OBJECTIVE: To investigate the protective effect of miR-129-5p on ischemia-reperfusion (I/R) injury via targeting high mobility group box-1 (HMGB1). MATERIALS AND METHODS: Rat models of myocardial I/R and hypoxia/reoxygenation (H/R) cardiomyocytes were established, and the miR-129-5p and HMGB1 expression levels in myocardium of I/R rats and in cardiomyocytes of H/R rats were quantified by RT-PCR. The over-expression of miR-129-5p was performed on I/R rats, and the over-expression of miR-129-5p and down-regulation of HMGB1 were performed on cardiomyocytes of H/R rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size (IS). TUNEL (TdT-mediated dUTP end nick labeling) staining was employed to observe cardiomyocyte apoptosis in the myocardium of rats, and flow cytometry to observe cardiomyocyte apoptosis of I/R and H/R rats respectively. Dual-Luciferase reporter assay was used to verify the target relation between miR-129-5p and HMGB1. RESULTS: MiR-129-5p was lowly expressed and HMGB1 was highly expressed in myocardial I/R injury rats and cardiomyocytes of H/R rats. Over-expression of miR-129-5p effectively reduced myocardial IS and cardiomyocyte apoptosis in rats with myocardial I/R injury, and significantly down-regulated the pro-apoptotic protein Bax, as well as significantly up-regulated the anti-apoptotic protein Bcl-2. Either over-expression of miR-129-5p or low-expression of HMGB1 in cardiomyocytes of H/R rats also achieved the same effects as described above. Dual-Luciferase reporter assay determined that miR-129-5p was a target for HMGB1. CONCLUSIONS: MiR-129-5p plays a protective role on myocardial I/R injury by regulating HMGB1 expression. Besides, it inhibits cardiomyocyte apoptosis and is expected to become a novel molecular marker or therapeutic target for myocardial I/R injury.
OBJECTIVE: To investigate the protective effect of miR-129-5p on ischemia-reperfusion (I/R) injury via targeting high mobility group box-1 (HMGB1). MATERIALS AND METHODS:Rat models of myocardial I/R and hypoxia/reoxygenation (H/R) cardiomyocytes were established, and the miR-129-5p and HMGB1 expression levels in myocardium of I/R rats and in cardiomyocytes of H/R rats were quantified by RT-PCR. The over-expression of miR-129-5p was performed on I/R rats, and the over-expression of miR-129-5p and down-regulation of HMGB1 were performed on cardiomyocytes of H/R rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size (IS). TUNEL (TdT-mediated dUTP end nick labeling) staining was employed to observe cardiomyocyte apoptosis in the myocardium of rats, and flow cytometry to observe cardiomyocyte apoptosis of I/R and H/R rats respectively. Dual-Luciferase reporter assay was used to verify the target relation between miR-129-5p and HMGB1. RESULTS:MiR-129-5p was lowly expressed and HMGB1 was highly expressed in myocardial I/R injury rats and cardiomyocytes of H/R rats. Over-expression of miR-129-5p effectively reduced myocardial IS and cardiomyocyte apoptosis in rats with myocardial I/R injury, and significantly down-regulated the pro-apoptotic protein Bax, as well as significantly up-regulated the anti-apoptotic protein Bcl-2. Either over-expression of miR-129-5p or low-expression of HMGB1 in cardiomyocytes of H/R rats also achieved the same effects as described above. Dual-Luciferase reporter assay determined that miR-129-5p was a target for HMGB1. CONCLUSIONS:MiR-129-5p plays a protective role on myocardial I/R injury by regulating HMGB1 expression. Besides, it inhibits cardiomyocyte apoptosis and is expected to become a novel molecular marker or therapeutic target for myocardial I/R injury.