microRNA‐135a protects against myocardial ischemia‐reperfusion injury in rats by targeting protein tyrosine phosphatase 1B

microRNAs are an emerging class of molecules that regulate pathogenesis of cardiovascular diseases. Here we aim to elucidate the effects and mechanism of miR‐135a, a previously reported regulator of ischemia‐reperfusion (I/R) injury, in myocardial I/R injury. Quantitative real‐time polymerase chain reaction analysis revealed that the expression level of miR‐135a was significantly decreased both in the rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation. Overexpression of miR‐135a in vivo markedly decreased the infarct size and inhibited the I/R‐induced cardiomyocyte apoptosis. Overexpression of miR‐135a in H9c2 also exerted antiapoptosis effects. Furthermore, bioinformatics analysis, luciferase activity, and the Western blot assay indicated that protein tyrosine phosphatase 1B (PTP1B) is a direct target of miR‐135a. In addition, the expression of proapoptotic‐related genes, such as p53, Bax, and cleaved caspase3, were decreased in association with the downregulation of PTP1B. In summary, this study demonstrates that miR‐135a exerts protective effects against myocardial I/R injury by targeting PTP1B. In this paper, we aim to elucidate the effects and mechanism of miR‐135a, a previously reported regulator of ischemia‐reperfusion (I/R) injury, in myocardial I/R injury. Our results demonstrated that miR‐135a exerts protective effects against myocardial I/R injury by targeting protein tyrosine phosphatase 1B.