Increased p53 protein expression in human failing myocardium

BackgroundThe p53 gene is a tumor-suppressor gene which involves apoptosis and cell-cycle arrest under certain stress stimulate. However, the status of the p53 gene expression in human myocardium in congestive heart failure (CHF) remains unclear. Therefore, the current study was designed to investigate the expression of the p53 protein in human myocardium in normal subjects and in patients with severe CHF.MethodsHuman ventricular cardiac tissue was obtained from 7 normal subjects and 7 end-stage CHF patients during cardiac transplantation. The expression of p53 protein was determined by immunohistochemical staining. The cardiac apoptosis was determined by TUNEL staining.ResultsThe p53 protein was minimally stained in normal human ventricular cardiomyocytes. In contrast, the staining density and positive stained nuclear (%) of p53 was significantly increased in ventricular cardiomyocytes of patients with severe CHF. Apoptosis in CHF human myocardium also markedly increased.ConclusionsThe significantly increased expression of p53 in CHF human cardiomyocytes suggests that p53 may play an important pathophysiological role in the process of CHF through mechanisms involving myocardial apoptosis. Copyright (C) 1999 International Society for Heart and Lung Transplantation.