Expression of miRNA‑214 in the sera of elderly patients with acute myocardial infarction and its effect on cardiomyocyte apoptosis

Abstract

The aim of the present study was to investigate the expression of microRNA (miRNA/miR)‑214 in the sera of elderly patients with acute myocardial infarction (AMI) and the mechanism of how its expression affects cardiomyocyte apoptosis in these patients. The expression levels of miRNA‑214 in elderly patients with AMI, unstable angina (UA) and healthy elderly subjects were detected by reverse transcription‑quantitative polymerase chain reaction, and the correlation between the relative expressions of sera miRNA‑214 and myocardial enzymes in elderly patients with AMI was examined by Pearson's analysis. Human cardiomyocyte (HCM) cell lines with a high expression miRNA‑214 were established. The apoptotic rates of the different groups of cells were detected by flow cytometry and TUNEL assay. The expression of miRNA‑214 target genes in the different groups of cells was detected by western blot assay. The relative expression levels of sera miR‑214 in elderly AMI patients, UA patients and healthy subjects (as determined by physical examination) were 15.79±4.66, 4.60±2.51 and 2.07±0.99, respectively. The differences between each group were statistically significant (P<0.05). The relative expression of sera miRNA‑214 in elderly AMI patients was positively correlated with sera aspartate aminotransferase (r=0.361, P=0.0174), lactate dehydrogenase (r=0.425, P=0.0045), creatine kinase‑MB (r=0.835, P<0.001) and cardiac troponin (r=0.770, P<0.001). When compared with normal HCMs, the expressions of p53‑upregulated modulator of apoptosis (PUMA), phosphatase and tensin homolog (PTEN), B‑cell lymphoma‑2‑associated X protein (Bax) and caspase 7 proteins was decreased in HCMs overexpressing miRNA‑214 following H2O2 induction, and the rate of apoptosis decreased by 63.64, 21.95, 46.67 and 50.05%, respectively. miRNA‑214 was highly expressed in the sera of elderly patients with AMI, which may inhibit myocardial cell apoptosis by inhibiting the expression of miR‑214 target genes including PUMA, PTEN, Bax and caspase 7.