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The mechanism of myocardial hypertrophy regulated by the interaction between mhrt and myocardin.

Abstract
As a strong transactivator of promoters containing CarG boxes, myocardin was critical for the cardiac muscle program and necessary for normal cardiogenesis. So it probably represents a viable therapeutic biomarker in the setting of cardiac hypertrophy and failure. In recent years, the studies of regulation of cardiac hypertrophy via myocardin are so common, and the molecular mechanism is becoming more and more clear. Here, we have revealed a kind of interaction between mhrt and myocardin shown as a feedback regulatory mechanism in the regulation of cardiac hypertrophy. That is, the lncRNA mhrt can affect the acetylation of myocardin by HDAC5 to inhibit cardiac hypertrophy induced by myocardin. Moreover, myocardin also can directly activate the mhrt transcription through binding to the CarG box. Thus, mhrt and myocardin form a regulation loop in the process of cardiac hypertrophy. This finding may play a positive role in revealing the complete mechanisms of cardiac hypertrophy.
AuthorsYing Luo, Yao Xu, Chen Liang, Weibing Xing, Tongcun Zhang
JournalCellular signalling (Cell Signal) Vol. 43 Pg. 11-20 (03 2018) ISSN: 1873-3913 [Electronic] England
PMID29199045 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2017. Published by Elsevier Inc.
Chemical References
  • Cardiotonic Agents
  • Nuclear Proteins
  • RNA, Long Noncoding
  • Trans-Activators
  • long non-coding RNA Mhrt, rat
  • myocardin
  • Hdac5 protein, rat
  • Histone Deacetylases
Topics
  • Acetylation
  • Animals
  • Cardiomegaly (genetics, metabolism, pathology)
  • Cardiotonic Agents (metabolism)
  • Gene Expression Regulation
  • Histone Deacetylases (metabolism)
  • Models, Biological
  • Myocardium (metabolism, pathology)
  • Myocytes, Cardiac (metabolism, pathology)
  • Nuclear Proteins (genetics, metabolism)
  • Promoter Regions, Genetic
  • Protein Binding
  • RNA, Long Noncoding (genetics, metabolism)
  • Rats, Sprague-Dawley
  • Trans-Activators (genetics, metabolism)

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