Document Detail


Cardiac remodeling is not modulated by overexpression of muscle LIM protein (MLP).
MedLine Citation:
PMID:  22421737     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Muscle LIM protein (MLP) has been proposed to be a central player in the pathogenesis of heart muscle disease. In line with this notion, the homozygous loss of MLP results in cardiac hypertrophy and dilated cardiomyopathy. Moreover, MLP is induced in several models of cardiac hypertrophy such as aortic banding and myocardial infarction. We thus hypothesized that overexpression of MLP might change the hypertrophic response to cardiac stress. In order to answer the question whether MLP modulates cardiac hypertrophy in vivo, we generated a novel transgenic mouse model with cardiac-specific overexpression of MLP. Three independent transgenic lines did not show a pathological phenotype under baseline conditions. Specifically, contractile function and heart weight to body weight ratios at different ages were normal. Next, the transgenic animals were challenged with pressure overload due to aortic constriction. Surprisingly, transgenic mice developed cardiac hypertrophy to the same extent as their wild-type littermates. Moreover, neither contractile dysfunction nor pathological gene expression in response to pressure overload were differentially affected by MLP overexpression. Finally, in a milder in vivo model of hypertrophy induced by chronic infusion of angiotensin-II, cardiac mass and hypertrophic gene expression were again identical in MLP transgenic mice and controls. Taken together, we provide evidence that cardiac overexpression of MLP does not modulate the heart's response to various forms of pathological stress.
Authors:
Christian Kuhn; Derk Frank; Franziska Dierck; Ulrike Oehl; Jutta Krebs; Rainer Will; Lorenz H Lehmann; Johannes Backs; Hugo A Katus; Norbert Frey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-03-16
Journal Detail:
Title:  Basic research in cardiology     Volume:  107     ISSN:  1435-1803     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-03-16     Completed Date:  2012-07-09     Revised Date:  2014-08-20    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  262     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II
Animals
Animals, Newborn
Aorta / surgery
Blood Pressure
Cardiomegaly / etiology,  genetics,  metabolism*,  physiopathology,  ultrasonography
Cells, Cultured
Disease Models, Animal
Gene Expression Regulation
Genotype
LIM Domain Proteins / genetics,  metabolism*
Ligation
Mice
Mice, 129 Strain
Mice, Transgenic
Muscle Proteins / genetics,  metabolism*
Myocardial Contraction
Myocardium / metabolism*,  pathology
Phenotype
Rats
Rats, Wistar
Ventricular Function, Left
Ventricular Remodeling*
Chemical
Reg. No./Substance:
0/LIM Domain Proteins; 0/Muscle Proteins; 0/cysteine and glycine-rich protein 3; 11128-99-7/Angiotensin II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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