Source:http://linkedlifedata.com/resource/pubmed/id/14699015
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2004-3-5
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| pubmed:abstractText |
Angiotensin II type 1 (AT1) receptor activation as well as proinflammatory cytokines such as interleukin-6 (IL-6) are involved in the development and progression of atherosclerosis. The detailed underlying mechanisms including interactions between inflammatory agonists and the renin-angiotensin system are poorly understood. Stimulation of cultured rat aortic vascular smooth muscle cells (VSMCs) with IL-6 led to upregulation of AT1 receptor mRNA and protein expression, as assessed by Northern and Western blot experiments. Nuclear run-on and transcription blockade experiments showed that IL-6 increases AT1 receptor mRNA de novo synthesis but not mRNA stability. Preincubation of VSMCs with IL-6 resulted in an enhanced angiotensin II-induced production of reactive oxygen species, as assessed by DCF fluorescence laser microscopy. Treatment of C57BL/6J mice with IL-6 for 18 days increased vascular AT1 receptor expression (real-time RT-PCR) and angiotensin II-induced vasoconstriction, enhanced vascular superoxide production (L-012 chemiluminescence, DHE fluorescence), and impaired endothelium-dependent vasodilatation. These effects were completely omitted in AT1 receptor knockout mice (AT1A-/- mice). Upregulation of vascular AT1 receptor expression in vitro and in vivo is decisively involved in IL-6-induced propagation of oxidative stress and endothelial dysfunction. This interaction of the proinflammatory cytokine IL-6 with the renin-angiotensin system may represent an important pathogenetic mechanism in the atherosclerotic process.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
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| pubmed:issn |
1524-4571
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
5
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| pubmed:volume |
94
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
534-41
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14699015-Animals,
pubmed-meshheading:14699015-Aortic Diseases,
pubmed-meshheading:14699015-Arteriosclerosis,
pubmed-meshheading:14699015-Crosses, Genetic,
pubmed-meshheading:14699015-Endothelium, Vascular,
pubmed-meshheading:14699015-Gene Expression Regulation,
pubmed-meshheading:14699015-Inflammation,
pubmed-meshheading:14699015-Interleukin-6,
pubmed-meshheading:14699015-Male,
pubmed-meshheading:14699015-Mice,
pubmed-meshheading:14699015-Mice, Inbred C57BL,
pubmed-meshheading:14699015-Mice, Knockout,
pubmed-meshheading:14699015-Muscle, Smooth, Vascular,
pubmed-meshheading:14699015-Oxidative Stress,
pubmed-meshheading:14699015-Rats,
pubmed-meshheading:14699015-Reactive Oxygen Species,
pubmed-meshheading:14699015-Receptor, Angiotensin, Type 1,
pubmed-meshheading:14699015-Recombinant Proteins,
pubmed-meshheading:14699015-Renin-Angiotensin System
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Interleukin-6 induces oxidative stress and endothelial dysfunction by overexpression of the angiotensin II type 1 receptor.
|
| pubmed:affiliation |
Medizinische Klinik und Poliklinik, Innere Medizin III, Universitätskliniken des Saarlandes, D-66421 Homburg/Saar, Germany. wassmann@med-in.uni-saarland.de
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|