JOURNAL ARTICLE

miR-192-5p mediates hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3

Yuefeng Zhang, Risheng Huang, Weihe Zhou, Qifeng Zhao, Zhenye Lü
Journal of Biochemical and Molecular Toxicology 2017, 31 (4)
27780314
Myocardial ischemia/reperfusion (I/R) injury is a leading cause of morbidity and mortality. In this study, we investigated the role of miR-192-5p in hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. H9c2 cardiomyocytes were subjected to H/R and tested for miR-192-5p expression. Overexpression and knockdown experiments were performed to determine the effects of manipulating miR-192-5p on apoptotic responses. H/R-treated H9c2 cells exhibited a 2.2-fold increase in miR-192-5p levels. Overexpression of miR-192-5p significantly augmented apoptosis in H9c2 cells after H/R, which was accompanied by a significant increase in the ratio of Bax/Bcl-2. In contrast, delivery of anti-miR-192-5p inhibitors significantly reduced apoptosis induced by H/R. FABP3 was identified to be a functional target of miR-192-5p. Restoration of FABP3 prevented apoptosis in miR-192-5p-transfected H9c2 cells, whereas downregulation of FABP3 enhanced apoptosis in H/R-exposed H9c2 cells. In conclusion, miR-192-5p mediates H/R-induced apoptosis in cardiomyocytes by targeting FABP3 and represents a potential target for prevention of myocardial I/R injury.

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