Immuno-detection of PPAR overexpression with no change protein turnover endocardial tissues suggests major alterations in energy metabolism during ischemic and dilated cardiomyopathy conditions of heart
Immuno-Detection of PPAR Overexpression in Protein Turnover in Endocardial Tissues Suggesting Alterations in Energy Metabolism during Ischemic and Dilated Cardiomyopathy Conditions
The peroxisome proliferator-activated receptor (PPAR) family regulates genes encoding enzymes involved in fatty acid and glucose metabolism. This role in the high-energy consuming heart organ has been a major target in cardiomyopathy studies. PPARs and nuclear protein levels were investigated in endocardial tissues samples obtained from ischemic and dilated cardiomyopathy male patients. Control samples were obtained from male accident victims of same age group. The expression of PPAR isoforms in each sample was analyzed by, protein assay, SDS-PAGE, western blotting and densitometry. The mean milligram nuclear protein of endocardial tissues for each of the three groups was measured as follows: ischemic 17.6 ± 8.1; dilated 13.7 ± 3.4; control 21.0 ± 6.0; (n=3 per group). The range of protein variability by Pearson correlation coefficient r was -0.91 ≤ r ≤ +0.77, (n=9). However, the sample means of the ischemic and dilated groups were not significantly different from the control mean, P>0.5 in each case by student’s test. The isoforms of PPAR are strongly expressed in cardiomyopathy conditions without change in nuclear protein turnover. The results also show that PPAR-α and PPAR-γ may be more predominant in the heart than PPAR-ß. Furthermore, the expression of the spliced variants of PPAR-α and PPAR-γ were not affected by the cardiomyopathy conditions and PPAR-ß have no spliced variant in the heart. The study provides an evidence of alteration in the heart’s energy metabolic processes during cardiomyopathies.