Abstract:
RATIONALE:Sustained cardiac hypertrophy is often accompanied by maladaptive cardiac remodeling leading to decreased compliance and increased risk for heart failure. Maladaptive hypertrophy is considered to be a therapeutic target for heart failure. MicroRNAs (miRNAs) and long noncoding RNAs (lncRNAs) have various biological functions and have been extensively investigated in past years. OBJECTIVE:We identified miR-489 and lncRNAs (cardiac hypertrophy related factor, CHRF) from hypertrophic cardiomyocytes. Here, we tested the hypothesis that miR-489 and CHRF can participate in the regulation of cardiac hypertrophy in vivo and in vitro. METHODS AND RESULTS:A microarray was performed to analyze miRNAs in response to angiotensin II treatment, and we found miR-489 was substantially reduced. Enforced expression of miR-489 in cardiomyocytes and transgenic overexpression of miR-489 both exhibited reduced hypertrophic response on angiotensin II treatment. We identified myeloid differentiation primary response gene 88 (Myd88) as a miR-489 target to mediate the function of miR-489 in cardiac hypertrophy. Knockdown of Myd88 in cardiomyocytes and Myd88-knockout mice both showed attenuated hypertrophic responses. Furthermore, we explored the molecular mechanism by which miR-489 expression is regulated and found that an lncRNA that we named CHRF acts as an endogenous sponge of miR-489, which downregulates miR-489 expression levels. CHRF is able to directly bind to miR-489 and regulate Myd88 expression and hypertrophy. CONCLUSIONS:Our present study reveals a novel cardiac hypertrophy regulating model that is composed of CHRF, miR-489, and Myd88. The modulation of their levels may provide a new approach for tackling cardiac hypertrophy.
journal_name
Circ Resjournal_title
Circulation researchauthors
Wang K,Liu F,Zhou LY,Long B,Yuan SM,Wang Y,Liu CY,Sun T,Zhang XJ,Li PFdoi
10.1161/CIRCRESAHA.114.302476subject
Has Abstractpub_date
2014-04-25 00:00:00pages
1377-88issue
9eissn
0009-7330issn
1524-4571pii
CIRCRESAHA.114.302476journal_volume
114pub_type
杂志文章abstract:RATIONALE:Myofibroblasts are believed to evolve from precursor cells; however, whether noncardiomyocyte cardiac cells (NMCCs; ie, endothelial cells, smooth muscle cells, pericytes, and fibroblasts) that have been derived from human-induced pluripotent stem cells (hiPSCs) can transdifferentiate into myofibroblast-like c...
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journal_title:Circulation research
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doi:
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abstract::Smooth muscle cell migration in response to platelet-derived growth factor (PDGF) is a key event in several vascular pathologies, including atherosclerosis and restenosis. PDGF increases intracellular levels of reactive oxygen species (ROS) in vascular smooth muscle cells (VSMCs), but the ROS sensitivity of migration ...
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journal_title:Circulation research
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journal_title:Circulation research
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doi:10.1161/hh0102.103221
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abstract::Left ventricular (LV) remodeling after experimental myocardial infarction (MI) is associated with hypertrophy of noninfarcted myocardium and electrophysiological alterations. We have recently shown that post-MI hypertrophied LV myocytes have prolonged action potential duration (APD) and generate triggered activity fro...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.79.4.669
更新日期:1996-10-01 00:00:00
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doi:10.1161/01.res.39.1.106
更新日期:1976-07-01 00:00:00
abstract::Inhibition of vascular smooth muscle (VSM) delayed rectifier K+ channels (K(DR)) by 4-aminopyridine (4-AP; 200 micromol/L) or correolide (1 micromol/L), a selective inhibitor of Kv1 channels, enhanced myogenic contraction of rat mesenteric arteries (RMAs) in response to increases in intraluminal pressure. The molecula...
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pub_type: 杂志文章
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更新日期:2005-02-04 00:00:00
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doi:10.1161/01.res.49.1.141
更新日期:1981-07-01 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.84.8.929
更新日期:1999-04-30 00:00:00
abstract::In response to hypoxia and reoxygenation, mammalian cells are known to express a variety of genes to adapt to these external stresses or lead to further cell damage. We investigated the intracellular signaling cascades in cultured rat cardiac myocytes subjected to hypoxia followed by reoxygenation (hypoxia/reoxygenati...
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doi:10.1161/01.res.78.1.82
更新日期:1996-01-01 00:00:00
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doi:10.1161/01.res.55.2.155
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更新日期:1977-01-01 00:00:00
abstract::The recent discovery of neutral active choline and ethanolamine glycerophospholipid specific phospholipase C in myocardium (Wolf RA, Gross RW. J Biol Chem 1985;260:7295) has demonstrated a novel catabolic pathway that potentially contributes to the accumulation of amphiphilic metabolites during myocardial ischemia. To...
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更新日期:1989-01-01 00:00:00
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更新日期:2010-06-11 00:00:00
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更新日期:1978-08-01 00:00:00
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更新日期:2014-09-12 00:00:00