Document Detail


Stress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice.
MedLine Citation:
PMID:  20978354     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
MicroRNAs inhibit mRNA translation or promote mRNA degradation by binding complementary sequences in 3' untranslated regions of target mRNAs. MicroRNA-21 (miR-21) is upregulated in response to cardiac stress, and its inhibition by a cholesterol-modified antagomir has been reported to prevent cardiac hypertrophy and fibrosis in rodents in response to pressure overload. In contrast, we have shown here that miR-21-null mice are normal and, in response to a variety of cardiac stresses, display cardiac hypertrophy, fibrosis, upregulation of stress-responsive cardiac genes, and loss of cardiac contractility comparable to wild-type littermates. Similarly, inhibition of miR-21 through intravenous delivery of a locked nucleic acid-modified (LNA-modified) antimiR oligonucleotide also failed to block the remodeling response of the heart to stress. We therefore conclude that miR-21 is not essential for pathological cardiac remodeling.
Authors:
David M Patrick; Rusty L Montgomery; Xiaoxia Qi; Susanna Obad; Sakari Kauppinen; Joseph A Hill; Eva van Rooij; Eric N Olson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-18
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  120     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-02     Completed Date:  2010-12-07     Revised Date:  2014-09-22    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3912-6     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomegaly / metabolism,  pathology*
Hypertension / pathology
Mice
Mice, Knockout
MicroRNAs / genetics,  metabolism*
Myocardial Contraction / physiology
Myocardium* / metabolism,  pathology
Oligonucleotides, Antisense / genetics,  metabolism
Stress, Physiological*
Ventricular Remodeling / physiology*
Grant Support
ID/Acronym/Agency:
R01 HL077439/HL/NHLBI NIH HHS; R01 HL077439-01/HL/NHLBI NIH HHS; R01 HL077439-02/HL/NHLBI NIH HHS; R01 HL077439-03/HL/NHLBI NIH HHS; R01 HL077439-04/HL/NHLBI NIH HHS; R01 HL077439-05/HL/NHLBI NIH HHS; R01 HL077439-06/HL/NHLBI NIH HHS; R01 HL077439-06W1/HL/NHLBI NIH HHS; R01 HL077439-07/HL/NHLBI NIH HHS; R01 HL077439-08/HL/NHLBI NIH HHS; R01 HL093039/HL/NHLBI NIH HHS; R01 HL093039-01A1/HL/NHLBI NIH HHS; R01 HL093039-01A1W1/HL/NHLBI NIH HHS; R01 HL093039-02/HL/NHLBI NIH HHS; R01 HL093039-03/HL/NHLBI NIH HHS; R37 HL053351/HL/NHLBI NIH HHS; R37 HL053351-09S1/HL/NHLBI NIH HHS; R37 HL053351-10/HL/NHLBI NIH HHS; R37 HL053351-11/HL/NHLBI NIH HHS; R37 HL053351-12/HL/NHLBI NIH HHS; R37 HL053351-13/HL/NHLBI NIH HHS; R37 HL053351-14/HL/NHLBI NIH HHS; R37 HL053351-15/HL/NHLBI NIH HHS; U01 HL100401/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/MIRN21 microRNA, mouse; 0/MicroRNAs; 0/Oligonucleotides, Antisense
Comments/Corrections
Comment In:
J Clin Invest. 2011 Feb;121(2):461-2; author reply 462-3   [PMID:  21285516 ]
J Clin Invest. 2010 Nov;120(11):3817-9   [PMID:  20978356 ]

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