The expression of microRNA-23a regulates acute myocardial infarction in patients and in vitro through targeting PTEN

Cardiovascular disease is responsible for one of the highest rates of fatality worldwide. The present study investigated the presence and influence of microRNA (miRNA)-23a in the regulation of acute myocardial infarction (AMI). A total of 6 patients with AMI and 6 normal volunteers without myocardial disease were included, and blood samples were taken to analyze the expression of miRNA-23a by reverse transcription-quantitative polymerase chain reaction. miRNA-23a expression in patients with AMI was downregulated compared with the normal group. In H9C2 cells treated with H2O2, upregulation of miRNA-23a expression increased the superoxide dismutase, glutathione and catalase activity levels, and suppressed the malonaldehyde activity level, as determined by ELISA. Western blot analysis and a caspase-3 substrate assay demonstrated that upregulation of miRNA-23a expression suppressed the Bcl-2-associated X (Bax)/Bcl-2 protein expression ratio, caspase-3 activity level and tumor suppressor p53 (p53) protein expression in H2O2-induced H9C2 cells. Furthermore, downregulation of phosphatase and tensin homolog (PTEN), by the PTEN inhibitor bpV(HOpic), increased miRNA-23a expression and suppressed the Bax/Bcl-2 protein expression ratio, caspase-3 activity level and p53 protein expression in H2O2-induced H9C2 cells. Therefore, the results of the present study indicate that the expression of miRNA-23a may regulate AMI through targeting PTEN in patients and in vitro, and PTEN/miRNA-23a may therefore be potential targets for the clinical treatment of AMI.