microRNA-30e up-regulation alleviates myocardial ischemia-reperfusion injury and promotes ventricular remodeling via SOX9 repression.

Abstract Aim At present, studies have focused on microRNAs (miRNAs) in myocardial ischemia-reperfusion injury (MI/RI). But the specific role of miR-30e hasn’t been fully explored. Thus, this study is to uncover the mechanism of miR-30e in MI/RI. Methods MI/RI models of rats and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established. Rats were injected with miR-30e and SRY-related high mobility group-box gene 9 (SOX9)-related oligonucleotides or vectors to explore their roles in MI/RI. H9C2 cardiomyocytes were transfected with restored miR-30e and depleted SOX9 to decipher their function in H/R injury. miR-30e and SOX9 expression in myocardial tissues and cardiomyocytes were detected. Online website prediction and luciferase activity assay were applied to validate the targeting relationship between miR-30e and SOX9. Results Decreased miR-30e and increased SOX9 were found in myocardial tissues of MI/RI rats and H/R-treated cardiomyocytes. miR-30e targeted SOX9. miR-30e up-regulation or SOX9 down-regulation reduced cardiac function damage and suppressed oxidative stress, inflammation, cardiomyocyte apoptosis and myocardial enzymes in myocardial tissues of MI/RI rats. Restoring miR-30e or silencing SOX9 energized cell viability and inhibited apoptosis of H/R-treated cardiomyocytes. Down-regulating SOX9 reversed the effects of miR-30e down-regulation on myocardial injury, ventricular remodeling, cardiomyocyte damage and apoptosis in MI/RI. Conclusion It is concluded that miR-30e elevation alleviated cardiac function damage and promoted ventricular remodeling via SOX9 repression.