Research Papers:
MicroRNA1555p suppresses cardiomyocytes apoptosis induced by hypoxia/reoxygenation via targeting fosrelated antigen 2
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Ge Jin1, Xue Qiang Guan1, Jia Li1 and Jun Ma1
1The Department of Cardiology, 2nd Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
Correspondence to:
Jun Ma, email: [email protected]
Keywords: hypoxia/reoxygenation; cardiomyocyte; apoptosis; microRNA-155-5p; FRA2
Received: September 12, 2017 Accepted: November 13, 2017 Published: January 30, 2018
ABSTRACT
Myocardial ischemia/reperfusion (I/R) injury results in cardiomyocytes apoptosis and cardiac fibrosis, which accompanied with fibroblasts trans-differentiate to myofibroblasts and the deposition of collagen. Substantive researches have demonstrated that microRNAs are involved in myocardial I/R injury. Nevertheless, the behind mechanisms remain not well investigation. In this study, cardiomyocyte (M6200 cells) were exposed to hypoxia/reoxygenation (H/R). Our results implied that H/R induced M6200 cells apoptosis and increased the expression of fibrosis-associated proteins, including collagen I, collagen II, collagen III and fibronectin, as well as decreased the level of miR-155-5p. Over-expression of miR-155-5p inhibited H/R-induced apoptosis and the fibrosis of cardiomyocyte M6200 cells. Both the bioinformatics analysis and luciferase reporter assay demonstrated fos-related antigen 2 (FRA2) is one of the direct targets of miR-155-5p, and miR-155-5p negatively regulated the expression of FRA2 in M6200 cells. Moreover, knocked-down of FRA2 accelerated cell growth whereas suppressed the apoptosis and fibrosis in M6200 cells induced by H/R. Altogether, our results demonstrated that miR-155-5p restrain H/R-induced both cellular apoptosis and fibrosis of cardiomyocytes, partly via directly inhibit FRA2.