Journal
ARCHIVES OF MEDICAL SCIENCE
Volume 16, Issue 5, Pages 1119-1129Publisher
TERMEDIA PUBLISHING HOUSE LTD
DOI: 10.5114/aoms.2019.85405
Keywords
ischemic heart diseases; miR-214-5p; FASLG; cell apoptosis
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Funding
- Youth Science Foundation program of China [81700231]
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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, malondial-dehyde 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.
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