• Yuan Lu, Jue Xi, Yao Zhang, Chenzong Li, Wensu Chen, Xiaoqin Hu, Min Zhang, Fengyun Zhang, Hui Wei, Zhi Li, and Zhirong Wang.
• Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
• Arch Med Sci. 2020 Jan 1; 16 (5): 1119-1129.

IntroductionMicroRNAs (miRNAs) are considered as crucial modulators in myocardial ischemia and reperfusion (I/R) injury. The present study aimed to investigate the expression and biological functions of miR-214-5p via targeting Fas ligand (FASLG) in I/R injury.Material And MethodsLactate dehydrogenase, casein kinase, malondialdehyde assay, reactive oxygen species (ROS) detection and cell apoptosis analysis measured cell damage and cell apoptosis in H9c2 cells under hypoxia/reperfusion (H/R) treatment. Bioinformatics and dual luciferase reporter assays demonstrated the molecular mechanism of miR-214-5p in cardiac cells. 2,3,5-Triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining and adenovirus injection were performed in I/R treated mice.ResultsThe expression of miR-214-5p was decreased in H/R injured H9c2 cells compared with control cells (p < 0.001). Overexpression of miR-214-5p reduced cell damage and apoptosis in H9c2 cells under H/R treatment (p < 0.001). Further study revealed that FASLG was a target of miR-214-5p. Enhanced expression of FASLG attenuated the protective function of miR-214-5p in H9c2 cells subjected to H/R injury (P < 0.001). Moreover, the elevated expression of miR-214-5p by adenovirus injection protected cardiac cells from I/R injury in mice (n = 6/per group).ConclusionsWe found that miR-214-5p exerted a protective role in I/R injured cardiac cells by direct targeting FASLG in vitro and in vivo.Copyright: © 2019 Termedia & Banach.

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