Exosomes derived miR-126 attenuates oxidative stress and apoptosis from ischemia and reperfusion injury by targeting ERRFI1

Aims: Acute myocardial infarction is one of the most threaten disease in the world. In previous studies, exosome derived miR-126 has been verified that exert an pro-angiogenic function through exosomal transfer. However, the function of miR-126 in ischemic reperfusion injury remains unknown. The aim of the study was to investigate the function and mechanism of miR-126 in ischemic reperfusion injury. Methods: H2O2 and CoCl2-treated neonatal rat ventricular cardiomyocytes were used to analyze the function of miR-126 in vitro. Tunel, JC-1, ROS, LDH and cell survival rates were detected to evaluate the function of miR-126. Rat acute myocardial infarction was performed to elucidate the function of miR-126 in vivo. Results: We found that miR-126 could reduce the apoptosis and improved cell survival of H2O2-treated and CoCl2-treated neonatal rat ventricular cardiomyocytes. MiR-126 also attenuates the ROS elevation and mitochondrial membrane potential through JC-1 detection. miR-126 also improved the cardiac function in vivo. Luciferase activity revealed that miR-126 could bind to ERRFI1, suggesting miR-126 functioned through regulating ERRFI1. Conclusion: We verified the function and mechanism of miR-126 and provide evidence that miR-126 may play important role in ischemic reperfusion injury, and understanding the precise role of miR-126 will undoubtedly shed new light on the clinical treatment.