Source:http://linkedlifedata.com/resource/pubmed/id/12065319
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2002-6-14
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| pubmed:abstractText |
Neointimal hyperplasia is a major cause of restenosis after coronary intervention. Because vascular injury is now recognized to involve an inflammatory response, monocyte chemoattractant protein-1 (MCP-1) might be involved in underlying mechanisms of restenosis. In the present study, we demonstrate the important role of MCP-1 in neointimal hyperplasia after cuff-induced arterial injury. In the first set of experiments, placement of a nonconstricting cuff around the femoral artery of intact mice and monkeys resulted in inflammation in the early stages and subsequent neointimal hyperplasia at the late stages. We transfected with an N-terminal deletion mutant of the human MCP-1 gene into skeletal muscles to block MCP-1 activity in vivo. This mutant MCP-1 works as a dominant-negative inhibitor of MCP-1. This strategy inhibited early vascular inflammation (monocyte infiltration, increased expression of MCP-1, and inflammatory cytokines) and late neointimal hyperplasia. In the second set of experiments, the cuff-induced neointimal hyperplasia was found to be less in CCR2-deficient mice than in control CCR2(+/+) mice. The MCP-1/CCR2 pathway plays a central role in the pathogenesis of neointimal hyperplasia in cuffed femoral artery of mice and monkeys. Therefore, the MCP-1/CCR2 pathway can be a therapeutic target for human restenosis after coronary intervention.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCR2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ccr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
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| pubmed:issn |
1524-4571
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| pubmed:author |
pubmed-author:CharoIsrael FIF,
pubmed-author:EgashiraKensukeK,
pubmed-author:IchikiToshihiroT,
pubmed-author:InoueShujiroS,
pubmed-author:KataokaChuC,
pubmed-author:KatohMakotoM,
pubmed-author:NishidaKen-IchiK,
pubmed-author:OhtaniKishouK,
pubmed-author:TakeshitaAkiraA,
pubmed-author:UsuiMakotoM,
pubmed-author:ZhaoQingweiQ
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| pubmed:issnType |
Electronic
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| pubmed:day |
14
|
| pubmed:volume |
90
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1167-72
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12065319-Animals,
pubmed-meshheading:12065319-Chemokine CCL2,
pubmed-meshheading:12065319-Femoral Artery,
pubmed-meshheading:12065319-Gene Expression,
pubmed-meshheading:12065319-Genotype,
pubmed-meshheading:12065319-Humans,
pubmed-meshheading:12065319-Hyperplasia,
pubmed-meshheading:12065319-Immunohistochemistry,
pubmed-meshheading:12065319-Macaca fascicularis,
pubmed-meshheading:12065319-Male,
pubmed-meshheading:12065319-Mice,
pubmed-meshheading:12065319-Mice, Inbred C57BL,
pubmed-meshheading:12065319-Mice, Knockout,
pubmed-meshheading:12065319-Plasmids,
pubmed-meshheading:12065319-RNA, Messenger,
pubmed-meshheading:12065319-Receptors, CCR2,
pubmed-meshheading:12065319-Receptors, Chemokine,
pubmed-meshheading:12065319-Signal Transduction,
pubmed-meshheading:12065319-Time Factors,
pubmed-meshheading:12065319-Transfection,
pubmed-meshheading:12065319-Tunica Intima
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| pubmed:year |
2002
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| pubmed:articleTitle |
Importance of monocyte chemoattractant protein-1 pathway in neointimal hyperplasia after periarterial injury in mice and monkeys.
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| pubmed:affiliation |
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. egashira@cardiol.med.kyushu-u.ac.jp
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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