle, WA 98104, USA. dbannerm@u.washington.edu</Address><Web_URL>PM:12083783</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>BD<Refman><Cite><Author>Ha</Author><Year>2008</Year><RecNum>477</RecNum><IDText>Lipopolysaccharide-induced myocardial protection against ischaemia/reperfusion injury is mediated through a PI3K/Akt-dependent mechanism</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>477</Ref_ID><Title_Primary>Lipopolysaccharide-induced myocardial protection against ischaemia/reperfusion injury is mediated through a PI3K/Akt-dependent mechanism</Title_Primary><Authors_Primary>Ha,T.</Authors_Primary><Authors_Primary>Hua,F.</Authors_Primary><Authors_Primary>Liu,X.</Authors_Primary><Authors_Primary>Ma,J.</Authors_Primary><Authors_Primary>McMullen,J.R.</Authors_Primary><Authors_Primary>Shioi,T.</Authors_Primary><Authors_Primary>Izumo,S.</Authors_Primary><Authors_Primary>Kelley,J.</Authors_Primary><Authors_Primary>Gao,X.</Authors_Primary><Authors_Primary>Browder,W.</Authors_Primary><Authors_Primary>Williams,D.L.</Authors_Primary><Authors_Primary>Kao,R.L.</Authors_Primary><Authors_Primary>Li,C.</Authors_Primary><Date_Primary>2008/6/1</Date_Primary><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Apoptosis</Keywords><Keywords>Caspase 3</Keywords><Keywords>Chromones</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>drug effects</Keywords><Keywords>enzymology</Keywords><Keywords>genetics</Keywords><Keywords>Glycogen Synthase Kinase 3</Keywords><Keywords>Heart</Keywords><Keywords>Heat-Shock Proteins</Keywords><Keywords>HSP27 Heat-Shock Proteins</Keywords><Keywords>injuries</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Morpholines</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Reperfusion Injury</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphatidylinositol 3-Kinase</Keywords><Keywords>Phosphatidylinositol 3-Kinases</Keywords><Keywords>Phosphorylation</Keywords><Keywords>prevention &amp; control</Keywords><Keywords>Protein Kinase Inhibitors</Keywords><Keywords>Proteins</Keywords><Keywords>Proto-Oncogene Proteins</Keywords><Keywords>Proto-Oncogene Proteins c-akt</Keywords><Keywords>Signal Transduction</Keywords><Keywords>surgery</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Reprint>Not in File</Reprint><Start_Page>546</Start_Page><End_Page>553</End_Page><Periodical>Cardiovasc.Res.</Periodical><Volume>78</Volume><Issue>3</Issue><Address>Department of Surgery, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, PO Box 70575, TN 37614-0575, USA</Address><Web_URL>PM:18267957</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cardiovasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Arimilli</Author><Year>2007</Year><RecNum>113</RecNum><IDText>TLR-4 and -6 agonists reverse apoptosis and promote maturation of simian virus 5-infected human dendritic cells through NFkB-dependent pathways</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>113</Ref_ID><Title_Primary>TLR-4 and -6 agonists reverse apoptosis and promote maturation of simian virus 5-infected human dendritic cells through NFkB-dependent pathways</Title_Primary><Authors_Primary>Arimilli,S.</Authors_Primary><Authors_Primary>Johnson,J.B.</Authors_Primary><Authors_Primary>exander-Miller,M.A.</Authors_Primary><Authors_Primary>Parks,G.D.</Authors_Primary><Date_Primary>2007/8/15</Date_Primary><Keywords>agonists</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cell Death</Keywords><Keywords>Cell Survival</Keywords><Keywords>Dendritic Cells</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Infection</Keywords><Keywords>Ligands</Keywords><Keywords>MAP Kinase Signaling System</Keywords><Keywords>metabolism</Keywords><Keywords>microbiology</Keywords><Keywords>NF-kappa B</Keywords><Keywords>physiology</Keywords><Keywords>Simian virus 5</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Toll-Like Receptor 6</Keywords><Keywords>Toll-Like Receptors</Keywords><Keywords>virology</Keywords><Reprint>Not in File</Reprint><Start_Page>144</Start_Page><End_Page>156</End_Page><Periodical>Virology</Periodical><Volume>365</Volume><Issue>1</Issue><Address>Department of Microbiology and Immunology, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1064, USA</Address><Web_URL>PM:17459446</Web_URL><ZZ_JournalStdAbbrev><f name="System">Virology</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Wang</Author><Year>2009</Year><RecNum>216</RecNum><IDText>Lipopolysaccharides can protect mesenchymal stem cells (MSCs) from oxidative stress-induced apoptosis and enhance proliferation of MSCs via Toll-like receptor(TLR)-4 and PI3K/Akt</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>216</Ref_ID><Title_Primary>Lipopolysaccharides can protect mesenchymal stem cells (MSCs) from oxidative stress-induced apoptosis and enhance proliferation of MSCs via Toll-like receptor(TLR)-4 and PI3K/Akt</Title_Primary><Authors_Primary>Wang,Z.J.</Authors_Primary><Authors_Primary>Zhang,F.M.</Authors_Primary><Authors_Primary>Wang,L.S.</Authors_Primary><Authors_Primary>Yao,Y.W.</Authors_Primary><Authors_Primary>Zhao,Q.</Authors_Primary><Authors_Primary>Gao,X.</Authors_Primary><Date_Primary>2009/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>deficiency</Keywords><Keywords>drug effects</Keywords><Keywords>Hydrogen Peroxide</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Myeloid Differentiation Factor 88</Keywords><Keywords>Oxidative Stress</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphatidylinositol 3-Kinases</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Proto-Oncogene Proteins c-akt</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Toll-Like Receptors</Keywords><Keywords>Transcription Factor RelA</Keywords><Reprint>Not in File</Reprint><Start_Page>665</Start_Page><End_Page>674</End_Page><Periodical>Cell Biol.Int.</Periodical><Volume>33</Volume><Issue>6</Issue><Misc_3>S1065-6995(09)00075-4 [pii];10.1016/j.cellbi.2009.03.006 [doi]</Misc_3><Address>Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, Nanjing, PR China</Address><Web_URL>PM:19376254</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cell Biol.Int.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�%D<Refman><Cite><Author>Jung</Author><Year>2005</Year><RecNum>393</RecNum><IDText>TLR4, but not TLR2, signals autoregulatory apoptosis of cultured microglia: a critical role of IFN-beta as a decision maker</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>393</Ref_ID><Title_Primary>TLR4, but not TLR2, signals autoregulatory apoptosis of cultured microglia: a critical role of IFN-beta as a decision maker</Title_Primary><Authors_Primary>Jung,D.Y.</Authors_Primary><Authors_Primary>Lee,H.</Authors_Primary><Authors_Primary>Jung,B.Y.</Authors_Primary><Authors_Primary>Ock,J.</Authors_Primary><Authors_Primary>Lee,M.S.</Authors_Primary><Authors_Primary>Lee,W.H.</Authors_Primary><Authors_Primary>Suk,K.</Authors_Primary><Date_Primary>2005/5/15</Date_Primary><Keywords>Adaptor Proteins,Signal Transducing</Keywords><Keywords>agonists</Keywords><Keywords>Animals</Keywords><Keywords>Antigens,CD14</Keywords><Keywords>Antigens,Differentiation</Keywords><Keywords>Antigens,Ly</Keywords><Keywords>Apoptosis</Keywords><Keywords>biosynthesis</Keywords><Keywords>Brain</Keywords><Keywords>Caspase 3</Keywords><Keywords>Caspases</Keywords><Keywords>Cell Death</Keywords><Keywords>Cell Line</Keywords><Keywords>cytology</Keywords><Keywords>DNA-Binding Proteins</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Interferon Regulatory Factor-3</Keywords><Keywords>Interferon-beta</Keywords><Keywords>Jurkat Cells</Keywords><Keywords>Ligands</Keywords><Keywords>Lymphocyte Antigen 96</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C3H</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Knockout</Keywords><Keywords>Microglia</Keywords><Keywords>Myeloid Differentiation Factor 88</Keywords><Keywords>Peptidoglycan</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Receptors,Immunologic</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Toll-Like Receptor 2</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>6467</Start_Page><End_Page>6476</End_Page><Periodical>J.Immunol.</Periodical><Volume>174</Volume><Issue>10</Issue><Address>Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Korea</Address><Web_URL>PM:15879150</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Niu</Author><Year>2008</Year><RecNum>392</RecNum><IDText>Protection against lipopolysaccharide-induced myocardial dysfunction in mice by cardiac-specific expression of soluble Fas</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>392</Ref_ID><Title_Primary>Protection against lipopolysaccharide-induced myocardial dysfunction in mice by cardiac-specific expression of soluble 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Injury</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Myocardium</Keywords><Keywords>Necrosis</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Synthase Type II</Keywords><Keywords>Organ Specificity</Keywords><Keywords>pharmacology</Keywords><Keywords>physiopathology</Keywords><Keywords>Sepsis</Keywords><Keywords>Solubility</Keywords><Keywords>Toll-Like Receptor 4</Keywords><Keywords>Tyrosine</Keywords><Reprint>Not in File</Reprint><Start_Page>160</Start_Page><End_Page>169</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>44</Volume><Issue>1</Issue><Address>Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA. jniu@mail.ucf.edu</Address><Web_URL>PM:17996250</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell 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Quillen College of Medicine, East Tennessee State University, Johnson City, PO Box 70575, TN 37614-0575, USA</Address><Web_URL>PM:18267957</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cardiovasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Arimilli</Author><Year>2007</Year><RecNum>113</RecNum><IDText>TLR-4 and -6 agonists reverse apoptosis and promote maturation of simian virus 5-infected human dendritic cells through NFkB-dependent pathways</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>113</Ref_ID><Title_Primary>TLR-4 and -6 agonists reverse apoptosis and promote maturation of simian virus 5-infected human dendritic cells through NFkB-dependent 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Proteins</Keywords><Keywords>Infarction,Middle Cerebral Artery</Keywords><Keywords>injuries</Keywords><Keywords>Ischemia</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Nerve Regeneration</Keywords><Keywords>Neurogenesis</Keywords><Keywords>Neuronal Plasticity</Keywords><Keywords>Neurons</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proteins</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred SHR</Keywords><Keywords>Recovery of Function</Keywords><Keywords>Regeneration</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stroke</Keywords><Keywords>therapy</Keywords><Keywords>Transfection</Keywords><Keywords>Treatment Outcome</Keywords><Keywords>virology</Keywords><Reprint>Not in File</Reprint><Start_Page>153</Start_Page><End_Page>161</End_Page><Periodical>Stroke</Periodical><Volume>38</Volume><Issue>1</Issue><Address>Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. leker@cc.huji.ac.il</Address><Web_URL>PM:17122419</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stroke</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Koike</Author><Year>2004</Year><RecNum>664</RecNum><IDText>Tissue engineering: creation of long-lasting blood vessels</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>664</Ref_ID><Title_Primary>Tissue engineering: creation of long-lasting blood vessels</Title_Primary><Authors_Primary>Koike,N.</Authors_Primary><Authors_Primary>Fukumura,D.</Authors_Primary><Authors_Primary>Gralla,O.</Authors_Primary><Authors_Primary>Au,P.</Authors_Primary><Authors_Primary>Schechner,J.S.</Authors_Primary><Authors_Primary>Jain,R.K.</Authors_Primary><Date_Primary>2004/3/11</Date_Primary><Keywords>Animals</Keywords><Keywords>Biological Markers</Keywords><Keywords>blood</Keywords><Keywords>Blood 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Steele Laboratory, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA</Address><Web_URL>PM:15014486</Web_URL><ZZ_JournalFull><f name="System">Nature</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Nature</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Kinnaird</Author><Year>2004</Year><RecNum>645</RecNum><IDText>Local delivery of marrow-derived stromal cells augments collateral perfusion through paracrine mechanisms</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>645</Ref_ID><Title_Primary>Local delivery of marrow-derived stromal cells augments collateral perfusion through paracrine mechanisms</Title_Primary><Authors_Primary>Kinnaird,T.</Authors_Primary><Authors_Primary>Stabile,E.</Authors_Primary><Authors_Primary>Burnett,M.S.</Authors_Primary><Authors_Primary>Shou,M.</Authors_Primary><Authors_Primary>Lee,C.W.</Authors_Primary><Authors_Primary>Barr,S.</Authors_Primary><Authors_Primary>Fuchs,S.</Authors_Primary><Authors_Primary>Epstein,S.E.</Authors_Primary><Date_Primary>2004/3/30</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>blood supply</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemokine CCL2</Keywords><Keywords>Collateral Circulation</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>etiology</Keywords><Keywords>Femoral Artery</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Fibrosis</Keywords><Keywords>genetics</Keywords><Keywords>Growth Substances</Keywords><Keywords>Hindlimb</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Immunomagnetic Separation</Keywords><Keywords>Injections,Intramuscular</Keywords><Keywords>Ischemia</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred BALB C</Keywords><Keywords>Muscle Cells</Keywords><Keywords>Muscle,Skeletal</Keywords><Keywords>Muscle,Smooth,Vascular</Keywords><Keywords>Muscular Atrophy</Keywords><Keywords>Myocytes,Smooth Muscle</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pathology</Keywords><Keywords>Perfusion</Keywords><Keywords>pharmacology</Keywords><Keywords>physiopathology</Keywords><Keywords>Pregnancy</Keywords><Keywords>Pregnancy Proteins</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Stromal Cells</Keywords><Keywords>therapy</Keywords><Keywords>Transcription Factors</Keywords><Keywords>transplantation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>1543</Start_Page><End_Page>1549</End_Page><Periodical>Circulation</Periodical><Volume>109</Volume><Issue>12</Issue><Address>Cardiovascular Research Institute, Washington, DC 20010, USA. tim.kinnaird@medstar.net</Address><Web_URL>PM:15023891</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circulation</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>`D<Refman><Cite><Author>Wang</Author><Year>2008</Year><RecNum>386</RecNum><IDText>Hypoxic preconditioning attenuates hypoxia/reoxygenation-induced apoptosis in mesenchymal stem cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>386</Ref_ID><Title_Primary>Hypoxic preconditioning attenuates hypoxia/reoxygenation-induced apoptosis in mesenchymal stem cells</Title_Primary><Authors_Primary>Wang,J.A.</Authors_Primary><Authors_Primary>Chen,T.L.</Authors_Primary><Authors_Primary>Jiang,J.</Authors_Primary><Authors_Primary>Shi,H.</Authors_Primary><Authors_Primary>Gui,C.</Authors_Primary><Authors_Primary>Luo,R.H.</Authors_Primary><Authors_Primary>Xie,X.J.</Authors_Primary><Authors_Primary>Xiang,M.X.</Authors_Primary><Authors_Primary>Zhang,X.</Authors_Primary><Date_Primary>2008/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Apoptosis</Keywords><Keywords>blood</Keywords><Keywords>blood supply</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Survival</Keywords><Keywords>Cyclosporine</Keywords><Keywords>drug effects</Keywords><Keywords>In Situ Nick-End Labeling</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>methods</Keywords><Keywords>Mitochondria</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>74</Start_Page><End_Page>82</End_Page><Periodical>Acta Pharmacol.Sin.</Periodical><Volume>29</Volume><Issue>1</Issue><Misc_3>10.1111/j.1745-7254.2008.00716.x [doi]</Misc_3><Address>Department of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China. wang_jian_an@tom.com</Address><Web_URL>PM:18158868</Web_URL><ZZ_JournalFull><f name="System">Acta Pharmacol.Sin.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Acta Pharmacol.Sin.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Rochefort</Author><Year>2006</Year><RecNum>668</RecNum><IDText>Multipotential mesenchymal stem cells are mobilized into peripheral blood by hypoxia</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>668</Ref_ID><Title_Primary>Multipotential mesenchymal stem cells are mobilized into peripheral blood by hypoxia</Title_Primary><Authors_Primary>Rochefort,G.Y.</Authors_Primary><Authors_Primary>Delorme,B.</Authors_Primary><Authors_Primary>Lopez,A.</Authors_Primary><Authors_Primary>Herault,O.</Authors_Primary><Authors_Primary>Bonnet,P.</Authors_Primary><Authors_Primary>Charbord,P.</Authors_Primary><Authors_Primary>Eder,V.</Authors_Primary><Authors_Primary>Domenech,J.</Authors_Primary><Date_Primary>2006/10</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adipogenesis</Keywords><Keywords>Adult</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chondrocytes</Keywords><Keywords>Chondrogenesis</Keywords><Keywords>Colony-Forming Units Assay</Keywords><Keywords>cytology</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>immunology</Keywords><Keywords>Immunophenotyping</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Osteogenesis</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Wistar</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stromal Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>2202</Start_Page><End_Page>2208</End_Page><Periodical>Stem Cells</Periodical><Volume>24</Volume><Issue>10</Issue><Address>Upres-Ea3852, Universite Francois Rabelais de Tours and Chru de Tours, Tours, France</Address><Web_URL>PM:16778152</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cells</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Bates</Author><Year>2002</Year><RecNum>665</RecNum><IDText>Regulation of microvascular permeability by vascular endothelial growth factors</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>665</Ref_ID><Title_Primary>Regulation of microvascular permeability by vascular endothelial growth factors</Title_Primary><Authors_Primary>Bates,D.O.</Authors_Primary><Authors_Primary>Hillman,N.J.</Authors_Primary><Authors_Primary>Williams,B.</Authors_Primary><Authors_Primary>Neal,C.R.</Authors_Primary><Authors_Primary>Pocock,T.M.</Authors_Primary><Date_Primary>2002/6</Date_Primary><Keywords>Adult</Keywords><Keywords>Animals</Keywords><Keywords>blood</Keywords><Keywords>Blood Vessels</Keywords><Keywords>Calcium</Keywords><Keywords>Capillary Permeability</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelial Growth Factors</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Heart</Keywords><Keywords>Humans</Keywords><Keywords>Lymphokines</Keywords><Keywords>metabolism</Keywords><Keywords>Models,Biological</Keywords><Keywords>mortality</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>physiology</Keywords><Keywords>Protein-Tyrosine Kinases</Keywords><Keywords>Proteins</Keywords><Keywords>Proto-Oncogene Proteins</Keywords><Keywords>Receptor Protein-Tyrosine Kinases</Keywords><Keywords>Receptors,Growth Factor</Keywords><Keywords>Receptors,Vascular Endothelial Growth Factor</Keywords><Keywords>Research</Keywords><Keywords>Stroke</Keywords><Keywords>Tyrosine</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-1</Keywords><Keywords>Vascular Endothelial Growth Factors</Keywords><Keywords>veterinary</Keywords><Reprint>Not in File</Reprint><Start_Page>581</Start_Page><End_Page>597</End_Page><Periodical>J.Anat.</Periodical><Volume>200</Volume><Issue>6</Issue><Address>Department of Physiology, The Preclinical Veterinary School, University of Bristol, UK. 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inhibitors</Keywords><Keywords>Antibodies</Keywords><Keywords>Antibodies,Blocking</Keywords><Keywords>blood supply</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Brain</Keywords><Keywords>Brain Ischemia</Keywords><Keywords>Capillary Permeability</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in File</Reprint><Start_Page>59</Start_Page><End_Page>67</End_Page><Periodical>Microvasc.Res.</Periodical><Volume>75</Volume><Issue>1</Issue><Address>Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China</Address><Web_URL>PM:17662311</Web_URL><ZZ_JournalStdAbbrev><f name="System">Microvasc.Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>T(D<Refman><Cite><Author>De</Author><Year>2007</Year><RecNum>93</RecNum><IDText>Migration of culture-expanded human mesenchymal stem cells through bone marrow endothelium is regulated by matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-3</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>93</Ref_ID><Title_Primary>Migration of culture-expanded human mesenchymal stem cells through bone marrow endothelium is regulated by matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-3</Title_Primary><Authors_Primary>De,Becker A.</Authors_Primary><Authors_Primary>Van,Hummelen P.</Authors_Primary><Authors_Primary>Bakkus,M.</Authors_Primary><Authors_Primary>Vande,Broek,I</Authors_Primary><Authors_Primary>De,Wever J.</Authors_Primary><Authors_Primary>De,Waele 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Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Oligonucleotide Array Sequence Analysis</Keywords><Keywords>Organ Specificity</Keywords><Keywords>Osteocytes</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Polymerase Chain Reaction</Keywords><Keywords>Proteoglycans</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Small Interfering</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapeutic use</Keywords><Keywords>Tissue Inhibitor of Metalloproteinase-3</Keywords><Keywords>Transfection</Keywords><Keywords>transplantation</Keywords><Keywords>Up-Regulation</Keywords><Reprint>Not in File</Reprint><Start_Page>440</Start_Page><End_Page>449</End_Page><Periodical>Haematologica</Periodical><Volume>92</Volume><Issue>4</Issue><Address>Stem Cell Laboratory, Academic Hospital Vrije Universiteit Brussel Research group, Brussels, Belgium</Address><Web_URL>PM:17488654</Web_URL><ZZ_JournalStdAbbrev><f name="System">Haematologica</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ries</Author><Year>2007</Year><RecNum>96</RecNum><IDText>MMP-2, MT1-MMP, and TIMP-2 are essential for the invasive capacity of human mesenchymal stem cells: differential regulation by inflammatory cytokines</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>96</Ref_ID><Title_Primary>MMP-2, MT1-MMP, and TIMP-2 are essential for the invasive capacity of human mesenchymal stem cells: differential regulation by inflammatory cytokines</Title_Primary><Authors_Primary>Ries,C.</Authors_Primary><Authors_Primary>Egea,V.</Authors_Primary><Authors_Primary>Karow,M.</Authors_Primary><Authors_Primary>Kolb,H.</Authors_Primary><Authors_Primary>Jochum,M.</Authors_Primary><Authors_Primary>Neth,P.</Authors_Primary><Date_Primary>2007/5/1</Date_Primary><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Line</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Extracellular Matrix</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Inflammation</Keywords><Keywords>Matrix Metalloproteinase 14</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Rna</Keywords><Keywords>RNA Interference</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tissue Inhibitor of Metalloproteinase-2</Keywords><Reprint>Not in File</Reprint><Start_Page>4055</Start_Page><End_Page>4063</End_Page><Periodical>Blood</Periodical><Volume>109</Volume><Issue>9</Issue><Misc_3>blood-2006-10-051060 [pii];10.1182/blood-2006-10-051060 [doi]</Misc_3><Address>Division of Clinical Chemistry and Clinical Biochemistry, Surgical Department, Ludwig-Maximillians-University of Munich, Nussbaumstrasse 20, 80336 Munich, Germany. christian.ries@med.uni-muenchen.de</Address><Web_URL>PM:17197427</Web_URL><ZZ_JournalStdAbbrev><f name="System">Blood</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Steingen</Author><Year>2008</Year><RecNum>405</RecNum><IDText>Characterization of key mechanisms in transmigration and invasion of mesenchymal stem cells</IDText><MDL 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Cells</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Female</Keywords><Keywords>Gelatinases</Keywords><Keywords>Humans</Keywords><Keywords>Integrin alpha4beta1</Keywords><Keywords>Integrins</Keywords><Keywords>Male</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardium</Keywords><Keywords>Organ Specificity</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Pseudopodia</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time</Keywords><Keywords>Vascular Cell Adhesion Molecule-1</Keywords><Keywords>Veins</Keywords><Reprint>Not in File</Reprint><Start_Page>1072</Start_Page><End_Page>1084</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>44</Volume><Issue>6</Issue><Address>German Sport University Cologne, Institute for Cardiovascular Research and Sport Medicine, Department for Molecular and Cellular Sport Medicine, Cologne, Germany</Address><Web_URL>PM:18462748</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Liu</Author><Year>2008</Year><RecNum>15</RecNum><IDText>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>15</Ref_ID><Title_Primary>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic 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Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pharmacology</Keywords><Keywords>Protease Inhibitors</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Keywords>von Willebrand Factor</Keywords><Reprint>Not in 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Movement</Keywords><Keywords>Chemotactic Factors</Keywords><Keywords>Chemotaxis,Leukocyte</Keywords><Keywords>Collagen</Keywords><Keywords>Gelatin</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>Microbial Collagenase</Keywords><Keywords>Molecular Weight</Keywords><Keywords>Monocytes</Keywords><Keywords>Neutrophils</Keywords><Keywords>Oligopeptides</Keywords><Keywords>Peptides</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Research</Keywords><Reprint>Not in File</Reprint><Start_Page>289</Start_Page><End_Page>295</End_Page><Periodical>Matrix</Periodical><Volume>11</Volume><Issue>4</Issue><Address>Department of Medicine, St. Louis University, MO</Address><Web_URL>PM:1656175</Web_URL><ZZ_JournalStdAbbrev><f name="System">Matrix</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Steingen</Author><Year>2008</Year><RecNum>405</RecNum><IDText>Characterization of key mechanisms in transmigration 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Cells</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Female</Keywords><Keywords>Gelatinases</Keywords><Keywords>Humans</Keywords><Keywords>Integrin alpha4beta1</Keywords><Keywords>Integrins</Keywords><Keywords>Male</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardium</Keywords><Keywords>Organ Specificity</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Pseudopodia</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Keywords>Time</Keywords><Keywords>Vascular Cell Adhesion Molecule-1</Keywords><Keywords>Veins</Keywords><Reprint>Not in File</Reprint><Start_Page>1072</Start_Page><End_Page>1084</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>44</Volume><Issue>6</Issue><Address>German Sport University Cologne, Institute for Cardiovascular Research and Sport Medicine, Department for Molecular and Cellular Sport Medicine, Cologne, Germany</Address><Web_URL>PM:18462748</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Mauney</Author><Year>2010</Year><RecNum>127</RecNum><IDText>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen matrix</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>127</Ref_ID><Title_Primary>Matrix remodeling as stem cell recruitment event: a novel in vitro model for homing of human bone marrow stromal cells to the site of injury shows crucial role of extracellular collagen 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Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�#D<Refman><Cite><Author>Liu</Author><Year>2008</Year><RecNum>15</RecNum><IDText>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>15</Ref_ID><Title_Primary>The interactions between brain microvascular endothelial cells and mesenchymal stem cells under hypoxic conditions</Title_Primary><Authors_Primary>Liu,K.</Authors_Primary><Authors_Primary>Chi,L.</Authors_Primary><Authors_Primary>Guo,L.</Authors_Primary><Authors_Primary>Liu,X.</Authors_Primary><Authors_Primary>Luo,C.</Authors_Primary><Authors_Primary>Zhang,S.</Authors_Primary><Authors_Primary>He,G.</Authors_Primary><Date_Primary>2008/1</Date_Primary><Keywords>Animals</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Antibodies</Keywords><Keywords>Antibodies,Blocking</Keywords><Keywords>blood supply</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Brain</Keywords><Keywords>Brain Ischemia</Keywords><Keywords>Capillary Permeability</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>drug effects</Keywords><Keywords>Electric Impedance</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>enzymology</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Paracrine 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angiogenesis</Title_Primary><Authors_Primary>Jeon,S.H.</Authors_Primary><Authors_Primary>Chae,B.C.</Authors_Primary><Authors_Primary>Kim,H.A.</Authors_Primary><Authors_Primary>Seo,G.Y.</Authors_Primary><Authors_Primary>Seo,D.W.</Authors_Primary><Authors_Primary>Chun,G.T.</Authors_Primary><Authors_Primary>Kim,N.S.</Authors_Primary><Authors_Primary>Yie,S.W.</Authors_Primary><Authors_Primary>Byeon,W.H.</Authors_Primary><Authors_Primary>Eom,S.H.</Authors_Primary><Authors_Primary>Ha,K.S.</Authors_Primary><Authors_Primary>Kim,Y.M.</Authors_Primary><Authors_Primary>Kim,P.H.</Authors_Primary><Date_Primary>2007/2</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>biosynthesis</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chromatin</Keywords><Keywords>Chromatin Immunoprecipitation</Keywords><Keywords>drug effects</Keywords><Keywords>E1A-Associated p300 Protein</Keywords><Keywords>Enzyme-Linked Immunosorbent Assay</Keywords><Keywords>Gene Expression 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Proteins</Keywords><Keywords>Humans</Keywords><Keywords>Hydroxylation</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>metabolism</Keywords><Keywords>Oxygen</Keywords><Keywords>Procollagen-Proline Dioxygenase</Keywords><Keywords>Proline</Keywords><Keywords>Proteins</Keywords><Keywords>Receptors,Cell Surface</Keywords><Keywords>Repressor Proteins</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Transcription,Genetic</Keywords><Keywords>Von Hippel-Lindau Tumor Suppressor Protein</Keywords><Reprint>Not in File</Reprint><Start_Page>cm8</Start_Page><Periodical>Sci.STKE.</Periodical><Volume>2007</Volume><Issue>407</Issue><Address>Vascular Biology Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Broadway Research Building, Suite 671, 733 North Broadway, Baltimore, MD 21205, USA. gsemenza@jhmi.edu</Address><Web_URL>PM:17925579</Web_URL><ZZ_JournalStdAbbrev><f name="System">Sci.STKE.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Mendonca</Author><Year>2011</Year><RecNum>630</RecNum><IDText>NF-kappaB suppresses HIF-1alpha response by competing for P300 binding</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>630</Ref_ID><Title_Primary>NF-kappaB suppresses HIF-1alpha response by competing for P300 binding</Title_Primary><Authors_Primary>Mendonca,D.B.</Authors_Primary><Authors_Primary>Mendonca,G.</Authors_Primary><Authors_Primary>Aragao,F.J.</Authors_Primary><Authors_Primary>Cooper,L.F.</Authors_Primary><Date_Primary>2011/1/28</Date_Primary><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line</Keywords><Keywords>E1A-Associated p300 Protein</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Inflammation</Keywords><Keywords>metabolism</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Synthase Type II</Keywords><Keywords>Osteogenesis</Keywords><Keywords>Plasmids</Keywords><Keywords>Promoter Regions,Genetic</Keywords><Keywords>Proteins</Keywords><Keywords>Regeneration</Keywords><Keywords>Research</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cell Niche</Keywords><Keywords>Transcription Factor RelA</Keywords><Keywords>Transcriptional Activation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>997</Start_Page><End_Page>1003</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>404</Volume><Issue>4</Issue><Address>Universidade Catolica de Brasilia, Pos-Graduacao em Ciencias Genomicas e Biotecnologia, SGAN Quadra 916, Av. W5 Norte, 70790-160 Brasilia, DF, Brazil</Address><Web_URL>PM:21187066</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Lin</Author><Year>2008</Year><RecNum>671</RecNum><IDText>Hypoxia-inducible factor-1alpha regulates matrix metalloproteinase-1 activity in human bone marrow-derived mesenchymal stem cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>671</Ref_ID><Title_Primary>Hypoxia-inducible factor-1alpha regulates matrix metalloproteinase-1 activity in human bone marrow-derived mesenchymal stem cells</Title_Primary><Authors_Primary>Lin,J.L.</Authors_Primary><Authors_Primary>Wang,M.J.</Authors_Primary><Authors_Primary>Lee,D.</Authors_Primary><Authors_Primary>Liang,C.C.</Authors_Primary><Authors_Primary>Lin,S.</Authors_Primary><Date_Primary>2008/7/23</Date_Primary><Keywords>Aged</Keywords><Keywords>antagonists &amp; inhibitors</Keywords><Keywords>Bone Diseases</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>enzymology</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Matrix Metalloproteinase 1</Keywords><Keywords>Matrix Metalloproteinase 3</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Osteoarthritis</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>2615</Start_Page><End_Page>2619</End_Page><Periodical>FEBS Lett.</Periodical><Volume>582</Volume><Issue>17</Issue><Address>Orthopaedics Medicine, Miaoli General Hospital, Miaoli city, Taiwan</Address><Web_URL>PM:18588890</Web_URL><ZZ_JournalFull><f name="System">FEBS Lett.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">FEBS Lett.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>"D<Refman><Cite><Author>Pugh</Author><Year>2003</Year><RecNum>404</RecNum><IDText>Regulation of angiogenesis by hypoxia: role of the HIF system</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>404</Ref_ID><Title_Primary>Regulation of angiogenesis by hypoxia: role of the HIF system</Title_Primary><Authors_Primary>Pugh,C.W.</Authors_Primary><Authors_Primary>Ratcliffe,P.J.</Authors_Primary><Date_Primary>2003/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>blood supply</Keywords><Keywords>DNA-Binding Proteins</Keywords><Keywords>Gene Expression Regulation,Developmental</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Hydroxylation</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>metabolism</Keywords><Keywords>Neoplasms</Keywords><Keywords>Neovascularization,Pathologic</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>Nuclear Proteins</Keywords><Keywords>Oxygen</Keywords><Keywords>Phenotype</Keywords><Keywords>Protein Isoforms</Keywords><Keywords>Protein Subunits</Keywords><Keywords>Proteins</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>677</Start_Page><End_Page>684</End_Page><Periodical>Nat.Med.</Periodical><Volume>9</Volume><Issue>6</Issue><Address>The Henry Wellcome Building of Genomic Medicine, Roosevelt Drive, Oxford, OX3 7BN, UK</Address><Web_URL>PM:12778166</Web_URL><ZZ_JournalStdAbbrev><f name="System">Nat.Med.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Tipoe</Author><Year>2006</Year><RecNum>400</RecNum><IDText>Expression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemia</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>400</Ref_ID><Title_Primary>Expression and functions of vasoactive substances regulated by hypoxia-inducible factor-1 in chronic hypoxemia</Title_Primary><Authors_Primary>Tipoe,G.L.</Authors_Primary><Authors_Primary>Lau,T.Y.</Authors_Primary><Authors_Primary>Nanji,A.A.</Authors_Primary><Authors_Primary>Fung,M.L.</Authors_Primary><Date_Primary>2006/7</Date_Primary><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>Carotid Arteries</Keywords><Keywords>Chronic Disease</Keywords><Keywords>Endothelin-1</Keywords><Keywords>Erythropoietin</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Homeostasis</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Liver</Keywords><Keywords>metabolism</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Oxidative Stress</Keywords><Keywords>Oxygen</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Serum</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>199</Start_Page><End_Page>218</End_Page><Periodical>Cardiovasc.Hematol.Agents Med.Chem.</Periodical><Volume>4</Volume><Issue>3</Issue><Address>Department of Anatomy, The University of Hong Kong, Pokfulam, Hong Kong SAR, China</Address><Web_URL>PM:16842206</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cardiovasc.Hematol.Agents Med.Chem.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Jeon</Author><Year>2007</Year><RecNum>399</RecNum><IDText>Mechanisms underlying TGF-beta1-induced expression of VEGF and Flk-1 in mouse macrophages and their implications for angiogenesis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>399</Ref_ID><Title_Primary>Mechanisms underlying TGF-beta1-induced expression of VEGF and Flk-1 in mouse macrophages and their implications for angiogenesis</Title_Primary><Authors_Primary>Jeon,S.H.</Authors_Primary><Authors_Primary>Chae,B.C.</Authors_Primary><Authors_Primary>Kim,H.A.</Authors_Primary><Authors_Primary>Seo,G.Y.</Authors_Primary><Authors_Primary>Seo,D.W.</Authors_Primary><Authors_Primary>Chun,G.T.</Authors_Primary><Authors_Primary>Kim,N.S.</Authors_Primary><Authors_Primary>Yie,S.W.</Authors_Primary><Authors_Primary>Byeon,W.H.</Authors_Primary><Authors_Primary>Eom,S.H.</Authors_Primary><Authors_Primary>Ha,K.S.</Authors_Primary><Authors_Primary>Kim,Y.M.</Authors_Primary><Authors_Primary>Kim,P.H.</Authors_Primary><Date_Primary>2007/2</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>biosynthesis</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chromatin</Keywords><Keywords>Chromatin Immunoprecipitation</Keywords><Keywords>drug effects</Keywords><Keywords>E1A-Associated p300 Protein</Keywords><Keywords>Enzyme-Linked Immunosorbent Assay</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>immunology</Keywords><Keywords>Immunoprecipitation</Keywords><Keywords>Liver</Keywords><Keywords>Macrophages</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred BALB C</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pharmacology</Keywords><Keywords>Promoter Regions,Genetic</Keywords><Keywords>Protein Binding</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>secretion</Keywords><Keywords>Smad2 Protein</Keywords><Keywords>Smad3 Protein</Keywords><Keywords>Smad4 Protein</Keywords><Keywords>Structure-Activity Relationship</Keywords><Keywords>Transcription,Genetic</Keywords><Keywords>Transforming Growth Factor beta1</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-1</Keywords><Keywords>Vascular Endothelial Growth Factor Receptor-2</Keywords><Reprint>Not in File</Reprint><Start_Page>557</Start_Page><End_Page>566</End_Page><Periodical>J.Leukoc.Biol.</Periodical><Volume>81</Volume><Issue>2</Issue><Address>Department of Molecular Bioscience, School of Bioscience and Biotechnology, Kangwon National University, Chunchon, Korea</Address><Web_URL>PM:17053163</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Leukoc.Biol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Jensen</Author><Year>2006</Year><RecNum>642</RecNum><IDText>Inhibition of hypoxia inducible factor-1alpha (HIF-1alpha) decreases vascular endothelial growth factor (VEGF) secretion and tumor growth in malignant gliomas</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>642</Ref_ID><Title_Primary>Inhibition of hypoxia inducible factor-1alpha (HIF-1alpha) decreases vascular endothelial growth factor (VEGF) secretion and tumor growth in malignant gliomas</Title_Primary><Authors_Primary>Jensen,R.L.</Authors_Primary><Authors_Primary>Ragel,B.T.</Authors_Primary><Authors_Primary>Whang,K.</Authors_Primary><Authors_Primary>Gillespie,D.</Authors_Primary><Date_Primary>2006/7</Date_Primary><Keywords>Adult</Keywords><Keywords>Aged</Keywords><Keywords>Aged,80 and over</Keywords><Keywords>Anoxia</Keywords><Keywords>blood supply</Keywords><Keywords>Brain Neoplasms</Keywords><Keywords>Cell Line</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression Regulation,Neoplastic</Keywords><Keywords>Gene Silencing</Keywords><Keywords>genetics</Keywords><Keywords>Glioma</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>Ki-67 Antigen</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Neovascularization,Pathologic</Keywords><Keywords>pathology</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Tumor Cells,Cultured</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>233</Start_Page><End_Page>247</End_Page><Periodical>J.Neurooncol.</Periodical><Volume>78</Volume><Issue>3</Issue><Address>Department of Neurosurgery, University of Utah, Salt Lake City, Utah 84132-2303, USA. randy.jensen@hsc.utah.edu</Address><Web_URL>PM:16612574</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Neurooncol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>|D<Refman><Cite><Author>Mi</Author><Year>2008</Year><RecNum>627</RecNum><IDText>Synergystic induction of HIF-1alpha transcriptional activity by hypoxia and lipopolysaccharide in macrophages</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>627</Ref_ID><Title_Primary>Synergystic induction of HIF-1alpha transcriptional activity by hypoxia and lipopolysaccharide in macrophages</Title_Primary><Authors_Primary>Mi,Z.</Authors_Primary><Authors_Primary>Rapisarda,A.</Authors_Primary><Authors_Primary>Taylor,L.</Authors_Primary><Authors_Primary>Brooks,A.</Authors_Primary><Authors_Primary>Creighton-Gutteridge,M.</Authors_Primary><Authors_Primary>Melillo,G.</Authors_Primary><Authors_Primary>Varesio,L.</Authors_Primary><Date_Primary>2008/1/15</Date_Primary><Keywords>Animals</Keywords><Keywords>Binding Sites</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line</Keywords><Keywords>Dna</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>immunology</Keywords><Keywords>Lipopolysaccharides</Keywords><Keywords>Macrophages</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Synthase Type II</Keywords><Keywords>Research</Keywords><Keywords>Response Elements</Keywords><Keywords>Transcriptional Activation</Keywords><Keywords>Transfection</Keywords><Reprint>Not in File</Reprint><Start_Page>232</Start_Page><End_Page>241</End_Page><Periodical>Cell Cycle</Periodical><Volume>7</Volume><Issue>2</Issue><Address>Developmental Therapeutics Program, Istituto G. Gaslini, Genoa, Italy</Address><Web_URL>PM:18212534</Web_URL><ZZ_JournalStdAbbrev><f name="System">Cell Cycle</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Mendonca</Author><Year>2011</Year><RecNum>630</RecNum><IDText>NF-kappaB suppresses HIF-1alpha response by competing for P300 binding</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>630</Ref_ID><Title_Primary>NF-kappaB suppresses HIF-1alpha response by competing for P300 binding</Title_Primary><Authors_Primary>Mendonca,D.B.</Authors_Primary><Authors_Primary>Mendonca,G.</Authors_Primary><Authors_Primary>Aragao,F.J.</Authors_Primary><Authors_Primary>Cooper,L.F.</Authors_Primary><Date_Primary>2011/1/28</Date_Primary><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line</Keywords><Keywords>E1A-Associated p300 Protein</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Inflammation</Keywords><Keywords>metabolism</Keywords><Keywords>NF-kappa B</Keywords><Keywords>Nitric Oxide</Keywords><Keywords>Nitric Oxide Synthase Type II</Keywords><Keywords>Osteogenesis</Keywords><Keywords>Plasmids</Keywords><Keywords>Promoter Regions,Genetic</Keywords><Keywords>Proteins</Keywords><Keywords>Regeneration</Keywords><Keywords>Research</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cell Niche</Keywords><Keywords>Transcription Factor RelA</Keywords><Keywords>Transcriptional Activation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>997</Start_Page><End_Page>1003</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>404</Volume><Issue>4</Issue><Address>Universidade Catolica de Brasilia, Pos-Graduacao em Ciencias Genomicas e Biotecnologia, SGAN Quadra 916, Av. W5 Norte, 70790-160 Brasilia, DF, Brazil</Address><Web_URL>PM:21187066</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Dai</Author><Year>2007</Year><RecNum>388</RecNum><IDText>HIF-1alpha induced-VEGF overexpression in bone marrow stem cells protects cardiomyocytes against ischemia</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>388</Ref_ID><Title_Primary>HIF-1alpha induced-VEGF overexpression in bone marrow stem cells protects cardiomyocytes against ischemia</Title_Primary><Authors_Primary>Dai,Y.</Authors_Primary><Authors_Primary>Xu,M.</Authors_Primary><Authors_Primary>Wang,Y.</Authors_Primary><Authors_Primary>Pasha,Z.</Authors_Primary><Authors_Primary>Li,T.</Authors_Primary><Authors_Primary>Ashraf,M.</Authors_Primary><Date_Primary>2007/6</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>Antibodies</Keywords><Keywords>Apoptosis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>DNA Fragmentation</Keywords><Keywords>drug effects</Keywords><Keywords>Enzyme-Linked Immunosorbent Assay</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Hypoxia-Inducible Factor 1,alpha Subunit</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>injuries</Keywords><Keywords>Ischemia</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocytes,Cardiac</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Proteins</Keywords><Keywords>secretion</Keywords><Keywords>Stem Cells</Keywords><Keywords>Up-Regulation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>1036</Start_Page><End_Page>1044</End_Page><Periodical>J.Mol.Cell Cardiol.</Periodical><Volume>42</Volume><Issue>6</Issue><Address>Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA</Address><Web_URL>PM:17498737</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Mol.Cell Cardiol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ziello</Author><Year>2007</Year><RecNum>339</RecNum><IDText>Hypoxia-Inducible Factor (HIF)-1 regulatory pathway and its potential for therapeutic intervention in malignancy and ischemia</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>339</Ref_ID><Title_Primary>Hypoxia-Inducible Factor (HIF)-1 regulatory pathway and its potential for therapeutic intervention in malignancy and ischemia</Title_Primary><Authors_Primary>Ziello,J.E.</Authors_Primary><Authors_Primary>Jovin,I.S.</Authors_Primary><Authors_Primary>Huang,Y.</Authors_Primary><Date_Primary>2007/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Drug Delivery Systems</Keywords><Keywords>drug therapy</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>Gene Therapy</Keywords><Keywords>Homeostasis</Keywords><Keywords>Humans</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Ischemia</Keywords><Keywords>metabolism</Keywords><Keywords>methods</Keywords><Keywords>Models,Biological</Keywords><Keywords>Neoplasms</Keywords><Keywords>Oxygen</Keywords><Keywords>Signal Transduction</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>51</Start_Page><End_Page>60</End_Page><Periodical>Yale J.Biol.Med.</Periodical><Volume>80</Volume><Issue>2</Issue><User_Def_5>PMC2140184</User_Def_5><Address>Department of Medicine, Vascular Biology and Transplantation Program, Yale University, New Haven, Connecticut 06520, USA</Address><Web_URL>PM:18160990</Web_URL><ZZ_JournalStdAbbrev><f name="System">Yale J.Biol.Med.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Semenza</Author><Year>2000</Year><RecNum>11</RecNum><IDText>HIF-1: mediator of physiological and pathophysiological responses to hypoxia</IDText><MDL 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File</Reprint><Start_Page>1474</Start_Page><End_Page>1480</End_Page><Periodical>J.Appl.Physiol</Periodical><Volume>88</Volume><Issue>4</Issue><Address>Institute of Genetic Medicine, Departments of Pediatrics and Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21287-3914, USA. gsemenza@jhmi.edu</Address><Web_URL>PM:10749844</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Appl.Physiol</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Ye</Author><Year>2005</Year><RecNum>345</RecNum><IDText>Hypoxia down-regulates secretion of MMP-2, MMP-9 in porcine pulmonary artery endothelial and smooth muscle cells and the role of HIF-1</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>345</Ref_ID><Title_Primary>Hypoxia down-regulates secretion of MMP-2, MMP-9 in porcine pulmonary artery endothelial and smooth muscle cells and the role of HIF-1</Title_Primary><Authors_Primary>Ye,H.</Authors_Primary><Authors_Primary>Zheng,Y.</Authors_Primary><Authors_Primary>Ma,W.</Authors_Primary><Authors_Primary>Ke,D.</Authors_Primary><Authors_Primary>Jin,X.</Authors_Primary><Authors_Primary>Liu,S.</Authors_Primary><Authors_Primary>Wang,D.</Authors_Primary><Date_Primary>2005</Date_Primary><Keywords>Animals</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>cytology</Keywords><Keywords>Down-Regulation</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Enhancer Elements,Genetic</Keywords><Keywords>enzymology</Keywords><Keywords>Erythropoietin</Keywords><Keywords>genetics</Keywords><Keywords>Hypoxia-Inducible Factor 1</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix Metalloproteinase 9</Keywords><Keywords>metabolism</Keywords><Keywords>Muscle,Smooth,Vascular</Keywords><Keywords>pharmacology</Keywords><Keywords>Pulmonary Artery</Keywords><Keywords>secretion</Keywords><Keywords>Swine</Keywords><Keywords>Transfection</Keywords><Reprint>Not in File</Reprint><Start_Page>382</Start_Page><End_Page>4, 407</End_Page><Periodical>J.Huazhong.Univ Sci.Technolog.Med.Sci.</Periodical><Volume>25</Volume><Issue>4</Issue><Address>Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Pulmonary Laboratory of Ministry of Health of China, Wuhan 430030, China</Address><Web_URL>PM:16196282</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Huazhong.Univ Sci.Technolog.Med.Sci.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Annabi</Author><Year>2003</Year><RecNum>326</RecNum><IDText>Hypoxia promotes murine bone-marrow-derived stromal cell migration and tube formation</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>326</Ref_ID><Title_Primary>Hypoxia promotes murine bone-marrow-derived stromal cell migration and tube formation</Title_Primary><Authors_Primary>Annabi,B.</Authors_Primary><Authors_Primary>Lee,Y.T.</Authors_Primary><Authors_Primary>Turcotte,S.</Authors_Primary><Authors_Primary>Naud,E.</Authors_Primary><Authors_Primary>Desrosiers,R.R.</Authors_Primary><Authors_Primary>Champagne,M.</Authors_Primary><Authors_Primary>Eliopoulos,N.</Authors_Primary><Authors_Primary>Galipeau,J.</Authors_Primary><Authors_Primary>Beliveau,R.</Authors_Primary><Date_Primary>2003</Date_Primary><Keywords>Anoxia</Keywords><Keywords>Antibodies</Keywords><Keywords>Autocrine Communication</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Line</Keywords><Keywords>Cell Movement</Keywords><Keywords>Collagen</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Down-Regulation</Keywords><Keywords>Drug Combinations</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Extracellular Matrix</Keywords><Keywords>Gels</Keywords><Keywords>genetics</Keywords><Keywords>Glioma</Keywords><Keywords>Growth Substances</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Humans</Keywords><Keywords>Laminin</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix Metalloproteinases</Keywords><Keywords>Matrix Metalloproteinases,Membrane-Associated</Keywords><Keywords>metabolism</Keywords><Keywords>Metalloendopeptidases</Keywords><Keywords>Neoplasms</Keywords><Keywords>Neovascularization,Pathologic</Keywords><Keywords>Oxygen</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proteoglycans</Keywords><Keywords>secretion</Keywords><Keywords>Stromal Cells</Keywords><Keywords>Up-Regulation</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Reprint>Not in File</Reprint><Start_Page>337</Start_Page><End_Page>347</End_Page><Periodical>Stem Cells</Periodical><Volume>21</Volume><Issue>3</Issue><Misc_3>10.1634/stemcells.21-3-337 [doi]</Misc_3><Address>Laboratoire de Medecine Moleculaire and Division of Hematology-Oncology, Centre de Cancerologie Charles-Bruneau, Hopital Sainte-Justine and Universite du Quebec a Montreal, Montreal, Quebec, Canada</Address><Web_URL>PM:12743328</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cells</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Proulx-Bonneau</Author><Year>2011</Year><RecNum>341</RecNum><IDText>A concerted HIF-1alpha/MT1-MMP signalling axis regulates the expression of the 3BP2 adaptor protein in hypoxic mesenchymal stromal cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>341</Ref_ID><Title_Primary>A concerted HIF-1alpha/MT1-MMP signalling axis regulates the expression of the 3BP2 adaptor protein in hypoxic mesenchymal stromal cells</Title_Primary><Authors_Primary>Proulx-Bonneau,S.</Authors_Primary><Authors_Primary>Guezguez,A.</Authors_Primary><Authors_Primary>Annabi,B.</Authors_Primary><Date_Primary>2011</Date_Primary><Keywords>analysis</Keywords><Keywords>Gene Silencing</Keywords><Keywords>Protein Binding</Keywords><Keywords>Stromal Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>e21511</Start_Page><Periodical>PLoS.One.</Periodical><Volume>6</Volume><Issue>6</Issue><User_Def_5>PMC3124525</User_Def_5><Misc_3>10.1371/journal.pone.0021511 [doi];PONE-D-11-05842 [pii]</Misc_3><Address>Laboratoire d&apos;Oncologie Moleculaire, Centre de recherche BIOMED, Departement de Chimie, Universite du Quebec a Montreal, Quebec, Canada</Address><Web_URL>PM:21738685</Web_URL><ZZ_JournalStdAbbrev><f name="System">PLoS.One.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>��@@�@NormalCJ_HaJmH	sH	tH	DA@�DDefault Paragraph FontRi�RTable Normal�4�
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