Effects of miR-103a-3p on the autophagy and apoptosis of cardiomyocytes by regulating Atg5

Autophagy and apoptosis are associated with cardiovascular diseases. Emerging evidence shows that microRNAs (miRs) are critical in the development of pathological processes underlying cardiovascular diseases by regulating the induction of apoptosis and autophagy. The present study aimed to investigate the role of miR-103a-3p in cardiomyocyte injury through autophagy and apoptosis. H9c2 cells were cultured under hypoxia and reoxygenation (H/R) conditions and were used to mimic cells under ischemia. The transfection of cells with miR-103a-3p (mimics and inhibitors) was performed to examine its function in cardiomyocytes. The expression levels of miR-103a-3p were evaluated by reverse transcription-quantitative polymerase chain reaction analysis. Cell viability was determined using an MTT assay, and the lactate dehydrogenase assay (LDH) was used to investigate cell injury. The expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, Beclin-1, autophagy-related 5 (Atg5), cleaved caspase-3 and cleaved caspase-9 were detected using western blotting. Immunofluorescence assays were performed to detect the expression of LC3 as a marker of autophagy. The target gene of miR-103a-3p was identified using dual-luciferase reporter assays. The results revealed that the expression levels of miR-103a-3p were significantly downregulated in cardiomyocytes under H/R conditions. Injury of the cardiomyocytes was evaluated under H/R conditions. Following transfection of the cells with miR-103a-3p inhibitors, cell injury was increased, as determined by LDH and MTT assays. The expression levels of apoptotic proteins were consistent with the results obtained in the LDH and cell viability assays. The induction of autophagy was increased in cells under H/R conditions and cells with miR-103a-3p inhibitor transfection, whereas the induction of autophagy was decreased in cells transfected with miR-103a-3p mimics. In addition, the data indicated that miR-103a-3p directly targeted Atg5, which regulated the induction of autophagy and apoptosis. Taken together, these findings indicate that, following the inhibition of miR-103a-3p, Atg5 promotes autophagy and apoptosis in cardiomyocytes by directly targeting Atg5. Therefore, miR-103a-3p can be considered a potential therapeutic target for myocardial ischemia.