Evidence of Apoptosis: Bax and Fas Expression in Acute Phase of Myocardial Infarction in Rats

Abstract

Myocardial infarction (MI) remains the leading cause of death from cardiovascular diseases over the past decades. Apoptosis is ‘programmed’ cell death which leads to clearance of ‘unwanted’ cells without disruption of tissue structure or function. Recently, we reported that angiotensin receptor subtype AT1 and AT2 mRNA levels were time dependently regulated after MI. AT1 and AT2 receptor mRNA levels markedly increased at 30 min and peaked 24 h post-MI. The time-dependent increase of AT1 and AT2 receptor mRNA is associated with the early remodeling process of the non-infarcted myocardium post MI. There is a further question raised whether the up-regulation of AT2 receptor is linked to apoptosis. Therefore, we investigated the apoptotic development and apoptotic related gene expression after MI at different time points in the current study. MI was induced in Wistar rats by ligation of the left anterior descending coronary artery. Bax gene expression was found to be increased at 12 h after MI and peaked at 24 h (4.3-fold). It declined at 72 h after MI. Fas gene started to over-express at 12 h after MI as well but it reached maximum at 72 h (4.7-fold). Protein levels of Bax and Fas expression were detected in the necrotic area and area at risk (surrounding area) at different time points after MI. Apoptosis was detected in the infarcted areas. No apoptosis was detected in the sham operated rats. In the MI groups, strongest staining of apoptosis was detected in rats 3 days post operation. Weak staining was found 1 day, 7 day post MI. Very fewer apoptotic cells were detected in the rats 2 weeks after MI. Our results demonstrate that apoptotic development after MI is time dependent in the ischemic area and there could be some linkage with the over expression of AT2 receptor post MI.