Document Detail


Disruption of caveolin-1 leads to enhanced nitrosative stress and severe systolic and diastolic heart failure.
MedLine Citation:
PMID:  16380094     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although caveolin-1 is not expressed in cardiomyocytes, this protein is assumed to act as a key regulator in the development of cardiomyopathy. In view of recent discordant findings we aimed to elucidate the cardiac phenotype of independently generated caveolin-1 knockout mice (cav-1(-/-)) and to unveil causative mechanisms. Invasive hemodynamic measurements of cav-1(-/-) show a severely reduced systolic and diastolic heart function. Additionally, genetic ablation of caveolin-1 leads to a striking biventricular hypertrophy and to a sustained eNOS-hyperactivation yielding increased systemic NO levels. Furthermore, a diminished ATP content and reduced levels of cyclic AMP in hearts of knockout animals were measured. Taken together, these results indicate that genetic disruption of caveolin-1 is sufficient to induce a severe biventricular hypertrophy with signs of systolic and diastolic heart failure. Collectively, our findings suggest a causative role of a sustained nitrosative stress in the development of the pronounced cardiac impairment.
Authors:
Carsten Wunderlich; Kristin Schober; Stefan A Lange; Marek Drab; Ruediger C Braun-Dullaeus; Michael Kasper; Carsten Schwencke; Alexander Schmeisser; Ruth H Strasser
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Publication Detail:
Type:  Journal Article     Date:  2005-12-20
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  340     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2006 Feb 
Date Detail:
Created Date:  2006-01-03     Completed Date:  2006-03-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  702-8     Citation Subset:  IM    
Affiliation:
University of Technology Dresden, Department of Cardiology, Medical Clinic, Fetscherstr. 76, D-01307 Dresden, Germany. carstenwunderlich@gmx.de
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Apoptosis / genetics
Cardiomyopathy, Hypertrophic / enzymology,  genetics,  metabolism*,  physiopathology
Caveolin 1 / deficiency*,  genetics*
Cyclic AMP / metabolism
Heart Failure / genetics,  metabolism*,  physiopathology
Hypertrophy, Left Ventricular / enzymology,  genetics,  physiopathology
Hypertrophy, Right Ventricular / enzymology,  genetics,  physiopathology
Mice
Mice, Knockout
Mice, Transgenic
Myocardium / enzymology,  metabolism*
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type II / metabolism
Nitric Oxide Synthase Type III / metabolism*
Severity of Illness Index
Chemical
Reg. No./Substance:
0/Caveolin 1; 10102-43-9/Nitric Oxide; 56-65-5/Adenosine Triphosphate; 60-92-4/Cyclic AMP; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse

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


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