Source:http://linkedlifedata.com/resource/pubmed/id/11016940
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
52
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pubmed:dateCreated |
2001-1-25
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pubmed:abstractText |
Chronic stimulation of the renin-angiotensin system induces an elevation of blood pressure and the development of cardiac hypertrophy via the actions of its effector, angiotensin II. In cardiomyocytes, mitogen-activated protein kinases as well as protein kinase C isoforms have been shown to be important in the transduction of trophic signals. The Ca(2+)/calmodulin-dependent phosphatase calcineurin has also been suggested to play a role in cardiac growth. In the present report, we investigate possible cross-talks between calcineurin, protein kinase C, and mitogen-activated protein kinase pathways in controlling angiotensin II-induced hypertrophy. Angiotensin II-stimulated cardiomyocytes and mice with angiotensin II-dependent renovascular hypertension were treated with the calcineurin inhibitor cyclosporin A. Calcineurin, protein kinase C, and mitogen-activated protein kinase activations were determined. We show that cyclosporin A blocks angiotensin II-induced mitogen-activated protein kinase activation in cultured primary cardiomyocytes and in the heart of hypertensive mice. Cyclosporin A also inhibits specific protein kinase C isoforms. In vivo, cyclosporin A prevents the development of cardiac hypertrophy, and this effect appears to be independent of hemodynamic changes. These data suggest cross-talks between the calcineurin pathway, the protein kinase C, and the mitogen-activated protein kinase signaling cascades in transducing angiotensin II-mediated stimuli in cardiomyocytes and could provide the basis for an integrated model of cardiac hypertrophy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Calcineurin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
29
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pubmed:volume |
275
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
40867-73
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11016940-Angiotensin II,
pubmed-meshheading:11016940-Animals,
pubmed-meshheading:11016940-Calcineurin,
pubmed-meshheading:11016940-Cardiomegaly,
pubmed-meshheading:11016940-Cyclosporine,
pubmed-meshheading:11016940-Enzyme Activation,
pubmed-meshheading:11016940-Hypertension, Renovascular,
pubmed-meshheading:11016940-Male,
pubmed-meshheading:11016940-Mice,
pubmed-meshheading:11016940-Mice, Inbred C57BL,
pubmed-meshheading:11016940-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11016940-Myocardium,
pubmed-meshheading:11016940-Protein Kinase C
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pubmed:year |
2000
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pubmed:articleTitle |
Calcineurin blockade prevents cardiac mitogen-activated protein kinase activation and hypertrophy in renovascular hypertension.
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pubmed:affiliation |
Division of Hypertension, University of Lausanne Medical School, CH-1011 Lausanne, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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