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- Title
MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand.
- Authors
Yuan Lu; Jue Xi; Yao Zhang; Chenzong Li; Wensu Chen; Xiaoqin Hu; Min Zhang; Fengyun Zhang; Hui Wei; Zhi Li; Zhirong Wang; Lu, Yuan; Xi, Jue; Zhang, Yao; Li, Chenzong; Chen, Wensu; Hu, Xiaoqin; Zhang, Min; Zhang, Fengyun; Wei, Hui
- Abstract
<bold>Introduction: </bold>MicroRNAs (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.<bold>Material and Methods: </bold>Lactate 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.<bold>Results: </bold>The 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).<bold>Conclusions: </bold>We found that miR-214-5p exerted a protective role in I/R injured cardiac cells by direct targeting FASLG in vitro and in vivo.
- Subjects
MYOCARDIAL reperfusion; CORONARY disease; REACTIVE oxygen species; REPERFUSION injury; HEART cells
- Publication
Archives of Medical Science, 2020, Vol 16, Issue 5, p1119
- ISSN
1734-1922
- Publication type
journal article
- DOI
10.5114/aoms.2019.85405