Cargando…

miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1

Objective: miRNAs play critical roles in the regulation of many cardiovascular diseases. However, its role and potential mechanism in cardiac injury caused by obstructive sleep apnea (OSA) remain poorly elucidated. In the present study, we aimed to investigate the effects of miR-3574 on cardiomyocyt...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Qingshi, Lin, Guofu, Chen, Yongfa, Li, Chaowei, Wu, Lizhen, Hu, Xin, Lin, Qichang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8034950/
https://www.ncbi.nlm.nih.gov/pubmed/33582657
http://dx.doi.org/10.18632/aging.202480
_version_ 1783676626780815360
author Chen, Qingshi
Lin, Guofu
Chen, Yongfa
Li, Chaowei
Wu, Lizhen
Hu, Xin
Lin, Qichang
author_facet Chen, Qingshi
Lin, Guofu
Chen, Yongfa
Li, Chaowei
Wu, Lizhen
Hu, Xin
Lin, Qichang
author_sort Chen, Qingshi
collection PubMed
description Objective: miRNAs play critical roles in the regulation of many cardiovascular diseases. However, its role and potential mechanism in cardiac injury caused by obstructive sleep apnea (OSA) remain poorly elucidated. In the present study, we aimed to investigate the effects of miR-3574 on cardiomyocyte injury under intermittent hypoxia (IH). Results: We confirmed that IH inhibited cell viability, induced cell apoptosis and suppressed miR-3574 expression in the H9c2. miR-3574 overexpression could ameliorate the effects of IH on the cell viability and cell apoptosis in the H9c2. Axin1 was a target gene of miR-3574, and miR-3574 overexpression reduced the expression of Axin1. miR-3574 could inhibit the IH-induced cardiomyocyte injury via downregulating Axin1. However, Axin1 could partially reverse these effects of miR-3574. Conclusion: Our study first reveals that miR-3574 could alleviate IH-induced cardiomyocyte injury by targeting Axin1, which may function as a novel and promising therapy target for OSA-associated cardiovascular diseases. Methods: H9c2 were exposed to IH condition. CCK-8 assay was applied to determine cell viability of H9c2. qRT-PCR was conducted to measure the expression level of mRNA and miRNA. Western blot assay was then performed to detect the protein levels. Finally, we used dual-luciferase reporter assay identify the potential target of miR-3574.
format Online
Article
Text
id pubmed-8034950
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Impact Journals
record_format MEDLINE/PubMed
spelling pubmed-80349502021-04-16 miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1 Chen, Qingshi Lin, Guofu Chen, Yongfa Li, Chaowei Wu, Lizhen Hu, Xin Lin, Qichang Aging (Albany NY) Research Paper Objective: miRNAs play critical roles in the regulation of many cardiovascular diseases. However, its role and potential mechanism in cardiac injury caused by obstructive sleep apnea (OSA) remain poorly elucidated. In the present study, we aimed to investigate the effects of miR-3574 on cardiomyocyte injury under intermittent hypoxia (IH). Results: We confirmed that IH inhibited cell viability, induced cell apoptosis and suppressed miR-3574 expression in the H9c2. miR-3574 overexpression could ameliorate the effects of IH on the cell viability and cell apoptosis in the H9c2. Axin1 was a target gene of miR-3574, and miR-3574 overexpression reduced the expression of Axin1. miR-3574 could inhibit the IH-induced cardiomyocyte injury via downregulating Axin1. However, Axin1 could partially reverse these effects of miR-3574. Conclusion: Our study first reveals that miR-3574 could alleviate IH-induced cardiomyocyte injury by targeting Axin1, which may function as a novel and promising therapy target for OSA-associated cardiovascular diseases. Methods: H9c2 were exposed to IH condition. CCK-8 assay was applied to determine cell viability of H9c2. qRT-PCR was conducted to measure the expression level of mRNA and miRNA. Western blot assay was then performed to detect the protein levels. Finally, we used dual-luciferase reporter assay identify the potential target of miR-3574. Impact Journals 2021-02-11 /pmc/articles/PMC8034950/ /pubmed/33582657 http://dx.doi.org/10.18632/aging.202480 Text en Copyright: © 2021 Chen et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Chen, Qingshi
Lin, Guofu
Chen, Yongfa
Li, Chaowei
Wu, Lizhen
Hu, Xin
Lin, Qichang
miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title_full miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title_fullStr miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title_full_unstemmed miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title_short miR-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting Axin1
title_sort mir-3574 ameliorates intermittent hypoxia-induced cardiomyocyte injury through inhibiting axin1
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8034950/
https://www.ncbi.nlm.nih.gov/pubmed/33582657
http://dx.doi.org/10.18632/aging.202480
work_keys_str_mv AT chenqingshi mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT linguofu mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT chenyongfa mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT lichaowei mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT wulizhen mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT huxin mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1
AT linqichang mir3574amelioratesintermittenthypoxiainducedcardiomyocyteinjurythroughinhibitingaxin1