Cargando…

miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST

MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with significant risks of heart failure. However, many microRNAs are still not recognized for their functions in pathophysiological processes. In this study, we evaluated effects of miR-218 in ca...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Jing-Jing, Zhao, Cui-Mei, Li, Zhi-Gang, Wang, Yu-Mei, Miao, Wei, Wu, Xiu-Juan, Wang, Wen-Jing, Liu, Chang, Wang, Duo, Wang, Kang, Li, Li, Peng, Lu-Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926382/
https://www.ncbi.nlm.nih.gov/pubmed/27258257
http://dx.doi.org/10.3390/ijms17060848
_version_ 1782440100261527552
author Liu, Jing-Jing
Zhao, Cui-Mei
Li, Zhi-Gang
Wang, Yu-Mei
Miao, Wei
Wu, Xiu-Juan
Wang, Wen-Jing
Liu, Chang
Wang, Duo
Wang, Kang
Li, Li
Peng, Lu-Ying
author_facet Liu, Jing-Jing
Zhao, Cui-Mei
Li, Zhi-Gang
Wang, Yu-Mei
Miao, Wei
Wu, Xiu-Juan
Wang, Wen-Jing
Liu, Chang
Wang, Duo
Wang, Kang
Li, Li
Peng, Lu-Ying
author_sort Liu, Jing-Jing
collection PubMed
description MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with significant risks of heart failure. However, many microRNAs are still not recognized for their functions in pathophysiological processes. In this study, we evaluated effects of miR-218 in cardiomyocyte hypertrophy using both in vitro and in vivo models. We found that miR-218 was evidently downregulated in a transverse aortic constriction (TAC) mouse model. Overexpression of miR-218 is sufficient to reduce hypertrophy, whereas the suppression of miR-218 aggravates hypertrophy in primary cardiomyocytes induced by isoprenaline (ISO). In addition, we identified RE1-silencing transcription factor (REST) as a novel target of miR-218; it negatively regulated the expression of REST in hypertrophic cardiomyocytes and the TAC model. These results showed that miR-218 plays a crucial role in cardiomyocyte hypertrophy, likely via targeting REST, suggesting a potential candidate target for interfering hypertrophy.
format Online
Article
Text
id pubmed-4926382
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-49263822016-07-06 miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST Liu, Jing-Jing Zhao, Cui-Mei Li, Zhi-Gang Wang, Yu-Mei Miao, Wei Wu, Xiu-Juan Wang, Wen-Jing Liu, Chang Wang, Duo Wang, Kang Li, Li Peng, Lu-Ying Int J Mol Sci Article MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with significant risks of heart failure. However, many microRNAs are still not recognized for their functions in pathophysiological processes. In this study, we evaluated effects of miR-218 in cardiomyocyte hypertrophy using both in vitro and in vivo models. We found that miR-218 was evidently downregulated in a transverse aortic constriction (TAC) mouse model. Overexpression of miR-218 is sufficient to reduce hypertrophy, whereas the suppression of miR-218 aggravates hypertrophy in primary cardiomyocytes induced by isoprenaline (ISO). In addition, we identified RE1-silencing transcription factor (REST) as a novel target of miR-218; it negatively regulated the expression of REST in hypertrophic cardiomyocytes and the TAC model. These results showed that miR-218 plays a crucial role in cardiomyocyte hypertrophy, likely via targeting REST, suggesting a potential candidate target for interfering hypertrophy. MDPI 2016-05-31 /pmc/articles/PMC4926382/ /pubmed/27258257 http://dx.doi.org/10.3390/ijms17060848 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Liu, Jing-Jing
Zhao, Cui-Mei
Li, Zhi-Gang
Wang, Yu-Mei
Miao, Wei
Wu, Xiu-Juan
Wang, Wen-Jing
Liu, Chang
Wang, Duo
Wang, Kang
Li, Li
Peng, Lu-Ying
miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title_full miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title_fullStr miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title_full_unstemmed miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title_short miR-218 Involvement in Cardiomyocyte Hypertrophy Is Likely through Targeting REST
title_sort mir-218 involvement in cardiomyocyte hypertrophy is likely through targeting rest
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926382/
https://www.ncbi.nlm.nih.gov/pubmed/27258257
http://dx.doi.org/10.3390/ijms17060848
work_keys_str_mv AT liujingjing mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT zhaocuimei mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT lizhigang mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT wangyumei mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT miaowei mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT wuxiujuan mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT wangwenjing mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT liuchang mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT wangduo mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT wangkang mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT lili mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest
AT pengluying mir218involvementincardiomyocytehypertrophyislikelythroughtargetingrest