Source:http://linkedlifedata.com/resource/pubmed/id/16923992
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
2006-9-22
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| pubmed:abstractText |
To explore the role of angiotensin II Type 1 receptor-associated protein (ATRAP) in vascular remodeling, we developed transgenic mice for mouse ATRAP cDNA and examined remodeling after inflammatory vascular injury induced by polyethylene cuff placement. In ATRAP transgenic (ATRAP-Tg) mice, ATRAP mRNA was increased 3- to 4-fold in the heart, aorta, and femoral artery. ATRAP-Tg mice showed no significant change in body weight, systolic blood pressure, heart rate, and heart/body weight ratio. However, cell proliferation and neointimal formation in the injured artery were attenuated in ATRAP-Tg mice. The increase in NADPH oxidase activity and the expression of p22(phox), a reduced nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide phosphate oxidase subunit, after cuff placement was also attenuated in ATRAP-Tg mice. Moreover, activation of extracellular signal-regulated kinase, signal transducer and activator of transcription 1, and signal transducer and activator of transcription 3 after cuff placement was significantly reduced in ATRAP-Tg mice. Pressor response and cardiac hypertrophy induced by angiotensin II infusion and pressure overload were also attenuated in ATRAP-Tg mice. These results suggest that ATRAP plays an important role in vascular remodeling as a negative regulator.
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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
|
| pubmed:month |
Oct
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| pubmed:issn |
1524-4563
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
48
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
671-6
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16923992-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:16923992-Animals,
pubmed-meshheading:16923992-Blood Pressure,
pubmed-meshheading:16923992-Cardiomegaly,
pubmed-meshheading:16923992-Cell Proliferation,
pubmed-meshheading:16923992-Constriction,
pubmed-meshheading:16923992-Femoral Artery,
pubmed-meshheading:16923992-Heart Rate,
pubmed-meshheading:16923992-Inflammation,
pubmed-meshheading:16923992-Intracellular Membranes,
pubmed-meshheading:16923992-Male,
pubmed-meshheading:16923992-Mice,
pubmed-meshheading:16923992-Mice, Inbred C57BL,
pubmed-meshheading:16923992-Mice, Transgenic,
pubmed-meshheading:16923992-Muscle, Smooth, Vascular,
pubmed-meshheading:16923992-Myocytes, Smooth Muscle,
pubmed-meshheading:16923992-Oxidative Stress,
pubmed-meshheading:16923992-Signal Transduction,
pubmed-meshheading:16923992-Tunica Intima,
pubmed-meshheading:16923992-Wounds and Injuries
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Attenuation of inflammatory vascular remodeling by angiotensin II type 1 receptor-associated protein.
|
| pubmed:affiliation |
Department of Molecular and Cellular Biology, Ehime University School of Medicine, Tohon, Ehime, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|