Background: According to recent data, the pathology of cardiomyocyte death during and after myocardial infarction involves both necrosis and apoptosis. Although both mechanisms eventually lead to cell death, the participation of apoptosis in this process carries the potential of developing strategies to influence at least part of the population of dying cells. Therefore, the aim of this study was to determine expression profiles of genes associated with apoptosis in post-infarction myocardium, chronically ischemic myocardium as well as in a healthy heart muscle with the use of oligonucleotide microarrays.
Material and methods: The tissue samples used were sections from the right cardiac auricles obtained during elective surgery performed on 3 patients, as stated above. Then, the expression of 141 genes involved in fibrosis was assessed using an Affymetrix HG_U133A microarray. The similarity of the patients’ transcriptomes was compared using hierarchical clusterisation.
Results: Hierarchical clusterisation demonstrated that the profile of gene expression in post-infarction myocardium was different than that in the remaining specimens. Regression analysis showed that in post-infraction sample genes encoding caspase 4, PDCD8, BBC3, BIT1 and DIABLO were overexpressed, whereas transcriptional activity of 2 genes encoding TNFα receptors presented a lower expression in the post-infarction sample.
Conclusions: The profile of apoptosis-associated genes is significantly different in post-myocardial infarction (post-MI) myocardium compared to chronically ischemic and non-ischemic myocardium. Our data suggest the importance of proapoptotic factors associated with mitochondria. Genes encoding a cascade of caspases were undifferentiating, while 2 genes encoding TNFa receptors were underexpressed in post-infarction tissue.