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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
18
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pubmed:dateCreated |
2000-11-6
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pubmed:abstractText |
Chronic inhibition of endothelial nitric oxide (NO) synthesis by the administration of N:(omega)-nitro-L-arginine methyl ester (L-NAME) to rats induces early vascular inflammatory changes (monocyte infiltration into coronary vessels and monocyte chemoattractant protein-1 [MCP-1] expression) as well as subsequent arteriosclerosis (medial thickening and perivascular fibrosis) and cardiac fibrosis. However, the role of MCP-1 in this process is not known.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidyl-Dipeptidase A,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tgfb1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1524-4539
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
31
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pubmed:volume |
102
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2243-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11056100-Animals,
pubmed-meshheading:11056100-Antibodies, Monoclonal,
pubmed-meshheading:11056100-Blood Pressure,
pubmed-meshheading:11056100-Cell Division,
pubmed-meshheading:11056100-Chemokine CCL2,
pubmed-meshheading:11056100-Chronic Disease,
pubmed-meshheading:11056100-Collagen,
pubmed-meshheading:11056100-Coronary Artery Disease,
pubmed-meshheading:11056100-Dermis,
pubmed-meshheading:11056100-Disease Models, Animal,
pubmed-meshheading:11056100-Dose-Response Relationship, Drug,
pubmed-meshheading:11056100-Fibrosis,
pubmed-meshheading:11056100-Inflammation,
pubmed-meshheading:11056100-Male,
pubmed-meshheading:11056100-Monocytes,
pubmed-meshheading:11056100-Myocardium,
pubmed-meshheading:11056100-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:11056100-Nitric Oxide Synthase,
pubmed-meshheading:11056100-Peptidyl-Dipeptidase A,
pubmed-meshheading:11056100-RNA, Messenger,
pubmed-meshheading:11056100-Rats,
pubmed-meshheading:11056100-Rats, Inbred WKY,
pubmed-meshheading:11056100-Recombinant Proteins,
pubmed-meshheading:11056100-Transforming Growth Factor beta,
pubmed-meshheading:11056100-Transforming Growth Factor beta1,
pubmed-meshheading:11056100-Ventricular Remodeling
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pubmed:year |
2000
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pubmed:articleTitle |
Role of monocyte chemoattractant protein-1 in cardiovascular remodeling induced by chronic blockade of nitric oxide synthesis.
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pubmed:affiliation |
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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