Apoptosis-related factors p53, bcl-2 and the defects of force transmission in dilated cardiomyopathy

Abstract

The etiology of heart failure in dilated cardiomyopathy involves multiple agents. The purpose of this study was to investigate the presence of apoptosis-related proteins p53, bcl-2, and the defects of force transmission in end-stage dilated cardiomyopathy. We studied myocardial samples from 20 hearts with histologic findings of dilated cardiomyopathy. Myocardial samples obtained from 10 normal hearts were used as controls. An immunohistochemical method was performed with the use of desmin, N-cadherin, p53, and bcl-2 antibodies. The expression of desmin and N-cadherin was much more pronounced in dilated cardiomyopathy, and both of them were arranged disorderly. On the other hand, increased expression of p53 is associated with progressive loss of myocytes by apoptosis in heart failure, and increased expression of bcl-2 represents a possible compensatory antiapoptotic mechanism. The increased amount and the irregular distribution of desmin and N-cadherin in dilated cardiomyopathy may compensate for the loss of cellular stability due to the loss of contractile material. These alterations contribute to the deterioration of contractile function in heart failure. Furthermore, the prevalence of an apoptotic or compensatory antiapoptotic mechanism may influence the evolution of heart failure in dilated cardiomyopathy.