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

Abstract 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 H 2 O 2 and CoCl 2 -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 H 2 O 2 -treated and CoCl 2 -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.