Source:http://linkedlifedata.com/resource/pubmed/id/14620933
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2003-11-17
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pubmed:abstractText |
A number of in vitro studies have suggested potential pathophysiological roles of human (h-) chymase. However, the lack of an appropriate animal model has left the in vivo roles of chymase unclear. To approach this problem, a transgenic mouse (TGM) model carrying the h-chymase gene was established. The h-chymase cDNA transgene was constructed with the chicken beta actin promoter and cytomegalovirus immediate early gene enhancer, and injected into mouse oocytes. Homozygous mice with a high copy number of the h-chymase gene suffered from intrauterine death. In three heterozygous TGM lines, h-chymase transgene expression was detected in entire organs, including the heart, vessels, skin, liver, lung, and brain. The h-chymase immunoreactivity was localized in the extracellular matrices of each organ, especially on the basement membranes of vessels. Aortic and hepatic chymase-dependent angiotensin II formations were significantly higher than those in the wild-type littermates. Three independent TGM lines showed the same phenotypic changes: elevation of blood pressure, left ventricular hypertrophy, emaciation with reduction in the lipid tissue, leukocytosis, and oligotrichia. The angiotensin II subtype 1 (AT1) receptor antagonist valsartan suppressed the elevated blood pressure completely and left ventricular hypertrophy incompletely, but did not affect the other phenotypes. These data suggested that in vivo expression of h-chymase caused mild hypertension (AT1 receptor-dependent) with left ventricular hypertrophy (partially AT1 receptor-dependent), and also chronic inflammatory changes (AT1 receptor-independent).
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0916-9636
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pubmed:author |
pubmed-author:ArakawaKikuoK,
pubmed-author:HoshinoTakafumiT,
pubmed-author:IdeishiMunehitoM,
pubmed-author:InoueYukikoY,
pubmed-author:KogaTakafumiT,
pubmed-author:MatsunagaAkiraA,
pubmed-author:MiyazakiJunichiJ,
pubmed-author:OkamotoTakehiroT,
pubmed-author:SakuKeijiroK,
pubmed-author:SuzukiMisaoM,
pubmed-author:UrataHidenoriH
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pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
759-68
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:14620933-Animals,
pubmed-meshheading:14620933-Chymases,
pubmed-meshheading:14620933-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:14620933-Humans,
pubmed-meshheading:14620933-Hypertension,
pubmed-meshheading:14620933-Hypertrophy, Left Ventricular,
pubmed-meshheading:14620933-Mice,
pubmed-meshheading:14620933-Mice, Transgenic,
pubmed-meshheading:14620933-Phenotype,
pubmed-meshheading:14620933-Serine Endopeptidases
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pubmed:year |
2003
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pubmed:articleTitle |
Human chymase expression in a mice induces mild hypertension with left ventricular hypertrophy.
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pubmed:affiliation |
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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