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MicroRNA-214 provokes cardiac hypertrophy via repression of EZH2.

Authors: Yang, T  Zhang, GF  Chen, XF  Gu, HH  Fu, SZ  Xu, HF  Feng, Q  Ni, YM 
Citation: Yang T, etal., Biochem Biophys Res Commun. 2013 Jul 12;436(4):578-84. doi: 10.1016/j.bbrc.2013.05.079. Epub 2013 May 29.
Pubmed: (View Article at PubMed) PMID:23727574
DOI: Full-text: DOI:10.1016/j.bbrc.2013.05.079

Micro RNAs are small, non-coding RNA molecules that regulate gene expression via either translational inhibition or mRNA degredation. Enhancer of zeste homolog 2 (EZH2)-mediated hypertrophic signaling is a major regulatory response to hypertrophic stimuli. In this study, we constructed AAC rat models and PE-induced hypertrophic cardiomyocytes. We demonstrated that miR-214 relative levels were upregulated, whereas EZH2 was downregulated in both vivo and vitro models. Further, one conserved base-pairing site in the EZH2 3'-untranslated region (UTR) was verified. Mutation of the site in the EZH2 3'-UTR completely blocked the negative effect of miR-214 on EZH2, suggesting that EZH2 is a direct target for miR-214 regulation. Using a gain-of-function approach, incorporating the lentivirus constructed miR-214 and its sponge, we demonstrated that miR-214 significantly regulated endogenous levels of EZH2 gene expression; whereas, changes in the expression of the Sine oculis homeobox homolog gene were induced by an adrenergic receptor agonist in the AAC rat model. Having made this study it is possible to conclude that the negative regulation of EZH2 expression contributed to miR-214-mediated cardiac hypertrophy.


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CRRD Object Information
CRRD ID: 9588322
Created: 2014-10-28
Species: All species
Last Modified: 2014-10-28
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.