CARDIOLOGY / BASIC RESEARCH
MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand
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Jue Xi 2
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Zhi Li 1
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1
Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
2
Department of Endocrinology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
Submission date: 2018-11-12
Final revision date: 2019-03-27
Acceptance date: 2019-04-16
Online publication date: 2019-05-28
Publication date: 2020-08-06
 
Arch Med Sci 2020;16(5):1119–1129
 
KEYWORDS
TOPICS
ABSTRACT
Introduction:
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.

Material and methods:
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.

Results:
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).

Conclusions:
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.

eISSN:1896-9151
ISSN:1734-1922