Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis

The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatme...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Zhang Guorong, Ni Xinghua
Formato: article
Lenguaje:EN
Publicado: De Gruyter 2021
Materias:
Acceso en línea:https://doaj.org/article/3d2860fd73f74c90a8325a753dc0e3af
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:3d2860fd73f74c90a8325a753dc0e3af
record_format dspace
spelling oai:doaj.org-article:3d2860fd73f74c90a8325a753dc0e3af2021-12-05T14:10:40ZKnockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis2391-541210.1515/biol-2021-0025https://doaj.org/article/3d2860fd73f74c90a8325a753dc0e3af2021-03-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0025https://doaj.org/toc/2391-5412The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatment in vitro. Levels of lncRNA TUG1, miR-497 and myocyte enhancer factor 2C (MEF2C) mRNA were assessed by quantitative reverse transcriptase PCR (qRT-PCR). Western blot assay was performed to determine the expression of MEF2C protein. The endogenous interactions among TUG1, miR-497 and MEF2C were confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that TUG1 was upregulated and miR-497 was downregulated in the TAC rat model and Ang II-induced cardiomyocytes. TUG1 knockdown or miR-497 overexpression alleviated the hypertrophy induced by Ang II in cardiomyocytes. Moreover, TUG1 acted as a sponge of miR-497, and MEF2C was directly targeted and repressed by miR-497. miR-497 overexpression mediated the protective role of TUG1 knockdown in Ang II-induced cardiomyocyte hypertrophy. MEF2C was a functional target of miR-497 in regulating Ang II-induced cardiomyocyte hypertrophy. In addition, TUG1 regulated MEF2C expression through sponging miR-497. Knockdown of TUG1 rescued Ang II-induced hypertrophy in cardiomyocytes at least partly through targeting the miR-497/MEF2C axis, highlighting a novel promising therapeutic target for cardiac hypertrophy treatment.Zhang GuorongNi XinghuaDe Gruyterarticlecardiac hypertrophytug1mir-497myocyte enhancer factor 2cBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 242-251 (2021)
institution DOAJ
collection DOAJ
language EN
topic cardiac hypertrophy
tug1
mir-497
myocyte enhancer factor 2c
Biology (General)
QH301-705.5
spellingShingle cardiac hypertrophy
tug1
mir-497
myocyte enhancer factor 2c
Biology (General)
QH301-705.5
Zhang Guorong
Ni Xinghua
Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
description The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatment in vitro. Levels of lncRNA TUG1, miR-497 and myocyte enhancer factor 2C (MEF2C) mRNA were assessed by quantitative reverse transcriptase PCR (qRT-PCR). Western blot assay was performed to determine the expression of MEF2C protein. The endogenous interactions among TUG1, miR-497 and MEF2C were confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that TUG1 was upregulated and miR-497 was downregulated in the TAC rat model and Ang II-induced cardiomyocytes. TUG1 knockdown or miR-497 overexpression alleviated the hypertrophy induced by Ang II in cardiomyocytes. Moreover, TUG1 acted as a sponge of miR-497, and MEF2C was directly targeted and repressed by miR-497. miR-497 overexpression mediated the protective role of TUG1 knockdown in Ang II-induced cardiomyocyte hypertrophy. MEF2C was a functional target of miR-497 in regulating Ang II-induced cardiomyocyte hypertrophy. In addition, TUG1 regulated MEF2C expression through sponging miR-497. Knockdown of TUG1 rescued Ang II-induced hypertrophy in cardiomyocytes at least partly through targeting the miR-497/MEF2C axis, highlighting a novel promising therapeutic target for cardiac hypertrophy treatment.
format article
author Zhang Guorong
Ni Xinghua
author_facet Zhang Guorong
Ni Xinghua
author_sort Zhang Guorong
title Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
title_short Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
title_full Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
title_fullStr Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
title_full_unstemmed Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis
title_sort knockdown of tug1 rescues cardiomyocyte hypertrophy through targeting the mir-497/mef2c axis
publisher De Gruyter
publishDate 2021
url https://doaj.org/article/3d2860fd73f74c90a8325a753dc0e3af
work_keys_str_mv AT zhangguorong knockdownoftug1rescuescardiomyocytehypertrophythroughtargetingthemir497mef2caxis
AT nixinghua knockdownoftug1rescuescardiomyocytehypertrophythroughtargetingthemir497mef2caxis
_version_ 1718371835458879488