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rdf:type |
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lifeskim:mentions |
umls-concept:C0018801,
umls-concept:C0021701,
umls-concept:C0033095,
umls-concept:C0033684,
umls-concept:C0205191,
umls-concept:C0871261,
umls-concept:C0893597,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
1
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pubmed:dateCreated |
2003-1-6
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pubmed:abstractText |
Cardiac hypertrophy is an adaptive response to a variety of mechanical and hormonal stimuli, and represents an early event in the clinical course leading to heart failure. By gene inactivation, we demonstrate here a crucial role of melusin, a muscle-specific protein that interacts with the integrin beta1 cytoplasmic domain, in the hypertrophic response to mechanical overload. Melusin-null mice showed normal cardiac structure and function in physiological conditions, but when subjected to pressure overload--a condition that induces a hypertrophic response in wild-type controls--they developed an abnormal cardiac remodeling that evolved into dilated cardiomyopathy and contractile dysfunction. In contrast, the hypertrophic response was identical in wild-type and melusin-null mice after chronic administration of angiotensin II or phenylephrine at doses that do not increase blood pressure--that is, in the absence of cardiac biomechanical stress. Analysis of intracellular signaling events induced by pressure overload indicated that phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) was specifically blunted in melusin-null hearts. Thus, melusin prevents cardiac dilation during chronic pressure overload by specifically sensing mechanical stress.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD29,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cytoskeletal Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/ITGB1BP2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Itgb1bp2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1078-8956
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pubmed:author |
pubmed-author:AltrudaFiorellaF,
pubmed-author:BrancaccioMaraM,
pubmed-author:De AcetisMarikaM,
pubmed-author:FrattaLuigiL,
pubmed-author:GuazzoneSimonaS,
pubmed-author:HirschEmilioE,
pubmed-author:LemboGiuseppeG,
pubmed-author:MarinoGennaroG,
pubmed-author:NotteAntonellaA,
pubmed-author:PouletRobertaR,
pubmed-author:SilengoLorenzoL,
pubmed-author:TaroneGuidoG,
pubmed-author:VecchioneCarmineC
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pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
68-75
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12496958-Angiotensin II,
pubmed-meshheading:12496958-Animals,
pubmed-meshheading:12496958-Antigens, CD29,
pubmed-meshheading:12496958-Aortic Coarctation,
pubmed-meshheading:12496958-Biomechanics,
pubmed-meshheading:12496958-Cardiac Output, Low,
pubmed-meshheading:12496958-Cardiomegaly,
pubmed-meshheading:12496958-Carrier Proteins,
pubmed-meshheading:12496958-Cytoskeletal Proteins,
pubmed-meshheading:12496958-Echocardiography,
pubmed-meshheading:12496958-Female,
pubmed-meshheading:12496958-Gene Silencing,
pubmed-meshheading:12496958-Heart Ventricles,
pubmed-meshheading:12496958-Hemodynamics,
pubmed-meshheading:12496958-Male,
pubmed-meshheading:12496958-Mice,
pubmed-meshheading:12496958-Mice, Knockout,
pubmed-meshheading:12496958-Muscle, Skeletal,
pubmed-meshheading:12496958-Muscle Proteins,
pubmed-meshheading:12496958-Myocardium,
pubmed-meshheading:12496958-Phenylephrine,
pubmed-meshheading:12496958-Signal Transduction,
pubmed-meshheading:12496958-Stress, Mechanical,
pubmed-meshheading:12496958-Vasoconstrictor Agents,
pubmed-meshheading:12496958-Ventricular Function
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pubmed:year |
2003
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pubmed:articleTitle |
Melusin, a muscle-specific integrin beta1-interacting protein, is required to prevent cardiac failure in response to chronic pressure overload.
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pubmed:affiliation |
Department of Genetics, Biology, and Biochemistry, Turin University, 10126 Turin, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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