[Expression of bcl-2 and Bax protein in the failing human heart--an inhibitor or accelerator of apoptosis?].
In general, myocyte death in myocardial infarctions (MI) is attributed to necrosis, but recently the involvement of apoptosis has been suggested. Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. The expression of two proto-oncogenes influence apoptosis. Myocytes with positive bcl-2 immunoreactivity were seen in the heart of acute MI, localized only in the salvaged areas surrounding the infarcted tissues. Myocytes with overexpressed positive Bax immunoreactivity were observed in the salvaged areas of old MI.
Chen
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Institute of Forensic Sciences, Ministry of Justice, Shanghai 200063, P. R. China.
D017209:Apoptosis; D005786:Gene Expression Regulation; D016158:Genes, p53 / Q000235:genetics; D006333:Heart Failure / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis* / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein