Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy

Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade lea...

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Main Authors:	Li, Qiaoling, Xie, Jun, Wang, Bingjian, Li, Ran, Bai, Jian, Ding, Liang, Gu, Rong, Wang, Lian, Xu, Biao
Format:	Online
Language:	English
Published:	Public Library of Science 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767297/

id	pubmed-4767297
recordtype	oai_dc
spelling	pubmed-47672972016-03-09 Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy Li, Qiaoling Xie, Jun Wang, Bingjian Li, Ran Bai, Jian Ding, Liang Gu, Rong Wang, Lian Xu, Biao Research Article Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade leading to cardiac hypertrophy is unknown. To evaluate the role of miR-99a in cardiac hypertrophy, we assessed the expression of miR-99a in hypertrophic cardiomyocytes induced by isoprenaline (ISO)/angiotensin-II (Ang II) and in mice model of cardiac hypertrophy induced by transverse aortic constriction (TAC). Expression of miR-99a was evaluated in these hypertrophic cells and hearts. We also found that miR-99a expression was highly correlated with cardiac function of mice with heart failure (8 weeks after TAC surgery). Overexpression of miR-99a attenuated cardiac hypertrophy in TAC mice and cellular hypertrophy in stimuli treated cardiomyocytes through down-regulation of expression of mammalian target of rapamycin (mTOR). These results indicate that miR-99a negatively regulates physiological hypertrophy through mTOR signaling pathway, which may provide a new therapeutic approach for pressure-overload heart failure. Public Library of Science 2016-02-25 /pmc/articles/PMC4767297/ /pubmed/26914935 http://dx.doi.org/10.1371/journal.pone.0148480 Text en © 2016 Li et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Li, Qiaoling Xie, Jun Wang, Bingjian Li, Ran Bai, Jian Ding, Liang Gu, Rong Wang, Lian Xu, Biao
spellingShingle	Li, Qiaoling Xie, Jun Wang, Bingjian Li, Ran Bai, Jian Ding, Liang Gu, Rong Wang, Lian Xu, Biao Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
author_facet	Li, Qiaoling Xie, Jun Wang, Bingjian Li, Ran Bai, Jian Ding, Liang Gu, Rong Wang, Lian Xu, Biao
author_sort	Li, Qiaoling
title	Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
title_short	Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
title_full	Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
title_fullStr	Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
title_full_unstemmed	Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
title_sort	overexpression of microrna-99a attenuates cardiac hypertrophy
description	Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade leading to cardiac hypertrophy is unknown. To evaluate the role of miR-99a in cardiac hypertrophy, we assessed the expression of miR-99a in hypertrophic cardiomyocytes induced by isoprenaline (ISO)/angiotensin-II (Ang II) and in mice model of cardiac hypertrophy induced by transverse aortic constriction (TAC). Expression of miR-99a was evaluated in these hypertrophic cells and hearts. We also found that miR-99a expression was highly correlated with cardiac function of mice with heart failure (8 weeks after TAC surgery). Overexpression of miR-99a attenuated cardiac hypertrophy in TAC mice and cellular hypertrophy in stimuli treated cardiomyocytes through down-regulation of expression of mammalian target of rapamycin (mTOR). These results indicate that miR-99a negatively regulates physiological hypertrophy through mTOR signaling pathway, which may provide a new therapeutic approach for pressure-overload heart failure.
publisher	Public Library of Science
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767297/
_version_	1613543350889086976

Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy

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