Linked Life Data

11511516

Source:http://linkedlifedata.com/resource/pubmed/id/11511516

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-10-19
pubmed:abstractText
Cardiac hypertrophy as an adaptation to increased blood pressure leads to an increase in ventricular expression of transforming growth factor Cardiac hypertrophy as an adaptation to increased blood pressure leads to an increase in ventricular expression of transforming growth factor b (TGF-b), probably via the renin-angiotensin system. We studied in vivo to determine whether angiotensin II affects TGF-b expression independent from mechanical effects caused by the concomitant increase in blood pressure and in vitro intracellular signaling involved in angiotensin II-dependent TGF-b1 induction. In vivo, the AT1 receptor antagonist losartan, but not reduction of blood pressure by hydralazine, inhibited the increase in TGF-b1 expression caused by angiotensin II. In vitro, angiotensin II caused an induction of TGF-b1 expression in adult ventricular cardiomyocytes and induced AP-1 binding activity. Transfection with "decoys" directed against the binding site of AP-1 binding proteins inhibited the angiotensin II-dependent TGF-b induction. Angiotensin II induced TGF-b expression in a p38-MAP kinase-dependent way. p38-MAP kinase activation was diminished in presence of the antioxidants or diphenyleneiodium chloride, or by pretreatment with antisense nucleotides directed against phox22 and nox, components of smooth muscle type NAD(P)H oxidase. Thus, our study identifies a previously unrecognized coupling of cardiac AT receptors to a NAD(P)H oxidase complex similar to that expressed in smooth muscle cells and identifies p38-MAP kinase activation as an important downstream target.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2291-3
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11511516-Angiotensin II, pubmed-meshheading:11511516-Animals, pubmed-meshheading:11511516-Cardiomegaly, pubmed-meshheading:11511516-Cells, Cultured, pubmed-meshheading:11511516-Enzyme Activation, pubmed-meshheading:11511516-Heart Ventricles, pubmed-meshheading:11511516-MAP Kinase Signaling System, pubmed-meshheading:11511516-Mitogen-Activated Protein Kinases, pubmed-meshheading:11511516-Models, Biological, pubmed-meshheading:11511516-Myocardium, pubmed-meshheading:11511516-Oxidation-Reduction, pubmed-meshheading:11511516-RNA, Messenger, pubmed-meshheading:11511516-Transcription Factor AP-1, pubmed-meshheading:11511516-Transcriptional Activation, pubmed-meshheading:11511516-Transforming Growth Factor beta, pubmed-meshheading:11511516-p38 Mitogen-Activated Protein Kinases
pubmed:year
2001
pubmed:articleTitle
Redox-sensitive intermediates mediate angiotensin II-induced p38 MAP kinase activation, AP-1 binding activity, and TGF-beta expression in adult ventricular cardiomyocytes.
pubmed:affiliation
Physiologisches Institut, Universität Giessen, Germany.
pubmed:publicationType
Journal Article