LAUSR

Oxidative stress injury, inducing cardiomyocyte injury, is the major denominator of many cardiovascular diseases. In present study, we aimed to explore the molecular mechanism of microRNA-208a (miR-208a) in oxidative stress-induced cardiomyocyte injury. In this study, hydrogen peroxide (H2O2)-induced injury in H9c2 and AC16 cardiomyocytes was used as a model of myocardial injury. The pro-apoptosis potential and mechanism of miR-208a for oxidative injury were evaluated by MTT, flow cytometry, qRT-PCR and Western blot assays. Intracellular reactive oxygen species and detection of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) were performed to analyze the effect of miR-208a on H2O2-induced injury in H9c2 cardiomyocytes. The association between miR-208a and activated protein C (APC) was confirmed by luciferase reporter and RIP assays. We foundthatmiR-208a mimic aggravated H2O2-induced apoptosis and oxidative injury in cardiomyocytes, while miR-208a inhibitor hadan inverse effect. APC was a target gene of miR-208a and miR-208a negatively regulated the expression of APC. APC reduced H2O2-induced injury in H9c2 cardiomyocytes. Knockdown of APC attenuated the inhibitiveeffect of miR-208a inhibitor on H2O2-induced injuryin H9c2 cardiomyocytes. We concluded thatmiR-208a could aggravate H2O2-induced injury in H9c2 cardiomyocytes by targeting APC. A new signaling pathway miR-208a/APC was first observed in myocardial injury.