Cargando…

miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP

MicroRNAs (miRNAs) have emerged as key modulators in the pathophysiologic processes of cardiovascular diseases. However, its function in cardiac injury induced by obstructive sleep apnea (OSA) remains unknown. The aim of the current study was to identify the effect and potential molecular mechanism...

Descripción completa

Detalles Bibliográficos
Autores principales: Lin, Guofu, Huang, Jiefeng, Chen, Qingshi, Chen, Lida, Feng, Dehuai, Zhang, Shuyi, Huang, Xiaoyun, Huang, Yaping, Lin, Qichang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6530234/
https://www.ncbi.nlm.nih.gov/pubmed/31205587
http://dx.doi.org/10.1155/2019/6581217
_version_ 1783420590250524672
author Lin, Guofu
Huang, Jiefeng
Chen, Qingshi
Chen, Lida
Feng, Dehuai
Zhang, Shuyi
Huang, Xiaoyun
Huang, Yaping
Lin, Qichang
author_facet Lin, Guofu
Huang, Jiefeng
Chen, Qingshi
Chen, Lida
Feng, Dehuai
Zhang, Shuyi
Huang, Xiaoyun
Huang, Yaping
Lin, Qichang
author_sort Lin, Guofu
collection PubMed
description MicroRNAs (miRNAs) have emerged as key modulators in the pathophysiologic processes of cardiovascular diseases. However, its function in cardiac injury induced by obstructive sleep apnea (OSA) remains unknown. The aim of the current study was to identify the effect and potential molecular mechanism of miR-146a-5p in intermittent hypoxia(IH)- induced myocardial damage. We exposed H9c2 cells to IH condition; the expression levels of miR-146a-5p were detected by RT-qPCR. Cell viability, cell apoptosis, and the expressions of apoptosis-associated proteins were assessed via Cell Counting Kit-8 (CCK-8), flow cytometry, and western blotting, respectively. Target genes of miR-146a-5p were confirmed by dual-luciferase reporter assay. IH remarkably lowered viability but enhanced cell apoptosis. Concomitantly, the miR-146a-5p expression level was increased in H9c2 cells after IH. Subsequent experiments showed that IH-induced injury was alleviated through miR-146a-5p silence. X-linked inhibitor of apoptosis protein (XIAP) was predicted by bioinformatics analysis and further confirmed as a direct target gene of miR-146a-5p. Surprisingly, the effect of miR-146a-5p inhibition under IH may be reversed by downregulating XIAP expression. In conclusion, our results demonstrated that miR-146a-5p could attenuate viability and promote the apoptosis of H9c2 by targeting XIAP, thus aggravating the H9c2 cell injury induced by IH, which could enhance our understanding of the mechanisms for OSA-associated cardiac injury.
format Online
Article
Text
id pubmed-6530234
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Hindawi
record_format MEDLINE/PubMed
spelling pubmed-65302342019-06-16 miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP Lin, Guofu Huang, Jiefeng Chen, Qingshi Chen, Lida Feng, Dehuai Zhang, Shuyi Huang, Xiaoyun Huang, Yaping Lin, Qichang Oxid Med Cell Longev Research Article MicroRNAs (miRNAs) have emerged as key modulators in the pathophysiologic processes of cardiovascular diseases. However, its function in cardiac injury induced by obstructive sleep apnea (OSA) remains unknown. The aim of the current study was to identify the effect and potential molecular mechanism of miR-146a-5p in intermittent hypoxia(IH)- induced myocardial damage. We exposed H9c2 cells to IH condition; the expression levels of miR-146a-5p were detected by RT-qPCR. Cell viability, cell apoptosis, and the expressions of apoptosis-associated proteins were assessed via Cell Counting Kit-8 (CCK-8), flow cytometry, and western blotting, respectively. Target genes of miR-146a-5p were confirmed by dual-luciferase reporter assay. IH remarkably lowered viability but enhanced cell apoptosis. Concomitantly, the miR-146a-5p expression level was increased in H9c2 cells after IH. Subsequent experiments showed that IH-induced injury was alleviated through miR-146a-5p silence. X-linked inhibitor of apoptosis protein (XIAP) was predicted by bioinformatics analysis and further confirmed as a direct target gene of miR-146a-5p. Surprisingly, the effect of miR-146a-5p inhibition under IH may be reversed by downregulating XIAP expression. In conclusion, our results demonstrated that miR-146a-5p could attenuate viability and promote the apoptosis of H9c2 by targeting XIAP, thus aggravating the H9c2 cell injury induced by IH, which could enhance our understanding of the mechanisms for OSA-associated cardiac injury. Hindawi 2019-05-07 /pmc/articles/PMC6530234/ /pubmed/31205587 http://dx.doi.org/10.1155/2019/6581217 Text en Copyright © 2019 Guofu Lin et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Lin, Guofu
Huang, Jiefeng
Chen, Qingshi
Chen, Lida
Feng, Dehuai
Zhang, Shuyi
Huang, Xiaoyun
Huang, Yaping
Lin, Qichang
miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title_full miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title_fullStr miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title_full_unstemmed miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title_short miR-146a-5p Mediates Intermittent Hypoxia-Induced Injury in H9c2 Cells by Targeting XIAP
title_sort mir-146a-5p mediates intermittent hypoxia-induced injury in h9c2 cells by targeting xiap
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6530234/
https://www.ncbi.nlm.nih.gov/pubmed/31205587
http://dx.doi.org/10.1155/2019/6581217
work_keys_str_mv AT linguofu mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT huangjiefeng mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT chenqingshi mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT chenlida mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT fengdehuai mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT zhangshuyi mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT huangxiaoyun mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT huangyaping mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap
AT linqichang mir146a5pmediatesintermittenthypoxiainducedinjuryinh9c2cellsbytargetingxiap