MicroRNA-147 inhibits myocardial inflammation and apoptosis following myocardial infarction via targeting HIPK2

Objective The incidence of acute myocardial infarction (AMI) is increasing year by year, and it has become one of the diseases with the highest mortality in humans. MicroRNAs (miRNAs) are involved in the regulation of many diseases, including AMI. This study aims to investigate the function of miR-147 in myocardial infarction (MI) and its underlying mechanism of action. Materials and methods Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect miR-147, Bcl-2 mRNA, and Bax mRNA expressions. Enzyme-linked immunosorbent assay (ELISA) kits were used to detect the levels of inflammatory factors (TNF-α, IL-6, IL-β) and lactate dehydrogenase (LDH). Besides, MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay was performed to detect cell viability. Cell apoptosis was observed using terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL). Moreover, echocardiography was utilized to measure cardiac function of rats. HIPK2 expression was detected by Western blot. Results MiR-147 expression was significantly decreased in rat MI model and H2O2 treated H9c2 cells. H2O2 treatment increased the expression of inflammatory factors in H9c2 cells and induced apoptosis, while such effects were inhibited by overexpression of miR-147. Overexpression of miR-147 reversed the decrease in Bcl-2 expression and the increase in Bax expression in H9c2 cells caused by H2O2. In addition, overexpression of miR-147 could improve cardiac function and reduce serum LDH levels in myocardial infarction rats. Through TargetScan, we found that HIPK2 might have a binding site for miR-147. Moreover, overexpression of miR-147 could inhibit the expression of HIPK2. Conclusions In MI, miR-147 expression is decreased in the myocardium and overexpression of miR-147 can inhibit myocardial inflammation and apoptosis and improve cardiac function in rats via targeting HIPK2.