MiR-19a-3p mitigates hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes by targeting SOCS3

Abstract

The available treatment strategies for myocardial ischemia-reperfusion (I/R) injuries have not been so much effective. MicroRNAs (miRNAs) from the miR-19 family, which includes miR-19a and miR-19b, modulate both proliferation and apoptosis in the myocardium. The correlation between I/R injury and miR-19a-3p is unknown. Here, the role of miR-19a-3p in injuries induced by I/R was investigated in H9C2 cardiomyocytes. The MiR-19a-3p Levels were determined to be reduced after hypoxia/reoxygenation (H/R) and miR-19a-3p overexpression reduced apoptosis resulting from H/R, improving the activity of the cells. The opposite effect was observed when miR-19a-3p was inhibited. Potential miR-19a-3p targets were investigated using bioinformatics, identifying Protein Suppressor of cytokine signaling-3 (SOCS3), which was verified by luciferase reporter assays. SOCS3 levels were lower by overexpression of miR-19a-3p. SOCS3 silencing prevented apoptosis induced by miR-19a-3p inhibition, whereas overexpression of SOCS3 blocked a miR-19a-3p mimic's effects on apoptosis. According to these findings, miR-19a-3p reduces apoptosis and injury induced by H/R in cardiomyocytes through targeting SOCS3, and that targeting miR-19a-3p/SOCS3 signalling may present a new strategy in the therapy of myocardial I/R injury.