MicroRNA-520d-3p alleviates hypoxia/reoxygenation-induced damage in human cardiomyocytes by targeting ATG-12.

Hypoxia/reoxygenation (H/R) induced injury results in extensive damages to myocardial tissue in patients with coronary heart disease, which leads to heart failure. MicroRNA (miRNA) is thought to be associated with myocardial H/R injury. The purpose of this study was to investigate the in vitro role of microRNA-520d-3p in human myocardial cell (HCM) myocardial H/R injury. MTT method and Annexin V-FITC flow cytometry were employed to measure the viability and apoptosis of H/R treated HCM. RT-qPCR was employed to determine miRNA and mRNA expression. MicroRNA-520d-3p mimic and microRNA-520d-3p inhibitor were used to overexpression and inhibit the expression of microRNA-520d-3p. In addition, pcDNA3.1-ATG12 was used to upregulate ATG12 expression. The protein levels of ATG12, Bcl-2 and autophagy related-genes were determined by western blotting. Hypoxia/reoxygenation (H/R) injury could inhibit cell viability, apoptosis and inhibited microRNA-520d-3p expression in HCM. The down-regulation of microRNA-520d-3p inhibited cell viability and induced apoptosis in HCM. The overexpression of microRNA-520d-3p attenuated the effects of H/R treatment on the viability and apoptosis of HCM cells. In addition, microRNA-520d-3p inhibited the expression of autophagy-associated 12 (ATG12). More importantly, H/R treatment could promote autophagy in HCM, and microRNA-520d-3p mimic transfection could significantly reverse this effect. Our result indicated that overexpression of microRNA-520d-3p attenuated the effect of H/R treatments on cell viability, apoptosis and autophagy, through partly regulating ATG12 expression in HCM.