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��ࡱ�>��	�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������}�	��0X�bjbj�5�5	:��_�_��%�������88{{{{{�������8���D�E8��`'"III$.Rf47676767676767$=9��;$Z7�{�$$��Z7{{II��7�#�#�#��{I{I47�#�47�#�#�42|�3I����p��b�f��r!��2 780E8�2�=N"�=$�3={�3tr>�,�#�$�rrrZ7Z7�"�rrrE8������������������������������������������������������������������������=rrrrrrrrr8	A:	Molecular strategies contributing to efficient homing of Bone Marrow Stem Cells

Fatemeh Pourrajaba, b,*, (PhD),  Seyed Khalil Forouzanniaa,(MD), Seyed Hossain Hekmatimoghadama, c, (MD)
Marjan tajik kord, (MSC)

aYazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
bDepartment of Clinical Biochemistry and Molecular Biology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
cSchool of paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran



Corresponding authors: Yazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Gomhoori BLV, Yazd, Iran, Postal Code: 8917945556. 
Tel: +98 351 5231421; fax: +98 351 5253335.
E-mail address: mina_poorrajab@yahoo.com (F. Pourrajab),  HYPERLINK "mailto:drforouzan_nia@yahoo.com" drforouzan_nia@yahoo.com (S.K. Forouzannia).

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

For successful systemic stem cell therapy, BMSCs must transmigrate across the endothelium and invade their target tissue. A prerequisite for a successful usage of BMSCs is that they exit the blood circulation via transmigration and invasion. The endothelial phenotype selectively modulates BMSCs transmigration and morphological changes. BMSCs exit the blood circulation by integrating into the endothelium, penetrating the basement membrane and invading the surrounding tissue via the formation of plasmic podia. Dependent on the degree of ischemia, chemotactics play important roles in the mobilization and homing of BMSCs. This information is crucial for achieving a better control over the human BMSCs expansion and transplantation processes. 

Keywords: Vascular phenotype; key mechanism; transmigration; homing; molecular mechanism. 


Vascular phenotype of ischemic milieu, the key mechanism of transmigration
Systemic delivery of BMSCs circumvents problems associated with site-specific delivery, such as calcification and tissue damage, since none of these complications have been reported. Moreover, systemic delivery enables the delivery of multiple doses  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (36). In various regions of the vascular tree, the endothelium is functionally different and its barrier function varies accordingly. It is known that different endothelial phenotypes hold functional differences, for example, variances in the amount of intercellular tight junctions exist at different points along the vascular tree, cause differences in the endothelial permeability  ADDIN REFMGR.CITE <Refman><Cite><Author>Dejana</Author><Year>1995</Year><RecNum>406</RecNum><IDText>Endothelial cell-to-cell junctions</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>406</Ref_ID><Title_Primary>Endothelial cell-to-cell junctions</Title_Primary><Authors_Primary>Dejana,E.</Authors_Primary><Authors_Primary>Corada,M.</Authors_Primary><Authors_Primary>Lampugnani,M.G.</Authors_Primary><Date_Primary>1995/7</Date_Primary><Keywords>Blood</Keywords><Keywords>Cell Movement</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Epithelial Cells</Keywords><Keywords>Gap Junctions</Keywords><Keywords>Humans</Keywords><Keywords>Intercellular Junctions</Keywords><Keywords>Leukocytes</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Signal Transduction</Keywords><Keywords>ultrastructure</Keywords><Reprint>Not in File</Reprint><Start_Page>910</Start_Page><End_Page>918</End_Page><Periodical>FASEB J.</Periodical><Volume>9</Volume><Issue>10</Issue><Address>CEA, Laboratories of Hematologie, INSERM U217, Departement de Biologie Moleculaire et Structurale, CEN-Grenoble, France</Address><Web_URL>PM:7615160</Web_URL><ZZ_JournalStdAbbrev><f name="System">FASEB J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(6). Results indicate that BMSCs transmigration is strongly influenced by the endothelial phenotype. Coronary artery endothelium, for instance, enable the fastest BMSC integration. In contrast, over time the transmigration of MSCs across venous endothelium is most efficient. Here in, MSCs adhere and transmigrate across venous vessels more efficiently  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (7, 32, 25).
Accordingly, the time course of adhesion, integration and transmigration depends on the endothelial phenotype and is most effective in venous vessels. Rolling and adherence of BMSCs on endothelial cells have been shown to be accompanied by a rapid extension of plasmic podia. Furthermore, transmigration not only requires the interaction of vascular cell adhesion molecule-1 (VCAM-1) and very late antigen-4 (VLA-4) as verified by blocking experiments, but also triggers the clustering of �1 integrins. The key players involved in transmigration and invasion of BMSCs are the endothelial phenotype, VCAM-1/VLA-4, �1 integrins, MMP secretion and cytokines  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (4, 14). This multi-step process involves several types of adhesion molecules, proteases and cytokines. The diapedesis of leukocytes can serve as a model mechanism  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (4, 7). Most of the leukocyte adhesion molecules, for instance �2 integrin linked molecules, are not expressed on the surface of BMSCs, while expressing VLA-4 (�4�1 integrin) and VCAM-1 ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (36, 14). 
Besides integrin �4�1, BMSCs express other combinations of integrin subunits such as �6�1, �8�1 and �9�1 verified that BMSCs bind to endothelial cells in a P-selectin dependent manner and that rolling BMSCs engage VLA-4/VCAM-1 to mediate firm adhesion to endothelial cells. BMSCs require VCAM-1 and VLA-4 (�4�1 integrin) to firmly adhere as well as to transmigrate across the endothelium. In addition, the distinct clustering of �1 integrins causes downstream effects such as accumulation of the cytoskeleton  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (32, 14) . 
After ischemia, cytokines up-regulation event plays an important role in increasing the expression of adhesion molecules on endothelial cells, in recruiting BMSCs to ischemic site and in the homing of stem cells  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (42). 
The migratory activity of BMSCs is accelerated by cytokines, in particular bFGF, but also IL-6 and VEGF. Transmigration is marginally influenced by bFGF, while EPO and VEGF improved migration capacity at the early points of time. Moreover, BMSCs homing through endothelium barrier needs a functional involvement of MMPs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (36, 31).
Extracellular collagen and matrix remodeling is also a novel event for recruitment and homing of BMSCs to the site of injury  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (24, 21). Injury of cells in collagen I or collagen IV matrix produces agents capable of attracting BMSCs toward the site of injury. The results show that upon injury, cells secrete proteases which interact with collagen matrix and produce BMSC homing agents. The collagen matrix appears to be digested by secreted proteases into fragments shown to be chemotactic  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (36, 25). Thereby, MMPs play an importatnt role for migration in the inflamed site, which facilitates invasion of the subendothelial matrix. BMSCs also, secrete MMPs to penetrate the basement membrane and to invade the surrounding extracellular matrix  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (24). 
In terms of the first scenario described above where both stress response and a matrix-initiated signaling pathway need to be concurrently active, no homing effect would be expected  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (36). In terms of the second scenario, however, putative proteases released into the medium as a result of stress should produce proteolytic fragments when combined with collagen matrix and thus generate the effect. 

The hypoxia cytokines and hematopoietic signals play roles in BMSC homing 
The role of regional cerebral neural precursor cells in restoration of the CNS activity during the development of hypoxic encephalopathy and the participation of BMSCs in the formation of blood system reactions in hypoxia have been well knpwn. Here, we present evidence that under hypoxic conditions, mobilization of BMSCs is enhanced by cytokine and hematopoietic growth factors such as granulocyte colony-stimulating factor (G-CSF), Macrophage migration inhibitory factor (MIF) and IL-6  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (17, 27). Data has revealed the chemokine receptor CXCR-4/stromal cell-derived factor-1 (SDF-1) complex as a pivotal element of stem cell mobilization and homing  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (2). The expression of CXCR-4 onto the surfaces of stem cells facilitates their migration along a gradient of the CXCR-4 ligand SDF-1. Following administration of G-CSF in the impaired border zone demonstrate increased expression of intercellular adhesion molecule-1 (ICAM-1) accompanied by an accumulation of bone marrow-derived stem cells and a pronounced proliferation of endothelial and smooth muscle cells accompanied by a marked reduction of scar formation  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (2, 35). The reports have pronounced neuroprotective effects of G-CSF in hypoxia of different origin (5). G-CSF stimulates mobilization and ensures determined homing of endogenous BMSCs into damaged CNS zones with subsequent differentiation into specialized elements. G-CSF also activates extra medullary and bone marrow erythropoiesis associated with increased production of erythrocytes, ensuring the optimal gaseous homeostasis in the body, essential for rapid recovery of CNS activity  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (2, 43). The mechanisms of neuroprotective effect of G-CSF in severe oxygen insufficiency have been implied.
This protein has been shown to be significantly up-regulated in many hypoxia models and in patients suffering from ischemic diseases. Several small-scale trials of G-CSF treatment alone confirm the safety and feasibility of the approach in patients with acute myocardial infarction  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (5, 2, 43). 
In other side, high level of IL-6 serves to attract and stimulate BMSCs toward the hypoxic milieu. IL-6 is a multifunctional cytokine that plays various roles in apoptosis, cell proliferation and survival. Particularly, BMSC increased migration is depend on IL-6 signaling through the IL-6 receptor  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (27, 15). IL-6 can be a critical component for recruitment of BMSCs to the hypoxic milieu. It binds to its cognate receptor leading to activation of the JAK/STAT signal transduction pathway  ADDIN REFMGR.CITE <Refman><Cite><Author>Kishimoto</Author><Year>2005</Year><RecNum>655</RecNum><IDText>Interleukin-6: from basic science to medicine--40 years in immunology</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>655</Ref_ID><Title_Primary>Interleukin-6: from basic science to medicine--40 years in immunology</Title_Primary><Authors_Primary>Kishimoto,T.</Authors_Primary><Date_Primary>2005</Date_Primary><Keywords>Allergy and Immunology</Keywords><Keywords>Antibodies</Keywords><Keywords>Arthritis</Keywords><Keywords>B-Lymphocytes</Keywords><Keywords>culture</Keywords><Keywords>history</Keywords><Keywords>History,20th Century</Keywords><Keywords>History,21st Century</Keywords><Keywords>Humans</Keywords><Keywords>Immunoglobulin M</Keywords><Keywords>immunology</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Japan</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>1</Start_Page><End_Page>21</End_Page><Periodical>Annu.Rev.Immunol.</Periodical><Volume>23</Volume><Address>Graduate School of Frontier Bioscience, Osaka University, Osaka 565-0871, Japan. kishimot@imed3.med.osaka-u.ac.jp</Address><Web_URL>PM:15771564</Web_URL><ZZ_JournalStdAbbrev><f name="System">Annu.Rev.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(18).  IL-6 triggers the activation of Stat3 and downstream effectors, leading to alignment of actin filaments and cytoskeletal reorganization within BMSCs. The stimulation activates both Stat3 and MAPK signaling pathways to enhance migratory potential and cell survival  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (27, 15). Collectively, increased IL-6 production under hypoxic milieu establishes a critical role for its signaling in the hypoxia-mediated migration of BMSCs.
MIF is another factor involved in both angiogenesis and vasculogenesis and to be relevant for the revascularization of ischemic and hypoxic tissues. MIF can be a potential inducer of BMSCs mobilization to enhance vasculogenesis. MIF is a structurally unique pleiotropic cytokine and has been suggested to play a role in BMSC recruitment and thus can be a target of neuroprotective stem cell therapy  ADDIN REFMGR.CITE <Refman><Cite><Author>Grieb</Author><Year>2010</Year><RecNum>40</RecNum><IDText>Macrophage migration inhibitory factor is a potential inducer of endothelial progenitor cell mobilization after flap operation</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>40</Ref_ID><Title_Primary>Macrophage migration inhibitory factor is a potential inducer of endothelial progenitor cell mobilization after flap operation</Title_Primary><Authors_Primary>Grieb,G.</Authors_Primary><Authors_Primary>Piatkowski,A.</Authors_Primary><Authors_Primary>Simons,D.</Authors_Primary><Authors_Primary>Hormann,N.</Authors_Primary><Authors_Primary>Dewor,M.</Authors_Primary><Authors_Primary>Steffens,G.</Authors_Primary><Authors_Primary>Bernhagen,J.</Authors_Primary><Authors_Primary>Pallua,N.</Authors_Primary><Date_Primary>2010/12/28</Date_Primary><Keywords>analysis</Keywords><Keywords>Antibodies</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Hand</Keywords><Keywords>Ischemia</Keywords><Keywords>methods</Keywords><Keywords>surgery</Keywords><Keywords>Time</Keywords><Keywords>Wound Healing</Keywords><Reprint>Not in File</Reprint><Periodical>Surgery</Periodical><Address>Department of Plastic Surgery and Hand Surgery, Burn Center, RWTH Aachen University, Aachen, Germany; Institute of Biochemistry and Molecular Cell Biology, RWTH Aachen University, Aachen, Germany</Address><Web_URL>PM:21193209</Web_URL><ZZ_JournalStdAbbrev><f name="System">Surgery</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(39). 
Conclusively, all chemotactic pointed markers play important roles in enhancing the mobilization and homing of BMSCs, which is also dependent on the degree of ischemia.

BMSCs molecular characteristics, critical for homing and migration
Clinical studies have demonstrated the significance of stem cell homing signals which play an important role in stem cell mobilization from the bone marrow to the ischemic site. Circulating stem cells of different origin have been demonstrated to improve repair of various organs both after systemic and local application. The molecular mechanisms that direct mobilization and homing of BMSCs are only partially understood  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA ( 21, 20, 23). One of the best-studied examples is the vascular endothelial growth factor and stromal-derived factor-1 loop (VEGF-SDF1 loop), leading to VEGF-dependent mobilization of hematopoietic cells to the blood, which are then ��trapped�� in the close proximity to angiogenic vessels by SDF1, that seems mainly expressed by perivascular myofibroblasts  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (19, 11). To date, the most prominent stem cell homing factor is the chemokine SDF-1 alpha/CXCL12. SDF-1� has been known as a therapeutic stem cell homing factor in myocardial infarction  ADDIN REFMGR.CITE <Refman><Cite><Author>Ghadge</Author><Year>2011</Year><RecNum>613</RecNum><IDText>SDF-1alpha as a therapeutic stem cell homing factor in myocardial infarction</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>613</Ref_ID><Title_Primary>SDF-1alpha as a therapeutic stem cell homing factor in myocardial infarction</Title_Primary><Authors_Primary>Ghadge,S.K.</Authors_Primary><Authors_Primary>Muhlstedt,S.</Authors_Primary><Authors_Primary>Ozcelik,C.</Authors_Primary><Authors_Primary>Bader,M.</Authors_Primary><Date_Primary>2011/1</Date_Primary><Keywords>blood</Keywords><Keywords>Blood Vessels</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Movement</Keywords><Keywords>Chemokine CXCL12</Keywords><Keywords>Chemokines</Keywords><Keywords>Clinical Trials as Topic</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Receptors,CXCR4</Keywords><Keywords>Research</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>97</Start_Page><End_Page>108</End_Page><Periodical>Pharmacol.Ther.</Periodical><Volume>129</Volume><Issue>1</Issue><Address>Department of Cardiovascular and Metabolic Disease Research, Max Delbruck Center for Molecular Medicine (MDC), Robert-Rossle-Str. 10, D-13125 Berlin, Germany</Address><Web_URL>PM:20965212</Web_URL><ZZ_JournalStdAbbrev><f name="System">Pharmacol.Ther.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(11, 9). SDF-1alpha/CXCR4 has been demonstrated to be the key factors to mediate migration of BMSCs to the impaired site, for example system
ically transplanted towards ischemic lesion in annimal models  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (9, 40, 22). SDF1 receptor CXCR4 on BMSCs contributes to this process, since neutralizing antibodies against CXCR4 profoundly inhibited VEGF- and SDF-1-induced migration as well as EPC-induced angiogenesis  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (11, 22). 
The intracellular adaptor molecule FROUNT is also another molecule involved in homing and migration of BMSCs. It is a unique clathrin heavy chain repeat homology protein which interacts with CCR2. FROUNT is required for polarization of BMSCs, resulting in clustering of CCR2 and reorganization of the cytoskeleton.  The recruitment of adaptor protein FROUNT to the activated CCR2 receptor is proposed to be an important component of VEGF-SDF1 loop. Over expression of FROUNT enhances signaling via CCR2 in monocytes and stimulates chemotaxis by linking activated CCR2 to the PI(3)K-Rac-lamellipodium protrusion cascade (37). 
CCR2, monocytes chemoattractant protein (MCPs) receptor is crucial for transmigration of immune cells and development of inflammatory responses, plays pivotal roles in homing and migration of BMSCs. The CCR2 is necessary for organ-specific homing of BMSCs and a major receptor for MCP-1 (CCL2) and other MCPs including CCL8 (MCP-2) and CCL7 (MCP-3). CCR2 is a G protein-coupled receptor that is activated by MCP-1/CCL2, CCL7, CCL8, CCL12, and CCL13. Activation of intracellular effectors of CCR2 such as adenylate cyclases, PLC�s, PI3Ks, MAPKs, and RhoGEFs occurs mostly via heterotrimeric G-proteins of the GI/O and the Gq family (37, 34, 30). 
Data has shown that BMSCs summoned by the CCR2 ligand MCPs/CCLs, express SDF1 which trap additional circulating stem and progenitor cells to remodel diseased organs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (9, 30). 
Both models; ischemia/reperfusion and MCP over expression characterized by a high degree of mononuclear cell infiltration and inflammatory reactions might demonstrate the physiological relevance of MCP FROUNT-mediated clustering of CCR2 for homing of BMSCs. Clearly, stimulation of the CCR2-PI(3)K signal transduction pathway may help to summon different populations of bone marrow-derived stem cells to the impaired tissues in order to contribute to tissue remodeling  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (30, 3, 41). 
Before stimulation, CCR2 and FROUNT are evenly distributed within the cytoplasm or at a perinuclear localization. Binding of MCPs to CCR2 activates the receptor and recruits FROUNT, resulting in the clustering of CCR2 and FROUNT at the plasma membrane. The formation of clusters of CCR2 and FROUNT goes along with the polarization of cells as indicated by the asymmetric distribution of CCR2/FROUNT clusters at either side of the nucleus. The association of FROUNT with CCR2 leads to activation of PI(3)K, which results in localized formation of actin filaments and lamellipodia protrusions. The polarization of BMSCs may even be enhanced by a strong positive feedback loop that selectively amplifies the signal at the specific site  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (29, 30, 33). FROUNT expression implies profound changes in proliferation and morphology of BMSCs after activation of PI(3)K-Rac pathway  ADDIN REFMGR.CITE <Refman><Cite><Author>Charo</Author><Year>2003</Year><RecNum>292</RecNum><IDText>Chemokine receptor 2 (CCR2) in atherosclerosis, infectious diseases, and regulation of T-cell polarization</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>292</Ref_ID><Title_Primary>Chemokine receptor 2 (CCR2) in atherosclerosis, infectious diseases, and regulation of T-cell polarization</Title_Primary><Authors_Primary>Charo,I.F.</Authors_Primary><Authors_Primary>Peters,W.</Authors_Primary><Date_Primary>2003/6</Date_Primary><Keywords>Animals</Keywords><Keywords>Arteriosclerosis</Keywords><Keywords>Cell Polarity</Keywords><Keywords>Humans</Keywords><Keywords>Infection</Keywords><Keywords>Inflammation</Keywords><Keywords>Macrophages</Keywords><Keywords>metabolism</Keywords><Keywords>Monocyte Chemoattractant Proteins</Keywords><Keywords>physiology</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Receptors,Chemokine</Keywords><Keywords>T-Lymphocytes</Keywords><Reprint>Not in File</Reprint><Start_Page>259</Start_Page><End_Page>264</End_Page><Periodical>Microcirculation.</Periodical><Volume>10</Volume><Issue>3-4</Issue><Misc_3>10.1038/sj.mn.7800191 [doi];7800191 [pii]</Misc_3><Address>Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141-9100, USA. icharo@gladstone.ucsf.edu</Address><Web_URL>PM:12851643</Web_URL><ZZ_JournalFull><f name="System">Microcirculation.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Microcirculation.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(37). FROUNT pathway mediates expression of SDF-1 which therefore initiates an additional regulatory circuit  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (9, 37). CCR2-dependent pathway is also necessary for monocytes and macrophages recruitment and infiltration then inhibition of FROUNT may be used to fight various chronic inflammatory immune diseases by preventing infiltration  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (37, 34). Such an approach must certainly block homing of BMSCs, which seems to modulate inflammatory response and improve repair processes. Along another suggestion: a simple enhancement of tissue engraftment of BMSCs by over expression or injection of a single chemoattractant will most likely lead to engraftment of multiple cell types , including inflammatory cells, which might cause an enhanced inflammatory reaction thereby interfering with tissue repair.

Hypoxia enhances BMSC angiogenesis while preventing osteoblastic capacity
Since effective neo-vascularization is crucial for shortening the hypoxic episodes to which transplanted BMSCs are exposed, it seems to be worth investigating the stimulatory effects of hypoxia on angiogenic and growth factor expression by BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (1, 12). O2 tensions d" 4% are termed hypoxic conditions (as these conditions represent the hypoxia to which MSCs transplanted in vivo are subjected) and 21% O2 tensions are termed control conditions (as these conditions represent standard cell culture conditions). In vitro seeded BMSCs (expanded in vitro in 21% O2), when transplanted in vivo undergo temporary oxygen deprivation due to the lack of pre-existing blood vessels within bio-scaffolds  ADDIN REFMGR.CITE <Refman><Cite><Author>Heppenstall</Author><Year>1975</Year><RecNum>648</RecNum><IDText>Tissue gas tensions and oxygen consumption in healing bone defects</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>648</Ref_ID><Title_Primary>Tissue gas tensions and oxygen consumption in healing bone defects</Title_Primary><Authors_Primary>Heppenstall,R.B.</Authors_Primary><Authors_Primary>Grislis,G.</Authors_Primary><Authors_Primary>Hunt,T.K.</Authors_Primary><Date_Primary>1975/1</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Regeneration</Keywords><Keywords>Carbon Dioxide</Keywords><Keywords>complications</Keywords><Keywords>Dogs</Keywords><Keywords>instrumentation</Keywords><Keywords>metabolism</Keywords><Keywords>Oxygen</Keywords><Keywords>Oxygen Consumption</Keywords><Keywords>pathology</Keywords><Keywords>Research</Keywords><Keywords>Rib Fractures</Keywords><Keywords>Ribs</Keywords><Keywords>Time Factors</Keywords><Keywords>Tonometry,Ocular</Keywords><Keywords>Wound Healing</Keywords><Reprint>Not in File</Reprint><Start_Page>357</Start_Page><End_Page>365</End_Page><Periodical>Clin.Orthop.Relat Res.</Periodical><Issue>106</Issue><Web_URL>PM:1126089</Web_URL><ZZ_JournalStdAbbrev><f name="System">Clin.Orthop.Relat Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>(13). Since angiogenesis is known to contribute crucially to alleviating hypoxia, the effects of temporary hypoxia on angiogenic factor expression by BMSCs lead to a 2-fold increase in VEGF expression at both the mRNA and protein levels. Whereas, other growth factors and cytokines secreted by MSCs under control conditions (namely bFGF, TGF�1 and IL-8) is not affected by temporary exposure to hypoxia  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (26). The reports indicate that the temporary exposure of BMSCs to hypoxia leads to limited stimulation of angiogenic factor secretion but to persistent down-regulation of several osteoblastic markers, which suggests that the exposure of BMSCs transplanted in vivo to hypoxia may inhibit their bone forming potential, permanently. These findings prompt for the development of appropriate cell culture or in vivo transplantation conditions preserving the survival potential and preventing unwanted full osteogenic potential of BMSCs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (28, 38, 10).
However under hypoxia, BMSCs secrete a wide variety of angiogenic factors including VEGF, transforming growth factor-�1 (TGF�1), and basic fibroblast growth factor (bFGF), therefore modulate angiogenic processes and participate in the vascular invasion of engineered constructs  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (26, 33). Even though, hypoxia exposure up-regulates the VEGF expression but, data strongly indicate that the secretion levels of multiple angiogenic factors by BMSCs, even if they are not up-regulated by hypoxia, suffice to promote vascular invasion of ischemic tissues. BMSCs stimulate the secretion of angiogenic factors by other cell types.
The BMSC viability does not seem to be affected by temporary short-term (<72 h) hypoxia which are in agreement with previously published data, while temporary Long-term culturing (9, 16 or 24 days) of BMSCs under hypoxic conditions (~ 2% O2) results in decreased cell proliferation but not in increased apoptosis. Other reports imply prolonged exposure (120 h) to hypoxia results in increased cell death rates, whereas 48 or 72 h exposure dose not (28, 38, 10). The findings exhibit that the temporary exposure to hypoxia results in down-regulation of cbfa-1/Runx2 transcription factor which plays an essential role in controlling osteoblastic differentiation, and long-lasting inhibition of osteocalcin, a late osteogenic differentiation marker when its inhibition is associated with a large decrease in the rate of bone formation. The level of type I collagen expression is also durably and strongly inhibited by temporary exposure to hypoxia. Type I collagen is the main component of bone matrix and plays a central role in the mineralization process  ADDIN REFMGR.CITE  ADDIN EN.CITE.DATA (8, 16).


Conclusion
The aim of this review is to show the key mechanisms involved in transmigration and homing of BMSCs. The endothelium forms the main barrier for the passage of macromolecules and cells from the blood to the surrounding. Different model systems have revealed that BMSCs quickly come into contact with the endothelium and subsequently exit the blood circulation by integrating into the endothelium, penetrating the basement membrane and invading the surrounding tissue via the formation of plasmic podia. 
Under hypoxic conditions, mobilization of BMSCs is enhanced by using cytokine and hematopoietic growth factors. Also, the trophic factors released by BMSCs are sufficient to prevent in milieu stress-induced apoptosis. Understanding the mechanisms involved in BMSC transmigration, homing and neuroprotection, is an important prerequisite to the design of future cell-based therapies for degenerative diseases. 

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����y�&���e�C�$���e�1�2�4�5�7�8�:�;�=�>�G�H�I���������������������������& #$gd�c
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�����^��gdg�����& #$gd�c81�h:p�p&��. ��A!�"�#��$��%�������(2*2�D���y������K�drforouzan_nia@yahoo.com���y������K�Xmailto:drforouzan_nia@yahoo.comyX��;H�,�]ą'c���	D<Refman><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 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mechanisms</Title_Primary><Authors_Primary>Segers,V.F.</Authors_Primary><Authors_Primary>Van,Riet,I</Authors_Primary><Authors_Primary>Andries,L.J.</Authors_Primary><Authors_Primary>Lemmens,K.</Authors_Primary><Authors_Primary>Demolder,M.J.</Authors_Primary><Authors_Primary>De Becker,A.J.</Authors_Primary><Authors_Primary>Kockx,M.M.</Authors_Primary><Authors_Primary>De Keulenaer,G.W.</Authors_Primary><Date_Primary>2006/4</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Capillaries</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>Coronary Vessels</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Heart</Keywords><Keywords>Inflammation</Keywords><Keywords>Intercellular Adhesion Molecule-1</Keywords><Keywords>Mesenchymal Stem 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Cells</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Gap Junctions</Keywords><Keywords>Humans</Keywords><Keywords>Inflammation</Keywords><Keywords>Intercellular Junctions</Keywords><Keywords>Leukocytes</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proteins</Keywords><Reprint>Not in File</Reprint><Start_Page>210</Start_Page><End_Page>219</End_Page><Periodical>Haemostasis</Periodical><Volume>26 Suppl 4</Volume><Address>Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy. dejana@irfmn.mnegri.it</Address><Web_URL>PM:8979126</Web_URL><ZZ_JournalStdAbbrev><f name="System">Haemostasis</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Ruster</Author><Year>2006</Year><RecNum>610</RecNum><IDText>Mesenchymal stem cells display coordinated rolling and adhesion behavior on endothelial cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>610</Ref_ID><Title_Primary>Mesenchymal stem cells display coordinated rolling and adhesion behavior on endothelial cells</Title_Primary><Authors_Primary>Ruster,B.</Authors_Primary><Authors_Primary>Gottig,S.</Authors_Primary><Authors_Primary>Ludwig,R.J.</Authors_Primary><Authors_Primary>Bistrian,R.</Authors_Primary><Authors_Primary>Muller,S.</Authors_Primary><Authors_Primary>Seifried,E.</Authors_Primary><Authors_Primary>Gille,J.</Authors_Primary><Authors_Primary>Henschler,R.</Authors_Primary><Date_Primary>2006/12/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Antigens</Keywords><Keywords>Antigens,CD34</Keywords><Keywords>biosynthesis</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Adhesion Molecules</Keywords><Keywords>Cell Movement</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Female</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Microscopy,Video</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stress,Mechanical</Keywords><Keywords>Umbilical Veins</Keywords><Reprint>Not in File</Reprint><Start_Page>3938</Start_Page><End_Page>3944</End_Page><Periodical>Blood</Periodical><Volume>108</Volume><Issue>12</Issue><Address>DRK Institute of Transfusion Medicine and Immune Hematology, Sandhofstrasse 1, 60528 Frankfurt, Germany</Address><Web_URL>PM:16896152</Web_URL><ZZ_JournalStdAbbrev><f name="System">Blood</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ip</Author><Year>2007</Year><RecNum>266</RecNum><IDText>Mesenchymal stem cells use integrin beta1 not CXC chemokine receptor 4 for myocardial migration and engraftment</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>266</Ref_ID><Title_Primary>Mesenchymal stem cells use integrin beta1 not CXC chemokine receptor 4 for myocardial migration and engraftment</Title_Primary><Authors_Primary>Ip,J.E.</Authors_Primary><Authors_Primary>Wu,Y.</Authors_Primary><Authors_Primary>Huang,J.</Authors_Primary><Authors_Primary>Zhang,L.</Authors_Primary><Authors_Primary>Pratt,R.E.</Authors_Primary><Authors_Primary>Dzau,V.J.</Authors_Primary><Date_Primary>2007/8</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Antigens,CD29</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Movement</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Genomics</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Ligands</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred BALB C</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Receptors,Cell Surface</Keywords><Keywords>Receptors,CXCR4</Keywords><Keywords>Reproducibility of Results</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>2873</Start_Page><End_Page>2882</End_Page><Periodical>Mol.Biol.Cell</Periodical><Volume>18</Volume><Issue>8</Issue><User_Def_5>PMC1949353</User_Def_5><Misc_3>E07-02-0166 [pii];10.1091/mbc.E07-02-0166 [doi]</Misc_3><Address>Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA</Address><Web_URL>PM:17507648</Web_URL><ZZ_JournalFull><f name="System">Mol.Biol.Cell</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Mol.Biol.Cell</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><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 M.</Authors_Primary><Authors_Primary>Van,Riet,I</Authors_Primary><Date_Primary>2007/4</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chondrocytes</Keywords><Keywords>Collagen</Keywords><Keywords>cytology</Keywords><Keywords>Drug Combinations</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelium</Keywords><Keywords>Gene Expression</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Hematopoietic Stem Cell Transplantation</Keywords><Keywords>Humans</Keywords><Keywords>Laminin</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix 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></Refman>�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 M.</Authors_Primary><Authors_Primary>Van,Riet,I</Authors_Primary><Date_Primary>2007/4</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chondrocytes</Keywords><Keywords>Collagen</Keywords><Keywords>cytology</Keywords><Keywords>Drug Combinations</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelium</Keywords><Keywords>Gene Expression</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Hematopoietic Stem Cell Transplantation</Keywords><Keywords>Humans</Keywords><Keywords>Laminin</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix 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>Dejana</Author><Year>1996</Year><RecNum>670</RecNum><IDText>Adhesive proteins at endothelial cell-to-cell junctions and leukocyte extravasation</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>670</Ref_ID><Title_Primary>Adhesive proteins at endothelial cell-to-cell junctions and leukocyte extravasation</Title_Primary><Authors_Primary>Dejana,E.</Authors_Primary><Authors_Primary>Zanetti,A.</Authors_Primary><Authors_Primary>Del,Maschio A.</Authors_Primary><Date_Primary>1996/10</Date_Primary><Keywords>Animals</Keywords><Keywords>Antigens</Keywords><Keywords>Antigens,CD31</Keywords><Keywords>Cadherins</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Adhesion Molecules</Keywords><Keywords>Cell Movement</Keywords><Keywords>chemistry</Keywords><Keywords>classification</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Gap Junctions</Keywords><Keywords>Humans</Keywords><Keywords>Inflammation</Keywords><Keywords>Intercellular Junctions</Keywords><Keywords>Leukocytes</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Proteins</Keywords><Reprint>Not in File</Reprint><Start_Page>210</Start_Page><End_Page>219</End_Page><Periodical>Haemostasis</Periodical><Volume>26 Suppl 4</Volume><Address>Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy. dejana@irfmn.mnegri.it</Address><Web_URL>PM:8979126</Web_URL><ZZ_JournalStdAbbrev><f name="System">Haemostasis</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Pittenger</Author><Year>2004</Year><RecNum>2</RecNum><IDText>Mesenchymal stem cells and their potential as cardiac therapeutics</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>2</Ref_ID><Title_Primary>Mesenchymal stem cells and their potential as cardiac therapeutics</Title_Primary><Authors_Primary>Pittenger,M.F.</Authors_Primary><Authors_Primary>Martin,B.J.</Authors_Primary><Date_Primary>2004/7/9</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cardiomyoplasty</Keywords><Keywords>cytology</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Neoplasms</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Rats</Keywords><Keywords>therapy</Keywords><Keywords>Transplantation,Homologous</Keywords><Reprint>Not in File</Reprint><Start_Page>9</Start_Page><End_Page>20</End_Page><Periodical>Circ.Res.</Periodical><Volume>95</Volume><Issue>1</Issue><Misc_3>10.1161/01.RES.0000135902.99383.6f [doi];95/1/9 [pii]</Misc_3><Address>Osiris Therapeutics, Inc., 2001 Aliceanna St, Baltimore, MD 21231, USA. mpittenger@osiristx.com</Address><Web_URL>PM:15242981</Web_URL><ZZ_JournalStdAbbrev><f name="System">Circ.Res.</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></Refman>�D<Refman><Cite><Author>Ruster</Author><Year>2006</Year><RecNum>610</RecNum><IDText>Mesenchymal stem cells display coordinated rolling and adhesion behavior on endothelial cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>610</Ref_ID><Title_Primary>Mesenchymal stem cells display coordinated rolling and adhesion behavior on endothelial cells</Title_Primary><Authors_Primary>Ruster,B.</Authors_Primary><Authors_Primary>Gottig,S.</Authors_Primary><Authors_Primary>Ludwig,R.J.</Authors_Primary><Authors_Primary>Bistrian,R.</Authors_Primary><Authors_Primary>Muller,S.</Authors_Primary><Authors_Primary>Seifried,E.</Authors_Primary><Authors_Primary>Gille,J.</Authors_Primary><Authors_Primary>Henschler,R.</Authors_Primary><Date_Primary>2006/12/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Antigens</Keywords><Keywords>Antigens,CD34</Keywords><Keywords>biosynthesis</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Adhesion Molecules</Keywords><Keywords>Cell Movement</Keywords><Keywords>cytology</Keywords><Keywords>Endothelial Cells</Keywords><Keywords>Female</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Microscopy,Video</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stress,Mechanical</Keywords><Keywords>Umbilical Veins</Keywords><Reprint>Not in File</Reprint><Start_Page>3938</Start_Page><End_Page>3944</End_Page><Periodical>Blood</Periodical><Volume>108</Volume><Issue>12</Issue><Address>DRK Institute of Transfusion Medicine and Immune Hematology, Sandhofstrasse 1, 60528 Frankfurt, Germany</Address><Web_URL>PM:16896152</Web_URL><ZZ_JournalStdAbbrev><f name="System">Blood</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ip</Author><Year>2007</Year><RecNum>266</RecNum><IDText>Mesenchymal stem cells use integrin beta1 not CXC chemokine receptor 4 for myocardial migration and engraftment</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>266</Ref_ID><Title_Primary>Mesenchymal stem cells use integrin beta1 not CXC chemokine receptor 4 for myocardial migration and engraftment</Title_Primary><Authors_Primary>Ip,J.E.</Authors_Primary><Authors_Primary>Wu,Y.</Authors_Primary><Authors_Primary>Huang,J.</Authors_Primary><Authors_Primary>Zhang,L.</Authors_Primary><Authors_Primary>Pratt,R.E.</Authors_Primary><Authors_Primary>Dzau,V.J.</Authors_Primary><Date_Primary>2007/8</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Antigens,CD29</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cell Movement</Keywords><Keywords>cytology</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Genomics</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Ligands</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred BALB C</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Receptors,Cell Surface</Keywords><Keywords>Receptors,CXCR4</Keywords><Keywords>Reproducibility of Results</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>2873</Start_Page><End_Page>2882</End_Page><Periodical>Mol.Biol.Cell</Periodical><Volume>18</Volume><Issue>8</Issue><User_Def_5>PMC1949353</User_Def_5><Misc_3>E07-02-0166 [pii];10.1091/mbc.E07-02-0166 [doi]</Misc_3><Address>Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA</Address><Web_URL>PM:17507648</Web_URL><ZZ_JournalFull><f name="System">Mol.Biol.Cell</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Mol.Biol.Cell</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Segers</Author><Year>2006</Year><RecNum>669</RecNum><IDText>Mesenchymal stem cell adhesion to cardiac microvascular endothelium: activators and mechanisms</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>669</Ref_ID><Title_Primary>Mesenchymal stem cell adhesion to cardiac microvascular endothelium: activators and mechanisms</Title_Primary><Authors_Primary>Segers,V.F.</Authors_Primary><Authors_Primary>Van,Riet,I</Authors_Primary><Authors_Primary>Andries,L.J.</Authors_Primary><Authors_Primary>Lemmens,K.</Authors_Primary><Authors_Primary>Demolder,M.J.</Authors_Primary><Authors_Primary>De Becker,A.J.</Authors_Primary><Authors_Primary>Kockx,M.M.</Authors_Primary><Authors_Primary>De Keulenaer,G.W.</Authors_Primary><Date_Primary>2006/4</Date_Primary><Keywords>Animals</Keywords><Keywords>Antibodies</Keywords><Keywords>Capillaries</Keywords><Keywords>Cell Adhesion</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Coculture Techniques</Keywords><Keywords>Coronary Vessels</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelium</Keywords><Keywords>Endothelium,Vascular</Keywords><Keywords>Heart</Keywords><Keywords>Inflammation</Keywords><Keywords>Intercellular Adhesion Molecule-1</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Microcirculation</Keywords><Keywords>Myocardium</Keywords><Keywords>Necrosis</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Regeneration</Keywords><Keywords>Research</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stem Cells</Keywords><Keywords>Tumor Necrosis Factor-alpha</Keywords><Keywords>Vascular Cell Adhesion Molecule-1</Keywords><Reprint>Not in File</Reprint><Start_Page>H1370</Start_Page><End_Page>H1377</End_Page><Periodical>Am.J.Physiol Heart Circ.Physiol</Periodical><Volume>290</Volume><Issue>4</Issue><Address>Laboratory of Physiology, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerp, Belgium</Address><Web_URL>PM:16243916</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>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>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 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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>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>Malone</Author><Year>1991</Year><RecNum>612</RecNum><IDText>Recruitment of peripheral mononuclear cells by mammalian collagenase digests of type I collagen</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>612</Ref_ID><Title_Primary>Recruitment of peripheral mononuclear cells by mammalian collagenase digests of type I collagen</Title_Primary><Authors_Primary>Malone,J.D.</Authors_Primary><Authors_Primary>Richards,M.</Authors_Primary><Authors_Primary>Jeffrey,J.J.</Authors_Primary><Date_Primary>1991/8</Date_Primary><Keywords>Cell 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>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 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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></Refman>�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 M.</Authors_Primary><Authors_Primary>Van,Riet,I</Authors_Primary><Date_Primary>2007/4</Date_Primary><Keywords>Adipocytes</Keywords><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>Antibodies</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Count</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chondrocytes</Keywords><Keywords>Collagen</Keywords><Keywords>cytology</Keywords><Keywords>Drug Combinations</Keywords><Keywords>drug effects</Keywords><Keywords>Endothelium</Keywords><Keywords>Gene Expression</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>genetics</Keywords><Keywords>Hematopoietic Stem Cell Transplantation</Keywords><Keywords>Humans</Keywords><Keywords>Laminin</Keywords><Keywords>Matrix Metalloproteinase 2</Keywords><Keywords>Matrix 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 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></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></Refman>�	D<Refman><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></Refman>�D<Refman><Cite><Author>Kuethe</Author><Year>2005</Year><RecNum>654</RecNum><IDText>Treatment with granulocyte colony-stimulating factor for mobilization of bone marrow cells in patients with acute myocardial infarction</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>654</Ref_ID><Title_Primary>Treatment with granulocyte colony-stimulating factor for mobilization of bone marrow cells in patients with acute myocardial infarction</Title_Primary><Authors_Primary>Kuethe,F.</Authors_Primary><Authors_Primary>Figulla,H.R.</Authors_Primary><Authors_Primary>Herzau,M.</Authors_Primary><Authors_Primary>Voth,M.</Authors_Primary><Authors_Primary>Fritzenwanger,M.</Authors_Primary><Authors_Primary>Opfermann,T.</Authors_Primary><Authors_Primary>Pachmann,K.</Authors_Primary><Authors_Primary>Krack,A.</Authors_Primary><Authors_Primary>Sayer,H.G.</Authors_Primary><Authors_Primary>Gottschild,D.</Authors_Primary><Authors_Primary>Werner,G.S.</Authors_Primary><Date_Primary>2005/7</Date_Primary><Keywords>Body Weight</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Feasibility Studies</Keywords><Keywords>Female</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Perfusion</Keywords><Keywords>Prospective Studies</Keywords><Keywords>Regeneration</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>115</Start_Page><Periodical>Am.Heart J.</Periodical><Volume>150</Volume><Issue>1</Issue><Address>Klinik fuer Innere Medizin I, Friedrich-Schiller-Universitaet Jena, Jena, Germany. friedhelm.kuethe@med.uni-jena.de</Address><Web_URL>PM:16086558</Web_URL><ZZ_JournalStdAbbrev><f name="System">Am.Heart J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Brunner</Author><Year>2008</Year><RecNum>39</RecNum><IDText>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>39</Ref_ID><Title_Primary>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</Title_Primary><Authors_Primary>Brunner,S.</Authors_Primary><Authors_Primary>Huber,B.C.</Authors_Primary><Authors_Primary>Fischer,R.</Authors_Primary><Authors_Primary>Groebner,M.</Authors_Primary><Authors_Primary>Hacker,M.</Authors_Primary><Authors_Primary>David,R.</Authors_Primary><Authors_Primary>Zaruba,M.M.</Authors_Primary><Authors_Primary>Vallaster,M.</Authors_Primary><Authors_Primary>Rischpler,C.</Authors_Primary><Authors_Primary>Wilke,A.</Authors_Primary><Authors_Primary>Gerbitz,A.</Authors_Primary><Authors_Primary>Franz,W.M.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Dna</Keywords><Keywords>DNA Primers</Keywords><Keywords>drug therapy</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Genes,Reporter</Keywords><Keywords>genetics</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Green Fluorescent Proteins</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Perfusion</Keywords><Keywords>Polymerase Chain Reaction</Keywords><Keywords>Proteins</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>surgery</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>695</Start_Page><End_Page>702</End_Page><Periodical>Exp.Hematol.</Periodical><Volume>36</Volume><Issue>6</Issue><Address>Ludwig-Maximilians-University, Klinikum Grosshadern, Medical Department I, Munich, Germany</Address><Web_URL>PM:18346841</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Hematol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Rattigan</Author><Year>2010</Year><RecNum>44</RecNum><IDText>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>44</Ref_ID><Title_Primary>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</Title_Primary><Authors_Primary>Rattigan,Y.</Authors_Primary><Authors_Primary>Hsu,J.M.</Authors_Primary><Authors_Primary>Mishra,P.J.</Authors_Primary><Authors_Primary>Glod,J.</Authors_Primary><Authors_Primary>Banerjee,D.</Authors_Primary><Date_Primary>2010/12/10</Date_Primary><Keywords>Antibodies</Keywords><Keywords>bcl-X Protein</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Breast Neoplasms</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line,Tumor</Keywords><Keywords>Cell Migration Assays</Keywords><Keywords>Cell Survival</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytoskeleton</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinase 1</Keywords><Keywords>Mitogen-Activated Protein Kinase 3</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Recombinant Proteins</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Small Interfering</Keywords><Keywords>Signal Transduction</Keywords><Keywords>STAT3 Transcription Factor</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>3417</Start_Page><End_Page>3424</End_Page><Periodical>Exp.Cell Res.</Periodical><Volume>316</Volume><Issue>20</Issue><Address>Department of Pharmacology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA</Address><Web_URL>PM:20633553</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Deindl</Author><Year>2006</Year><RecNum>48</RecNum><IDText>G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>48</Ref_ID><Title_Primary>G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis</Title_Primary><Authors_Primary>Deindl,E.</Authors_Primary><Authors_Primary>Zaruba,M.M.</Authors_Primary><Authors_Primary>Brunner,S.</Authors_Primary><Authors_Primary>Huber,B.</Authors_Primary><Authors_Primary>Mehl,U.</Authors_Primary><Authors_Primary>Assmann,G.</Authors_Primary><Authors_Primary>Hoefer,I.E.</Authors_Primary><Authors_Primary>Mueller-Hoecker,J.</Authors_Primary><Authors_Primary>Franz,W.M.</Authors_Primary><Date_Primary>2006/5</Date_Primary><Keywords>administration &amp; dosage</Keywords><Keywords>Animals</Keywords><Keywords>Arterioles</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cell Death</Keywords><Keywords>Coronary Vessels</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocardium</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>T-Lymphocyte Subsets</Keywords><Keywords>therapeutic use</Keywords><Reprint>Not in File</Reprint><Start_Page>956</Start_Page><End_Page>958</End_Page><Periodical>FASEB J.</Periodical><Volume>20</Volume><Issue>7</Issue><Address>Ludwig-Maximilians University, Klinikum Grosshadern, Medical Department I, Marchioninistr. 15, D-81377 Munich, Germany</Address><Web_URL>PM:16571777</Web_URL><ZZ_JournalStdAbbrev><f name="System">FASEB J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Brunner</Author><Year>2008</Year><RecNum>39</RecNum><IDText>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>39</Ref_ID><Title_Primary>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</Title_Primary><Authors_Primary>Brunner,S.</Authors_Primary><Authors_Primary>Huber,B.C.</Authors_Primary><Authors_Primary>Fischer,R.</Authors_Primary><Authors_Primary>Groebner,M.</Authors_Primary><Authors_Primary>Hacker,M.</Authors_Primary><Authors_Primary>David,R.</Authors_Primary><Authors_Primary>Zaruba,M.M.</Authors_Primary><Authors_Primary>Vallaster,M.</Authors_Primary><Authors_Primary>Rischpler,C.</Authors_Primary><Authors_Primary>Wilke,A.</Authors_Primary><Authors_Primary>Gerbitz,A.</Authors_Primary><Authors_Primary>Franz,W.M.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Dna</Keywords><Keywords>DNA Primers</Keywords><Keywords>drug therapy</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Genes,Reporter</Keywords><Keywords>genetics</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Green Fluorescent Proteins</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Perfusion</Keywords><Keywords>Polymerase Chain Reaction</Keywords><Keywords>Proteins</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>surgery</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>695</Start_Page><End_Page>702</End_Page><Periodical>Exp.Hematol.</Periodical><Volume>36</Volume><Issue>6</Issue><Address>Ludwig-Maximilians-University, Klinikum Grosshadern, Medical Department I, Munich, Germany</Address><Web_URL>PM:18346841</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Hematol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Deindl</Author><Year>2006</Year><RecNum>48</RecNum><IDText>G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>48</Ref_ID><Title_Primary>G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis</Title_Primary><Authors_Primary>Deindl,E.</Authors_Primary><Authors_Primary>Zaruba,M.M.</Authors_Primary><Authors_Primary>Brunner,S.</Authors_Primary><Authors_Primary>Huber,B.</Authors_Primary><Authors_Primary>Mehl,U.</Authors_Primary><Authors_Primary>Assmann,G.</Authors_Primary><Authors_Primary>Hoefer,I.E.</Authors_Primary><Authors_Primary>Mueller-Hoecker,J.</Authors_Primary><Authors_Primary>Franz,W.M.</Authors_Primary><Date_Primary>2006/5</Date_Primary><Keywords>administration &amp; dosage</Keywords><Keywords>Animals</Keywords><Keywords>Arterioles</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cardiomyopathies</Keywords><Keywords>Cell Death</Keywords><Keywords>Coronary Vessels</Keywords><Keywords>cytology</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Ischemia</Keywords><Keywords>Myocardium</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>T-Lymphocyte Subsets</Keywords><Keywords>therapeutic use</Keywords><Reprint>Not in File</Reprint><Start_Page>956</Start_Page><End_Page>958</End_Page><Periodical>FASEB J.</Periodical><Volume>20</Volume><Issue>7</Issue><Address>Ludwig-Maximilians University, Klinikum Grosshadern, Medical Department I, Marchioninistr. 15, D-81377 Munich, Germany</Address><Web_URL>PM:16571777</Web_URL><ZZ_JournalStdAbbrev><f name="System">FASEB J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman> D<Refman><Cite><Author>Kuethe</Author><Year>2004</Year><RecNum>109</RecNum><IDText>[Mobilization of stem cells by granulocyte colony-stimulating factor for the regeneration of myocardial tissue after myocardial infarction]</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>109</Ref_ID><Title_Primary>[Mobilization of stem cells by granulocyte colony-stimulating factor for the regeneration of myocardial tissue after myocardial infarction]</Title_Primary><Authors_Primary>Kuethe,F.</Authors_Primary><Authors_Primary>Figulla,H.R.</Authors_Primary><Authors_Primary>Voth,M.</Authors_Primary><Authors_Primary>Richartz,B.M.</Authors_Primary><Authors_Primary>Opfermann,T.</Authors_Primary><Authors_Primary>Sayer,H.G.</Authors_Primary><Authors_Primary>Krack,A.</Authors_Primary><Authors_Primary>Fritzenwanger,M.</Authors_Primary><Authors_Primary>Hoffken,K.</Authors_Primary><Authors_Primary>Gottschild,D.</Authors_Primary><Authors_Primary>Werner,G.S.</Authors_Primary><Date_Primary>2004/2/27</Date_Primary><Keywords>Adult</Keywords><Keywords>Aged</Keywords><Keywords>Angioplasty,Balloon,Coronary</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Electrocardiography</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Reperfusion</Keywords><Keywords>Myocardial Revascularization</Keywords><Keywords>Perfusion</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Safety</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stents</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>Tomography,Emission-Computed</Keywords><Keywords>Tomography,Emission-Computed,Single-Photon</Keywords><Keywords>Ventricular Function,Left</Keywords><Reprint>Not in File</Reprint><Start_Page>424</Start_Page><End_Page>428</End_Page><Periodical>Dtsch.Med.Wochenschr.</Periodical><Volume>129</Volume><Issue>9</Issue><Address>Klinik fur Innere Medizin I, Freiedrich-Schiller-Universitat, Jena. Friedheim.Kuethe@med.uni-jena.de</Address><Web_URL>PM:14970913</Web_URL><ZZ_JournalStdAbbrev><f name="System">Dtsch.Med.Wochenschr.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Zyuz&apos;kov</Author><Year>2005</Year><RecNum>657</RecNum><IDText>Role of stem cells in adaptation to hypoxia and mechanisms of neuroprotective effect of granulocytic colony-stimulating factor</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>657</Ref_ID><Title_Primary>Role of stem cells in adaptation to hypoxia and mechanisms of neuroprotective effect of granulocytic colony-stimulating factor</Title_Primary><Authors_Primary>Zyuz&apos;kov,G.N.</Authors_Primary><Authors_Primary>Suslov,N.I.</Authors_Primary><Authors_Primary>Dygai,A.M.</Authors_Primary><Authors_Primary>Zhdanov,V.V.</Authors_Primary><Authors_Primary>Gol&apos;dberg,E.D.</Authors_Primary><Date_Primary>2005/11</Date_Primary><Keywords>Animals</Keywords><Keywords>Anoxia</Keywords><Keywords>blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Central Nervous System</Keywords><Keywords>cytology</Keywords><Keywords>Erythroid Precursor Cells</Keywords><Keywords>Erythropoiesis</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred CBA</Keywords><Keywords>Neurons</Keywords><Keywords>Neuroprotective Agents</Keywords><Keywords>Oxygen</Keywords><Keywords>pharmacology</Keywords><Keywords>Research</Keywords><Keywords>Stem Cells</Keywords><Keywords>Time Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>606</Start_Page><End_Page>611</End_Page><Periodical>Bull.Exp.Biol.Med.</Periodical><Volume>140</Volume><Issue>5</Issue><Address>Institute of Pharmacology, Tomsk Research Center, Siberian Division of Russian Academy of Medical Sciences</Address><Web_URL>PM:16758637</Web_URL><ZZ_JournalFull><f name="System">Bull.Exp.Biol.Med.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Bull.Exp.Biol.Med.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Valgimigli</Author><Year>2005</Year><RecNum>658</RecNum><IDText>Use of granulocyte-colony stimulating factor during acute myocardial infarction to enhance bone marrow stem cell mobilization in humans: clinical and angiographic safety profile</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>658</Ref_ID><Title_Primary>Use of granulocyte-colony stimulating factor during acute myocardial infarction to enhance bone marrow stem cell mobilization in humans: clinical and angiographic safety profile</Title_Primary><Authors_Primary>Valgimigli,M.</Authors_Primary><Authors_Primary>Rigolin,G.M.</Authors_Primary><Authors_Primary>Cittanti,C.</Authors_Primary><Authors_Primary>Malagutti,P.</Authors_Primary><Authors_Primary>Curello,S.</Authors_Primary><Authors_Primary>Percoco,G.</Authors_Primary><Authors_Primary>Bugli,A.M.</Authors_Primary><Authors_Primary>Della,Porta M.</Authors_Primary><Authors_Primary>Bragotti,L.Z.</Authors_Primary><Authors_Primary>Ansani,L.</Authors_Primary><Authors_Primary>Mauro,E.</Authors_Primary><Authors_Primary>Lanfranchi,A.</Authors_Primary><Authors_Primary>Giganti,M.</Authors_Primary><Authors_Primary>Feggi,L.</Authors_Primary><Authors_Primary>Castoldi,G.</Authors_Primary><Authors_Primary>Ferrari,R.</Authors_Primary><Date_Primary>2005/9</Date_Primary><Keywords>Antigens</Keywords><Keywords>Antigens,CD34</Keywords><Keywords>blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Coronary Angiography</Keywords><Keywords>Coronary Circulation</Keywords><Keywords>Coronary Restenosis</Keywords><Keywords>Coronary Stenosis</Keywords><Keywords>etiology</Keywords><Keywords>Feasibility Studies</Keywords><Keywords>Female</Keywords><Keywords>Filgrastim</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>Humans</Keywords><Keywords>injuries</Keywords><Keywords>Male</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Perfusion</Keywords><Keywords>physiopathology</Keywords><Keywords>Recovery of Function</Keywords><Keywords>Research</Keywords><Keywords>Safety</Keywords><Keywords>Single-Blind Method</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>Treatment Outcome</Keywords><Keywords>Ventricular Dysfunction,Left</Keywords><Reprint>Not in File</Reprint><Start_Page>1838</Start_Page><End_Page>1845</End_Page><Periodical>Eur.Heart J.</Periodical><Volume>26</Volume><Issue>18</Issue><Address>Section of Cardiology, University of Ferrara and Cardiovascular Research Centre, Arcispedale S. Anna C.rso Giovecca 203, 44100 Ferrara, Italy. vlgmrc@unife.it</Address><Web_URL>PM:15860518</Web_URL><ZZ_JournalFull><f name="System">Eur.Heart J.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Eur.Heart J.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Kuethe</Author><Year>2004</Year><RecNum>109</RecNum><IDText>[Mobilization of stem cells by granulocyte colony-stimulating factor for the regeneration of myocardial tissue after myocardial infarction]</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>109</Ref_ID><Title_Primary>[Mobilization of stem cells by granulocyte colony-stimulating factor for the regeneration of myocardial tissue after myocardial infarction]</Title_Primary><Authors_Primary>Kuethe,F.</Authors_Primary><Authors_Primary>Figulla,H.R.</Authors_Primary><Authors_Primary>Voth,M.</Authors_Primary><Authors_Primary>Richartz,B.M.</Authors_Primary><Authors_Primary>Opfermann,T.</Authors_Primary><Authors_Primary>Sayer,H.G.</Authors_Primary><Authors_Primary>Krack,A.</Authors_Primary><Authors_Primary>Fritzenwanger,M.</Authors_Primary><Authors_Primary>Hoffken,K.</Authors_Primary><Authors_Primary>Gottschild,D.</Authors_Primary><Authors_Primary>Werner,G.S.</Authors_Primary><Date_Primary>2004/2/27</Date_Primary><Keywords>Adult</Keywords><Keywords>Aged</Keywords><Keywords>Angioplasty,Balloon,Coronary</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>drug effects</Keywords><Keywords>drug therapy</Keywords><Keywords>Electrocardiography</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>methods</Keywords><Keywords>Middle Aged</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardial Reperfusion</Keywords><Keywords>Myocardial Revascularization</Keywords><Keywords>Perfusion</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Regeneration</Keywords><Keywords>Safety</Keywords><Keywords>Stem Cells</Keywords><Keywords>Stents</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>Tomography,Emission-Computed</Keywords><Keywords>Tomography,Emission-Computed,Single-Photon</Keywords><Keywords>Ventricular Function,Left</Keywords><Reprint>Not in File</Reprint><Start_Page>424</Start_Page><End_Page>428</End_Page><Periodical>Dtsch.Med.Wochenschr.</Periodical><Volume>129</Volume><Issue>9</Issue><Address>Klinik fur Innere Medizin I, Freiedrich-Schiller-Universitat, Jena. Friedheim.Kuethe@med.uni-jena.de</Address><Web_URL>PM:14970913</Web_URL><ZZ_JournalStdAbbrev><f name="System">Dtsch.Med.Wochenschr.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Brunner</Author><Year>2008</Year><RecNum>39</RecNum><IDText>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>39</Ref_ID><Title_Primary>G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells</Title_Primary><Authors_Primary>Brunner,S.</Authors_Primary><Authors_Primary>Huber,B.C.</Authors_Primary><Authors_Primary>Fischer,R.</Authors_Primary><Authors_Primary>Groebner,M.</Authors_Primary><Authors_Primary>Hacker,M.</Authors_Primary><Authors_Primary>David,R.</Authors_Primary><Authors_Primary>Zaruba,M.M.</Authors_Primary><Authors_Primary>Vallaster,M.</Authors_Primary><Authors_Primary>Rischpler,C.</Authors_Primary><Authors_Primary>Wilke,A.</Authors_Primary><Authors_Primary>Gerbitz,A.</Authors_Primary><Authors_Primary>Franz,W.M.</Authors_Primary><Date_Primary>2008/6</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Blood</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Bone Marrow Transplantation</Keywords><Keywords>Cell Transplantation</Keywords><Keywords>Disease Models,Animal</Keywords><Keywords>Dna</Keywords><Keywords>DNA Primers</Keywords><Keywords>drug therapy</Keywords><Keywords>Flow Cytometry</Keywords><Keywords>Genes,Reporter</Keywords><Keywords>genetics</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Green Fluorescent Proteins</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cell Mobilization</Keywords><Keywords>methods</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Perfusion</Keywords><Keywords>Polymerase Chain Reaction</Keywords><Keywords>Proteins</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>surgery</Keywords><Keywords>therapeutic use</Keywords><Keywords>therapy</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>695</Start_Page><End_Page>702</End_Page><Periodical>Exp.Hematol.</Periodical><Volume>36</Volume><Issue>6</Issue><Address>Ludwig-Maximilians-University, Klinikum Grosshadern, Medical Department I, Munich, Germany</Address><Web_URL>PM:18346841</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Hematol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><Cite><Author>Kishimoto</Author><Year>2005</Year><RecNum>655</RecNum><IDText>Interleukin-6: from basic science to medicine--40 years in immunology</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>655</Ref_ID><Title_Primary>Interleukin-6: from basic science to medicine--40 years in immunology</Title_Primary><Authors_Primary>Kishimoto,T.</Authors_Primary><Date_Primary>2005</Date_Primary><Keywords>Allergy and Immunology</Keywords><Keywords>Antibodies</Keywords><Keywords>Arthritis</Keywords><Keywords>B-Lymphocytes</Keywords><Keywords>culture</Keywords><Keywords>history</Keywords><Keywords>History,20th Century</Keywords><Keywords>History,21st Century</Keywords><Keywords>Humans</Keywords><Keywords>Immunoglobulin M</Keywords><Keywords>immunology</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Japan</Keywords><Keywords>Research</Keywords><Keywords>Signal Transduction</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>1</Start_Page><End_Page>21</End_Page><Periodical>Annu.Rev.Immunol.</Periodical><Volume>23</Volume><Address>Graduate School of Frontier Bioscience, Osaka University, Osaka 565-0871, Japan. kishimot@imed3.med.osaka-u.ac.jp</Address><Web_URL>PM:15771564</Web_URL><ZZ_JournalStdAbbrev><f name="System">Annu.Rev.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Rattigan</Author><Year>2010</Year><RecNum>44</RecNum><IDText>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>44</Ref_ID><Title_Primary>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</Title_Primary><Authors_Primary>Rattigan,Y.</Authors_Primary><Authors_Primary>Hsu,J.M.</Authors_Primary><Authors_Primary>Mishra,P.J.</Authors_Primary><Authors_Primary>Glod,J.</Authors_Primary><Authors_Primary>Banerjee,D.</Authors_Primary><Date_Primary>2010/12/10</Date_Primary><Keywords>Antibodies</Keywords><Keywords>bcl-X Protein</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Breast Neoplasms</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line,Tumor</Keywords><Keywords>Cell Migration Assays</Keywords><Keywords>Cell Survival</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytoskeleton</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinase 1</Keywords><Keywords>Mitogen-Activated Protein Kinase 3</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Recombinant Proteins</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Small Interfering</Keywords><Keywords>Signal Transduction</Keywords><Keywords>STAT3 Transcription Factor</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>3417</Start_Page><End_Page>3424</End_Page><Periodical>Exp.Cell Res.</Periodical><Volume>316</Volume><Issue>20</Issue><Address>Department of Pharmacology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA</Address><Web_URL>PM:20633553</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>D<Refman><Cite><Author>Gao</Author><Year>2009</Year><RecNum>656</RecNum><IDText>Activation of signal transducers and activators of transcription 3 and focal adhesion kinase by stromal cell-derived factor 1 is required for migration of human mesenchymal stem cells in response to tumor cell-conditioned medium</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>656</Ref_ID><Title_Primary>Activation of signal transducers and activators of transcription 3 and focal adhesion kinase by stromal cell-derived factor 1 is required for migration of human mesenchymal stem cells in response to tumor cell-conditioned medium</Title_Primary><Authors_Primary>Gao,H.</Authors_Primary><Authors_Primary>Priebe,W.</Authors_Primary><Authors_Primary>Glod,J.</Authors_Primary><Authors_Primary>Banerjee,D.</Authors_Primary><Date_Primary>2009/4</Date_Primary><Keywords>analysis</Keywords><Keywords>Blotting,Western</Keywords><Keywords>Cell Line,Tumor</Keywords><Keywords>Cell Movement</Keywords><Keywords>Chemokine CXCL12</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytoskeleton</Keywords><Keywords>Extracellular Signal-Regulated MAP Kinases</Keywords><Keywords>Fluorescent Antibody Technique</Keywords><Keywords>Focal Adhesion Protein-Tyrosine Kinases</Keywords><Keywords>Gene Expression</Keywords><Keywords>Gene Expression Profiling</Keywords><Keywords>Gene Knockdown Techniques</Keywords><Keywords>Humans</Keywords><Keywords>Janus Kinase 2</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Protein-Tyrosine Kinases</Keywords><Keywords>Proteins</Keywords><Keywords>Receptors,CXCR</Keywords><Keywords>Receptors,CXCR4</Keywords><Keywords>Recombinant Proteins</Keywords><Keywords>Research</Keywords><Keywords>Reverse Transcriptase Polymerase Chain Reaction</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Small Interfering</Keywords><Keywords>Signal Transduction</Keywords><Keywords>STAT3 Transcription Factor</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>857</Start_Page><End_Page>865</End_Page><Periodical>Stem Cells</Periodical><Volume>27</Volume><Issue>4</Issue><Address>Department of Medicine, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey, USA</Address><Web_URL>PM:19350687</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cells</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Rattigan</Author><Year>2010</Year><RecNum>44</RecNum><IDText>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>44</Ref_ID><Title_Primary>Interleukin 6 mediated recruitment of mesenchymal stem cells to the hypoxic tumor milieu</Title_Primary><Authors_Primary>Rattigan,Y.</Authors_Primary><Authors_Primary>Hsu,J.M.</Authors_Primary><Authors_Primary>Mishra,P.J.</Authors_Primary><Authors_Primary>Glod,J.</Authors_Primary><Authors_Primary>Banerjee,D.</Authors_Primary><Date_Primary>2010/12/10</Date_Primary><Keywords>Antibodies</Keywords><Keywords>bcl-X Protein</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Breast Neoplasms</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Line,Tumor</Keywords><Keywords>Cell Migration Assays</Keywords><Keywords>Cell Survival</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Culture Media</Keywords><Keywords>Culture Media,Conditioned</Keywords><Keywords>Cytoskeleton</Keywords><Keywords>drug effects</Keywords><Keywords>Female</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>immunology</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinase 1</Keywords><Keywords>Mitogen-Activated Protein Kinase 3</Keywords><Keywords>Paracrine Communication</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Recombinant Proteins</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Small Interfering</Keywords><Keywords>Signal Transduction</Keywords><Keywords>STAT3 Transcription Factor</Keywords><Keywords>Stem Cells</Keywords><Reprint>Not in File</Reprint><Start_Page>3417</Start_Page><End_Page>3424</End_Page><Periodical>Exp.Cell Res.</Periodical><Volume>316</Volume><Issue>20</Issue><Address>Department of Pharmacology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA</Address><Web_URL>PM:20633553</Web_URL><ZZ_JournalStdAbbrev><f name="System">Exp.Cell Res.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Kishimoto</Author><Year>2005</Year><RecNum>655</RecNum><IDText>Interleukin-6: from basic science to medicine--40 years in immunology</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>655</Ref_ID><Title_Primary>Interleukin-6: from basic science to medicine--40 years in immunology</Title_Primary><Authors_Primary>Kishimoto,T.</Authors_Primary><Date_Primary>2005</Date_Primary><Keywords>Allergy 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Membrane</Keywords><Keywords>chemistry</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Clathrin Heavy Chains</Keywords><Keywords>Cloning,Molecular</Keywords><Keywords>cytology</Keywords><Keywords>Cytoplasm</Keywords><Keywords>Dna</Keywords><Keywords>DNA,Complementary</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>genetics</Keywords><Keywords>Glutathione Transferase</Keywords><Keywords>Humans</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>immunology</Keywords><Keywords>Inflammation</Keywords><Keywords>Ligands</Keywords><Keywords>Macrophages</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Microscopy,Fluorescence</Keywords><Keywords>Molecular Sequence Data</Keywords><Keywords>Monocytes</Keywords><Keywords>Mutation</Keywords><Keywords>Nuclear Pore Complex Proteins</Keywords><Keywords>Peptides</Keywords><Keywords>Peritonitis</Keywords><Keywords>Phosphatidylinositol 3-Kinases</Keywords><Keywords>physiology</Keywords><Keywords>Protein Transport</Keywords><Keywords>Pseudopodia</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Receptors,Chemokine</Keywords><Keywords>Retroviridae</Keywords><Keywords>Sequence Analysis,DNA</Keywords><Keywords>Sequence Homology,Amino Acid</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Subcellular Fractions</Keywords><Keywords>Time Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>827</Start_Page><End_Page>835</End_Page><Periodical>Nat.Immunol.</Periodical><Volume>6</Volume><Issue>8</Issue><Misc_3>ni1222 [pii];10.1038/ni1222 [doi]</Misc_3><Address>Department of Molecular Preventive Medicine (and Solution Oriented Research for Science and Technology), Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan</Address><Web_URL>PM:15995708</Web_URL><ZZ_JournalFull><f name="System">Nat.Immunol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Nat.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ghadge</Author><Year>2011</Year><RecNum>613</RecNum><IDText>SDF-1alpha as a therapeutic stem cell homing factor in myocardial infarction</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>613</Ref_ID><Title_Primary>SDF-1alpha as a therapeutic stem cell homing factor in myocardial infarction</Title_Primary><Authors_Primary>Ghadge,S.K.</Authors_Primary><Authors_Primary>Muhlstedt,S.</Authors_Primary><Authors_Primary>Ozcelik,C.</Authors_Primary><Authors_Primary>Bader,M.</Authors_Primary><Date_Primary>2011/1</Date_Primary><Keywords>blood</Keywords><Keywords>Blood Vessels</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Movement</Keywords><Keywords>Chemokine CXCL12</Keywords><Keywords>Chemokines</Keywords><Keywords>Clinical Trials as Topic</Keywords><Keywords>Heart</Keywords><Keywords>Hematopoietic Stem Cells</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Neovascularization,Physiologic</Keywords><Keywords>pathology</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>physiopathology</Keywords><Keywords>Receptors,CXCR4</Keywords><Keywords>Research</Keywords><Keywords>Stem Cell Transplantation</Keywords><Keywords>Stem Cells</Keywords><Keywords>therapy</Keywords><Reprint>Not in File</Reprint><Start_Page>97</Start_Page><End_Page>108</End_Page><Periodical>Pharmacol.Ther.</Periodical><Volume>129</Volume><Issue>1</Issue><Address>Department of Cardiovascular and Metabolic Disease Research, Max Delbruck Center for Molecular Medicine (MDC), Robert-Rossle-Str. 10, D-13125 Berlin, Germany</Address><Web_URL>PM:20965212</Web_URL><ZZ_JournalStdAbbrev><f name="System">Pharmacol.Ther.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Belema-Bedada</Author><Year>2008</Year><RecNum>83</RecNum><IDText>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>83</Ref_ID><Title_Primary>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</Title_Primary><Authors_Primary>Belema-Bedada,F.</Authors_Primary><Authors_Primary>Uchida,S.</Authors_Primary><Authors_Primary>Martire,A.</Authors_Primary><Authors_Primary>Kostin,S.</Authors_Primary><Authors_Primary>Braun,T.</Authors_Primary><Date_Primary>2008/6/5</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemokine CCL2</Keywords><Keywords>Clathrin Heavy Chains</Keywords><Keywords>cytology</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Microfilaments</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>Receptor Aggregation</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Reperfusion Injury</Keywords><Keywords>Stem Cells</Keywords><Keywords>Transfection</Keywords><Keywords>Transgenes</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>566</Start_Page><End_Page>575</End_Page><Periodical>Cell Stem Cell</Periodical><Volume>2</Volume><Issue>6</Issue><Misc_3>S1934-5909(08)00115-X [pii];10.1016/j.stem.2008.03.003 [doi]</Misc_3><Address>Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany</Address><Web_URL>PM:18522849</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>Belema-Bedada</Author><Year>2008</Year><RecNum>83</RecNum><IDText>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>83</Ref_ID><Title_Primary>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</Title_Primary><Authors_Primary>Belema-Bedada,F.</Authors_Primary><Authors_Primary>Uchida,S.</Authors_Primary><Authors_Primary>Martire,A.</Authors_Primary><Authors_Primary>Kostin,S.</Authors_Primary><Authors_Primary>Braun,T.</Authors_Primary><Date_Primary>2008/6/5</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemokine CCL2</Keywords><Keywords>Clathrin Heavy Chains</Keywords><Keywords>cytology</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Microfilaments</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>Receptor Aggregation</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Reperfusion Injury</Keywords><Keywords>Stem Cells</Keywords><Keywords>Transfection</Keywords><Keywords>Transgenes</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>566</Start_Page><End_Page>575</End_Page><Periodical>Cell Stem Cell</Periodical><Volume>2</Volume><Issue>6</Issue><Misc_3>S1934-5909(08)00115-X [pii];10.1016/j.stem.2008.03.003 [doi]</Misc_3><Address>Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany</Address><Web_URL>PM:18522849</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>Belema-Bedada</Author><Year>2008</Year><RecNum>83</RecNum><IDText>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>83</Ref_ID><Title_Primary>Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2</Title_Primary><Authors_Primary>Belema-Bedada,F.</Authors_Primary><Authors_Primary>Uchida,S.</Authors_Primary><Authors_Primary>Martire,A.</Authors_Primary><Authors_Primary>Kostin,S.</Authors_Primary><Authors_Primary>Braun,T.</Authors_Primary><Date_Primary>2008/6/5</Date_Primary><Keywords>Adult</Keywords><Keywords>Adult Stem Cells</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Movement</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Chemokine CCL2</Keywords><Keywords>Clathrin Heavy Chains</Keywords><Keywords>cytology</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Microfilaments</Keywords><Keywords>Myocardium</Keywords><Keywords>pathology</Keywords><Keywords>Receptor Aggregation</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Reperfusion Injury</Keywords><Keywords>Stem Cells</Keywords><Keywords>Transfection</Keywords><Keywords>Transgenes</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>566</Start_Page><End_Page>575</End_Page><Periodical>Cell Stem Cell</Periodical><Volume>2</Volume><Issue>6</Issue><Misc_3>S1934-5909(08)00115-X [pii];10.1016/j.stem.2008.03.003 [doi]</Misc_3><Address>Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany</Address><Web_URL>PM:18522849</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><Cite><Author>Terashima</Author><Year>2005</Year><RecNum>313</RecNum><IDText>Pivotal function for cytoplasmic protein FROUNT in CCR2-mediated monocyte chemotaxis</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>313</Ref_ID><Title_Primary>Pivotal function for cytoplasmic protein FROUNT in CCR2-mediated monocyte chemotaxis</Title_Primary><Authors_Primary>Terashima,Y.</Authors_Primary><Authors_Primary>Onai,N.</Authors_Primary><Authors_Primary>Murai,M.</Authors_Primary><Authors_Primary>Enomoto,M.</Authors_Primary><Authors_Primary>Poonpiriya,V.</Authors_Primary><Authors_Primary>Hamada,T.</Authors_Primary><Authors_Primary>Motomura,K.</Authors_Primary><Authors_Primary>Suwa,M.</Authors_Primary><Authors_Primary>Ezaki,T.</Authors_Primary><Authors_Primary>Haga,T.</Authors_Primary><Authors_Primary>Kanegasaki,S.</Authors_Primary><Authors_Primary>Matsushima,K.</Authors_Primary><Date_Primary>2005/8</Date_Primary><Keywords>Amino Acid Sequence</Keywords><Keywords>Animals</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Line</Keywords><Keywords>Cell Membrane</Keywords><Keywords>chemistry</Keywords><Keywords>Chemotaxis</Keywords><Keywords>Clathrin Heavy Chains</Keywords><Keywords>Cloning,Molecular</Keywords><Keywords>cytology</Keywords><Keywords>Cytoplasm</Keywords><Keywords>Dna</Keywords><Keywords>DNA,Complementary</Keywords><Keywords>Dose-Response Relationship,Drug</Keywords><Keywords>genetics</Keywords><Keywords>Glutathione Transferase</Keywords><Keywords>Humans</Keywords><Keywords>Immunohistochemistry</Keywords><Keywords>immunology</Keywords><Keywords>Inflammation</Keywords><Keywords>Ligands</Keywords><Keywords>Macrophages</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Inbred C57BL</Keywords><Keywords>Microscopy,Fluorescence</Keywords><Keywords>Molecular Sequence Data</Keywords><Keywords>Monocytes</Keywords><Keywords>Mutation</Keywords><Keywords>Nuclear Pore Complex Proteins</Keywords><Keywords>Peptides</Keywords><Keywords>Peritonitis</Keywords><Keywords>Phosphatidylinositol 3-Kinases</Keywords><Keywords>physiology</Keywords><Keywords>Protein Transport</Keywords><Keywords>Pseudopodia</Keywords><Keywords>Receptors,CCR2</Keywords><Keywords>Receptors,Chemokine</Keywords><Keywords>Retroviridae</Keywords><Keywords>Sequence Analysis,DNA</Keywords><Keywords>Sequence Homology,Amino Acid</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Subcellular Fractions</Keywords><Keywords>Time Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>827</Start_Page><End_Page>835</End_Page><Periodical>Nat.Immunol.</Periodical><Volume>6</Volume><Issue>8</Issue><Misc_3>ni1222 [pii];10.1038/ni1222 [doi]</Misc_3><Address>Department of Molecular Preventive Medicine (and Solution Oriented Research for Science and Technology), Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan</Address><Web_URL>PM:15995708</Web_URL><ZZ_JournalFull><f name="System">Nat.Immunol.</f></ZZ_JournalFull><ZZ_JournalStdAbbrev><f name="System">Nat.Immunol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>@	D<Refman><Cite><Author>Schenk</Author><Year>2007</Year><RecNum>291</RecNum><IDText>Monocyte chemotactic protein-3 is a myocardial mesenchymal stem cell homing factor</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>291</Ref_ID><Title_Primary>Monocyte chemotactic protein-3 is a myocardial mesenchymal stem cell homing factor</Title_Primary><Authors_Primary>Schenk,S.</Authors_Primary><Authors_Primary>Mal,N.</Authors_Primary><Authors_Primary>Finan,A.</Authors_Primary><Authors_Primary>Zhang,M.</Authors_Primary><Authors_Primary>Kiedrowski,M.</Authors_Primary><Authors_Primary>Popovic,Z.</Authors_Primary><Authors_Primary>McCarthy,P.M.</Authors_Primary><Authors_Primary>Penn,M.S.</Authors_Primary><Date_Primary>2007/1</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Cell Movement</Keywords><Keywords>Chemokine CCL7</Keywords><Keywords>Chemokines</Keywords><Keywords>Collagen</Keywords><Keywords>Coronary Vessels</Keywords><Keywords>Echocardiography</Keywords><Keywords>Fibroblasts</Keywords><Keywords>genetics</Keywords><Keywords>Heart</Keywords><Keywords>Heart Failure</Keywords><Keywords>injuries</Keywords><Keywords>Mesenchymal Stem Cell Transplantation</Keywords><Keywords>metabolism</Keywords><Keywords>Microscopy,Confocal</Keywords><Keywords>Models,Animal</Keywords><Keywords>Monocyte Chemoattractant Proteins</Keywords><Keywords>Myocardial Infarction</Keywords><Keywords>Myocardium</Keywords><Keywords>Oligonucleotide Array Sequence Analysis</Keywords><Keywords>pathology</Keywords><Keywords>physiology</Keywords><Keywords>Polymerase Chain Reaction</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Inbred Lew</Keywords><Keywords>Receptors,Chemokine</Keywords><Keywords>Regeneration</Keywords><Keywords>Time</Keywords><Keywords>transplantation</Keywords><Reprint>Not in File</Reprint><Start_Page>245</Start_Page><End_Page>251</End_Page><Periodical>Stem Cells</Periodical><Volume>25</Volume><Issue>1</Issue><Misc_3>2006-0293 [pii];10.1634/stemcells.2006-0293 [doi]</Misc_3><Address>Departments of Biomedical Engineering, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA</Address><Web_URL>PM:17053210</Web_URL><ZZ_JournalStdAbbrev><f name="System">Stem Cells</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><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><Cite><Author>Han</Author><Year>2005</Year><RecNum>646</RecNum><IDText>Potential of human bone marrow stromal cells to accelerate wound healing in vitro</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>646</Ref_ID><Title_Primary>Potential of human bone marrow stromal cells to accelerate wound healing in vitro</Title_Primary><Authors_Primary>Han,S.K.</Authors_Primary><Authors_Primary>Yoon,T.H.</Authors_Primary><Authors_Primary>Lee,D.G.</Authors_Primary><Authors_Primary>Lee,M.A.</Authors_Primary><Authors_Primary>Kim,W.K.</Authors_Primary><Date_Primary>2005/10</Date_Primary><Keywords>Adult</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Collagen</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>Pilot Projects</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Skin</Keywords><Keywords>Stromal Cells</Keywords><Keywords>surgery</Keywords><Keywords>Time</Keywords><Keywords>Time Factors</Keywords><Keywords>Tissue Transplantation</Keywords><Keywords>Transforming Growth Factor beta</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Wound Healing</Keywords><Reprint>Not in File</Reprint><Start_Page>414</Start_Page><End_Page>419</End_Page><Periodical>Ann.Plast.Surg.</Periodical><Volume>55</Volume><Issue>4</Issue><Address>Department of Plastic Surgery, Korea University College of Medicine, Seoul, Korea. pshan@kumc.or.kr</Address><Web_URL>PM:16186710</Web_URL><ZZ_JournalStdAbbrev><f name="System">Ann.Plast.Surg.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Sensebe</Author><Year>1997</Year><RecNum>647</RecNum><IDText>Cytokines active on granulomonopoiesis: release and consumption by human marrow myoid [corrected] stromal cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>647</Ref_ID><Title_Primary>Cytokines active on granulomonopoiesis: release and consumption by human marrow myoid [corrected] stromal cells</Title_Primary><Authors_Primary>Sensebe,L.</Authors_Primary><Authors_Primary>Mortensen,B.T.</Authors_Primary><Authors_Primary>Fixe,P.</Authors_Primary><Authors_Primary>Herve,P.</Authors_Primary><Authors_Primary>Charbord,P.</Authors_Primary><Date_Primary>1997/8</Date_Primary><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Line</Keywords><Keywords>Chemokine CCL3</Keywords><Keywords>Chemokine CCL4</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Granulocyte-Macrophage Colony-Stimulating Factor</Keywords><Keywords>Granulocytes</Keywords><Keywords>Hematopoiesis</Keywords><Keywords>Humans</Keywords><Keywords>Interleukin-3</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Macrophage Colony-Stimulating Factor</Keywords><Keywords>Macrophage Inflammatory Proteins</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Serum</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stromal Cells</Keywords><Keywords>Time</Keywords><Keywords>Transforming Growth Factor alpha</Keywords><Keywords>Transforming Growth Factor beta1</Keywords><Reprint>Not in File</Reprint><Start_Page>274</Start_Page><End_Page>282</End_Page><Periodical>Br.J.Haematol.</Periodical><Volume>98</Volume><Issue>2</Issue><Address>Laboratoire d&apos;Etude de l&apos;Hematopoiese, Etablissement de Transfusion Sanguine de Franche Comte, Besancon, France</Address><Web_URL>PM:9266919</Web_URL><ZZ_JournalStdAbbrev><f name="System">Br.J.Haematol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>bD<Refman><Cite><Author>Potier</Author><Year>2007</Year><RecNum>684</RecNum><IDText>Hypoxia affects mesenchymal stromal cell osteogenic differentiation and angiogenic factor expression</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>684</Ref_ID><Title_Primary>Hypoxia affects mesenchymal stromal cell osteogenic differentiation and angiogenic factor expression</Title_Primary><Authors_Primary>Potier,E.</Authors_Primary><Authors_Primary>Ferreira,E.</Authors_Primary><Authors_Primary>Andriamanalijaona,R.</Authors_Primary><Authors_Primary>Pujol,J.P.</Authors_Primary><Authors_Primary>Oudina,K.</Authors_Primary><Authors_Primary>Logeart-Avramoglou,D.</Authors_Primary><Authors_Primary>Petite,H.</Authors_Primary><Date_Primary>2007/4</Date_Primary><Keywords>Angiogenic Proteins</Keywords><Keywords>Base Sequence</Keywords><Keywords>blood</Keywords><Keywords>Blood Vessels</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>culture</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>DNA Primers</Keywords><Keywords>Down-Regulation</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Mesenchymal Stem Cells</Keywords><Keywords>metabolism</Keywords><Keywords>Multipotent Stem Cells</Keywords><Keywords>Osteocalcin</Keywords><Keywords>Osteogenesis</Keywords><Keywords>Osteopontin</Keywords><Keywords>Oxygen</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>secretion</Keywords><Keywords>Stromal Cells</Keywords><Keywords>transplantation</Keywords><Keywords>Up-Regulation</Keywords><Reprint>Not in File</Reprint><Start_Page>1078</Start_Page><End_Page>1087</End_Page><Periodical>Bone</Periodical><Volume>40</Volume><Issue>4</Issue><Address>Laboratoire de Recherches Orthopediques (B2OA), UMR CNRS 7052, Faculte de Medecine Lariboisiere-Saint-Louis, 10 Avenue de Verdun, 75010 Paris, France</Address><Web_URL>PM:17276151</Web_URL><ZZ_JournalStdAbbrev><f name="System">Bone</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><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></Refman>vD<Refman><Cite><Author>Ducy</Author><Year>2000</Year><RecNum>649</RecNum><IDText>Cbfa1: a molecular switch in osteoblast biology</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>649</Ref_ID><Title_Primary>Cbfa1: a molecular switch in osteoblast biology</Title_Primary><Authors_Primary>Ducy,P.</Authors_Primary><Date_Primary>2000/12</Date_Primary><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>Bone Development</Keywords><Keywords>Bone Matrix</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Chondrocytes</Keywords><Keywords>Cleidocranial Dysplasia</Keywords><Keywords>Collagen</Keywords><Keywords>Core Binding Factor Alpha 1 Subunit</Keywords><Keywords>cytology</Keywords><Keywords>Gene Expression Regulation,Developmental</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>Mice</Keywords><Keywords>Neoplasm Proteins</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Osteocalcin</Keywords><Keywords>Osteogenesis</Keywords><Keywords>physiology</Keywords><Keywords>Protein Binding</Keywords><Keywords>Protein Structure,Tertiary</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>461</Start_Page><End_Page>471</End_Page><Periodical>Dev.Dyn.</Periodical><Volume>219</Volume><Issue>4</Issue><Address>Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA. pducy@bcm.tmc.edu</Address><Web_URL>PM:11084646</Web_URL><ZZ_JournalStdAbbrev><f name="System">Dev.Dyn.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Ducy</Author><Year>1999</Year><RecNum>650</RecNum><IDText>A Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>650</Ref_ID><Title_Primary>A Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development</Title_Primary><Authors_Primary>Ducy,P.</Authors_Primary><Authors_Primary>Starbuck,M.</Authors_Primary><Authors_Primary>Priemel,M.</Authors_Primary><Authors_Primary>Shen,J.</Authors_Primary><Authors_Primary>Pinero,G.</Authors_Primary><Authors_Primary>Geoffroy,V.</Authors_Primary><Authors_Primary>Amling,M.</Authors_Primary><Authors_Primary>Karsenty,G.</Authors_Primary><Date_Primary>1999/4/15</Date_Primary><Keywords>Amino Acid Sequence</Keywords><Keywords>Animals</Keywords><Keywords>Animals,Newborn</Keywords><Keywords>Base Sequence</Keywords><Keywords>Biological Evolution</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Development</Keywords><Keywords>Bone Diseases,Metabolic</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Core Binding Factor Alpha 1 Subunit</Keywords><Keywords>Cos Cells</Keywords><Keywords>cytology</Keywords><Keywords>Dna</Keywords><Keywords>DNA,Complementary</Keywords><Keywords>Down-Regulation</Keywords><Keywords>etiology</Keywords><Keywords>Extracellular Matrix</Keywords><Keywords>Gene Expression</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>Mice</Keywords><Keywords>Mice,Transgenic</Keywords><Keywords>Molecular Sequence Data</Keywords><Keywords>Neoplasm Proteins</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Phenotype</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Transcription Factors</Keywords><Keywords>Transcriptional Activation</Keywords><Reprint>Not in File</Reprint><Start_Page>1025</Start_Page><End_Page>1036</End_Page><Periodical>Genes Dev.</Periodical><Volume>13</Volume><Issue>8</Issue><Address>Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA</Address><Web_URL>PM:10215629</Web_URL><ZZ_JournalStdAbbrev><f name="System">Genes Dev.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Komori</Author><Year>2005</Year><RecNum>537</RecNum><IDText>Regulation of skeletal development by the Runx family of transcription factors</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>537</Ref_ID><Title_Primary>Regulation of skeletal development by the Runx family of transcription factors</Title_Primary><Authors_Primary>Komori,T.</Authors_Primary><Date_Primary>2005/6/1</Date_Primary><Keywords>Animals</Keywords><Keywords>Bone and Bones</Keywords><Keywords>Bone Development</Keywords><Keywords>Cell Lineage</Keywords><Keywords>Chondrocytes</Keywords><Keywords>cytology</Keywords><Keywords>embryology</Keywords><Keywords>Gene Expression</Keywords><Keywords>Gene Expression Regulation,Developmental</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>445</Start_Page><End_Page>453</End_Page><Periodical>J.Cell Biochem.</Periodical><Volume>95</Volume><Issue>3</Issue><Address>Department of Developmental and Reconstructive Medicine, Division of Oral Cytology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8588, Japan. komorit@net.nagasaki-u.ac.jp</Address><Web_URL>PM:15786491</Web_URL><ZZ_JournalStdAbbrev><f name="System">J.Cell Biochem.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>�D<Refman><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><Cite><Author>Han</Author><Year>2005</Year><RecNum>646</RecNum><IDText>Potential of human bone marrow stromal cells to accelerate wound healing in vitro</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>646</Ref_ID><Title_Primary>Potential of human bone marrow stromal cells to accelerate wound healing in vitro</Title_Primary><Authors_Primary>Han,S.K.</Authors_Primary><Authors_Primary>Yoon,T.H.</Authors_Primary><Authors_Primary>Lee,D.G.</Authors_Primary><Authors_Primary>Lee,M.A.</Authors_Primary><Authors_Primary>Kim,W.K.</Authors_Primary><Date_Primary>2005/10</Date_Primary><Keywords>Adult</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Marrow</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Collagen</Keywords><Keywords>culture</Keywords><Keywords>cytology</Keywords><Keywords>Fibroblast Growth Factor 2</Keywords><Keywords>Fibroblasts</Keywords><Keywords>Humans</Keywords><Keywords>Male</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>Pilot Projects</Keywords><Keywords>Research</Keywords><Keywords>secretion</Keywords><Keywords>Skin</Keywords><Keywords>Stromal Cells</Keywords><Keywords>surgery</Keywords><Keywords>Time</Keywords><Keywords>Time Factors</Keywords><Keywords>Tissue Transplantation</Keywords><Keywords>Transforming Growth Factor beta</Keywords><Keywords>Vascular Endothelial Growth Factor A</Keywords><Keywords>Wound Healing</Keywords><Reprint>Not in File</Reprint><Start_Page>414</Start_Page><End_Page>419</End_Page><Periodical>Ann.Plast.Surg.</Periodical><Volume>55</Volume><Issue>4</Issue><Address>Department of Plastic Surgery, Korea University College of Medicine, Seoul, Korea. pshan@kumc.or.kr</Address><Web_URL>PM:16186710</Web_URL><ZZ_JournalStdAbbrev><f name="System">Ann.Plast.Surg.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Sensebe</Author><Year>1997</Year><RecNum>647</RecNum><IDText>Cytokines active on granulomonopoiesis: release and consumption by human marrow myoid [corrected] stromal cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>647</Ref_ID><Title_Primary>Cytokines active on granulomonopoiesis: release and consumption by human marrow myoid [corrected] stromal cells</Title_Primary><Authors_Primary>Sensebe,L.</Authors_Primary><Authors_Primary>Mortensen,B.T.</Authors_Primary><Authors_Primary>Fixe,P.</Authors_Primary><Authors_Primary>Herve,P.</Authors_Primary><Authors_Primary>Charbord,P.</Authors_Primary><Date_Primary>1997/8</Date_Primary><Keywords>Bone Marrow Cells</Keywords><Keywords>Cell Line</Keywords><Keywords>Chemokine CCL3</Keywords><Keywords>Chemokine CCL4</Keywords><Keywords>Cytokines</Keywords><Keywords>cytology</Keywords><Keywords>Granulocyte Colony-Stimulating Factor</Keywords><Keywords>Granulocyte-Macrophage Colony-Stimulating Factor</Keywords><Keywords>Granulocytes</Keywords><Keywords>Hematopoiesis</Keywords><Keywords>Humans</Keywords><Keywords>Interleukin-3</Keywords><Keywords>Interleukin-6</Keywords><Keywords>Macrophage Colony-Stimulating Factor</Keywords><Keywords>Macrophage Inflammatory Proteins</Keywords><Keywords>metabolism</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Serum</Keywords><Keywords>Stem Cell Factor</Keywords><Keywords>Stromal Cells</Keywords><Keywords>Time</Keywords><Keywords>Transforming Growth Factor alpha</Keywords><Keywords>Transforming Growth Factor beta1</Keywords><Reprint>Not in File</Reprint><Start_Page>274</Start_Page><End_Page>282</End_Page><Periodical>Br.J.Haematol.</Periodical><Volume>98</Volume><Issue>2</Issue><Address>Laboratoire d&apos;Etude de l&apos;Hematopoiese, Etablissement de Transfusion Sanguine de Franche Comte, Besancon, France</Address><Web_URL>PM:9266919</Web_URL><ZZ_JournalStdAbbrev><f name="System">Br.J.Haematol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>VD<Refman><Cite><Author>Matsuda</Author><Year>1998</Year><RecNum>651</RecNum><IDText>Proliferation and differentiation of human osteoblastic cells associated with differential activation of MAP kinases in response to epidermal growth factor, hypoxia, and mechanical stress in vitro</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>651</Ref_ID><Title_Primary>Proliferation and differentiation of human osteoblastic cells associated with differential activation of MAP kinases in response to epidermal growth factor, hypoxia, and mechanical stress in vitro</Title_Primary><Authors_Primary>Matsuda,N.</Authors_Primary><Authors_Primary>Morita,N.</Authors_Primary><Authors_Primary>Matsuda,K.</Authors_Primary><Authors_Primary>Watanabe,M.</Authors_Primary><Date_Primary>1998/8/19</Date_Primary><Keywords>Alkaline Phosphatase</Keywords><Keywords>Calcium-Calmodulin-Dependent Protein Kinases</Keywords><Keywords>Cell Differentiation</Keywords><Keywords>Cell Division</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cell Proliferation</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>cytology</Keywords><Keywords>Enzyme Activation</Keywords><Keywords>enzymology</Keywords><Keywords>Epidermal Growth Factor</Keywords><Keywords>Humans</Keywords><Keywords>JNK Mitogen-Activated Protein Kinases</Keywords><Keywords>metabolism</Keywords><Keywords>Mitogen-Activated Protein Kinases</Keywords><Keywords>Nerve Tissue</Keywords><Keywords>Nerve Tissue Proteins</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Periodontal Ligament</Keywords><Keywords>pharmacology</Keywords><Keywords>Phosphorylation</Keywords><Keywords>Protein Kinases</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Stress,Mechanical</Keywords><Reprint>Not in File</Reprint><Start_Page>350</Start_Page><End_Page>354</End_Page><Periodical>Biochem.Biophys.Res.Commun.</Periodical><Volume>249</Volume><Issue>2</Issue><Address>Nagasaki University Radioisotope Center, Nagasaki, Japan</Address><Web_URL>PM:9712699</Web_URL><ZZ_JournalStdAbbrev><f name="System">Biochem.Biophys.Res.Commun.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Park</Author><Year>2002</Year><RecNum>652</RecNum><IDText>Hypoxia decreases Runx2/Cbfa1 expression in human osteoblast-like cells</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>652</Ref_ID><Title_Primary>Hypoxia decreases Runx2/Cbfa1 expression in human osteoblast-like cells</Title_Primary><Authors_Primary>Park,J.H.</Authors_Primary><Authors_Primary>Park,B.H.</Authors_Primary><Authors_Primary>Kim,H.K.</Authors_Primary><Authors_Primary>Park,T.S.</Authors_Primary><Authors_Primary>Baek,H.S.</Authors_Primary><Date_Primary>2002/6/28</Date_Primary><Keywords>Alkaline Phosphatase</Keywords><Keywords>analysis</Keywords><Keywords>biosynthesis</Keywords><Keywords>blood</Keywords><Keywords>blood supply</Keywords><Keywords>Bone and Bones</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>Core Binding Factor Alpha 1 Subunit</Keywords><Keywords>culture</Keywords><Keywords>drug effects</Keywords><Keywords>Enzyme Induction</Keywords><Keywords>Gene Expression Regulation</Keywords><Keywords>genetics</Keywords><Keywords>Humans</Keywords><Keywords>metabolism</Keywords><Keywords>Neoplasm Proteins</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Osteocalcin</Keywords><Keywords>Osteoporosis</Keywords><Keywords>Oxygen</Keywords><Keywords>pharmacology</Keywords><Keywords>physiology</Keywords><Keywords>Proteins</Keywords><Keywords>Research</Keywords><Keywords>Rna</Keywords><Keywords>RNA,Messenger</Keywords><Keywords>Signal Transduction</Keywords><Keywords>Time</Keywords><Keywords>Transcription Factors</Keywords><Reprint>Not in File</Reprint><Start_Page>197</Start_Page><End_Page>203</End_Page><Periodical>Mol.Cell Endocrinol.</Periodical><Volume>192</Volume><Issue>1-2</Issue><Address>Division of Endocrinology and Metabolism, Department of Internal Medicine, Chonbuk National University Medical School and Research Institute of Clinical Medicine, #634-18, Keumam Dong, Dukjin Gu, Chonju, 561-712, Chonbuk, Republic of Korea</Address><Web_URL>PM:12088880</Web_URL><ZZ_JournalStdAbbrev><f name="System">Mol.Cell Endocrinol.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite><Cite><Author>Tuncay</Author><Year>1994</Year><RecNum>653</RecNum><IDText>Oxygen tension regulates osteoblast function</IDText><MDL Ref_Type="Journal"><Ref_Type>Journal</Ref_Type><Ref_ID>653</Ref_ID><Title_Primary>Oxygen tension regulates osteoblast function</Title_Primary><Authors_Primary>Tuncay,O.C.</Authors_Primary><Authors_Primary>Ho,D.</Authors_Primary><Authors_Primary>Barker,M.K.</Authors_Primary><Date_Primary>1994/5</Date_Primary><Keywords>Alkaline Phosphatase</Keywords><Keywords>analysis</Keywords><Keywords>Animals</Keywords><Keywords>biosynthesis</Keywords><Keywords>Bone Remodeling</Keywords><Keywords>Calcification,Physiologic</Keywords><Keywords>Carbon Dioxide</Keywords><Keywords>Cell Division</Keywords><Keywords>Cell Hypoxia</Keywords><Keywords>Cells,Cultured</Keywords><Keywords>Collagen</Keywords><Keywords>culture</Keywords><Keywords>Culture Media</Keywords><Keywords>Hydrogen-Ion Concentration</Keywords><Keywords>Hyperbaric Oxygenation</Keywords><Keywords>metabolism</Keywords><Keywords>Osteoblasts</Keywords><Keywords>Oxygen</Keywords><Keywords>Oxygen Consumption</Keywords><Keywords>Partial Pressure</Keywords><Keywords>physiology</Keywords><Keywords>Pressure</Keywords><Keywords>Rats</Keywords><Keywords>Rats,Sprague-Dawley</Keywords><Keywords>Research</Keywords><Reprint>Not in File</Reprint><Start_Page>457</Start_Page><End_Page>463</End_Page><Periodical>Am.J.Orthod.Dentofacial Orthop.</Periodical><Volume>105</Volume><Issue>5</Issue><Address>University of Mississippi Medical Center, Department of Orthodontics, Jackson</Address><Web_URL>PM:8166095</Web_URL><ZZ_JournalStdAbbrev><f name="System">Am.J.Orthod.Dentofacial Orthop.</f></ZZ_JournalStdAbbrev><ZZ_WorkformID>1</ZZ_WorkformID></MDL></Cite></Refman>^2���� 0@P`p������2(�� 0@P`p������ 0@P`p������ 0@P`p������ 0@P`p������ 0@P`p������ 0@P`p��8X�V~_HmH	nH	sH	tH	@`�@
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