Document Detail


Impaired cardiac contraction and relaxation and decreased expression of sarcoplasmic Ca2+-ATPase in mice lacking the CREM gene.
MedLine Citation:
PMID:  12475904     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Congestive heart failure is the common endpoint of various cardiac diseases representing a leading cause of cardiovascular mortality in Western countries. Characteristic functional alterations of the failing heart are explained by expressional changes of myocardial regulatory proteins; however, little is known about underlying mechanisms regulating cardiac gene expression in the failing heart. Here, we address the specific role of transcription factor CREM for cardiac function in CREM mutant mice with complete inactivation of the CREM gene. We show that CREM mutant mice display distinct alterations of cardiac function resembling characteristic functional defects of the failing heart. Left ventricular hemodynamic assessment of CREM mutant mice revealed impairment of both cardiac contraction and relaxation in basal state, as well as a decreased responsiveness to beta-adrenergic stimulation. The diminished cardiac contractile performance was associated with a selective down-regulation of beta1-adrenergic receptors and a decreased ventricular expression of SERCA, the Ca2+-ATPase of the sarcoplasmic reticulum. The cardiac phenotype of CREM mutant mice provides the first evidence that CREM represents an important key regulator of cardiac gene expression, which is essential for normal left ventricular contractile performance and response to beta-adrenoreceptor stimulation.
Authors:
Frank U Müller; Geertje Lewin; Marek Matus; Joachim Neumann; Burkhard Riemann; Joachim Wistuba; Günther Schütz; Wilhelm Schmitz
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Publication Detail:
Type:  Journal Article     Date:  2002-11-15
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  17     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-01-10     Completed Date:  2003-02-10     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  103-5     Citation Subset:  IM    
Affiliation:
Institute of Pharmacology and Toxicology, University of Münster, Germany. mullerf@uni-muenster.de
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology
Animals
Calcium-Transporting ATPases / metabolism*
Cardiomegaly / etiology
Cyclic AMP Response Element Modulator
DNA-Binding Proteins / genetics*,  physiology*
Dobutamine / pharmacology
Mice
Mice, Knockout
Models, Biological
Mutation
Myocardial Contraction*
Repressor Proteins*
Sarcoplasmic Reticulum Calcium-Transporting ATPases
Survival Analysis
Ventricular Dysfunction, Left / etiology
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/DNA-Binding Proteins; 0/Repressor Proteins; 135844-64-3/Cyclic AMP Response Element Modulator; 34368-04-2/Dobutamine; EC 3.6.3.8/Calcium-Transporting ATPases; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases

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


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