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MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand
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 dehydr...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444694/ https://www.ncbi.nlm.nih.gov/pubmed/32864001 http://dx.doi.org/10.5114/aoms.2019.85405 |
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author | Lu, Yuan Xi, Jue Zhang, Yao Li, Chenzong Chen, Wensu Hu, Xiaoqin Zhang, Min Zhang, Fengyun Wei, Hui Li, Zhi Wang, Zhirong |
author_facet | Lu, Yuan Xi, Jue Zhang, Yao Li, Chenzong Chen, Wensu Hu, Xiaoqin Zhang, Min Zhang, Fengyun Wei, Hui Li, Zhi Wang, Zhirong |
author_sort | Lu, Yuan |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7444694 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-74446942020-08-28 MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand Lu, Yuan Xi, Jue Zhang, Yao Li, Chenzong Chen, Wensu Hu, Xiaoqin Zhang, Min Zhang, Fengyun Wei, Hui Li, Zhi Wang, Zhirong Arch Med Sci Basic Research 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. Termedia Publishing House 2019-05-28 /pmc/articles/PMC7444694/ /pubmed/32864001 http://dx.doi.org/10.5114/aoms.2019.85405 Text en Copyright: © 2019 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license. |
spellingShingle | Basic Research Lu, Yuan Xi, Jue Zhang, Yao Li, Chenzong Chen, Wensu Hu, Xiaoqin Zhang, Min Zhang, Fengyun Wei, Hui Li, Zhi Wang, Zhirong MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title | MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title_full | MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title_fullStr | MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title_full_unstemmed | MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title_short | MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand |
title_sort | microrna-214-5p protects against myocardial ischemia reperfusion injury through targeting the fas ligand |
topic | Basic Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444694/ https://www.ncbi.nlm.nih.gov/pubmed/32864001 http://dx.doi.org/10.5114/aoms.2019.85405 |
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