Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:10024304rdf:typepubmed:Citationlld:pubmed
pubmed-article:10024304lifeskim:mentionsumls-concept:C0034721lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0034693lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0007272lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0128897lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0003241lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0008013lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C0020507lld:lifeskim
pubmed-article:10024304lifeskim:mentionsumls-concept:C1337092lld:lifeskim
pubmed-article:10024304pubmed:issue3lld:pubmed
pubmed-article:10024304pubmed:dateCreated1999-3-12lld:pubmed
pubmed-article:10024304pubmed:abstractTextMonocyte chemoattractant protein-1 (MCP-1)/monocyte chemotactic and activating factor (MCAF) has been suggested to promote atherogenesis. The effects of in vivo neutralization of MCP-1 in a rat model were examined in an effort to clarify the role of MCP-1 in the development of neointimal hyperplasia. Competitive polymerase chain reaction analysis revealed maximum MCP-1 mRNA expression at 4 hours after carotid arterial injury. Increased immunoreactivities of MCP-1 were also detected at 2 and 8 hours after injury. Either anti-MCP-1 antibody or nonimmunized goat IgG (10 mg/kg) was then administered every 12 hours to rats that had undergone carotid arterial injury. Treatment with 3 consecutive doses of anti-MCP-1 antibody within 24 hours (experiment 1) and every 12 hours for 5 days (experiment 2) significantly inhibited neointimal hyperplasia at day 14, resulting in a 27.8% reduction of the mean intima/media ratio (P<0.05) in experiment 1 and a 43.6% reduction (P<0.01) in experiment 2. This effect was still apparent at day 56 (55.6% inhibition; P<0.05). The number of vascular smooth muscle cells in the neointima at day 4 was significantly reduced by anti-MCP-1 treatment, demonstrating the important role of MCP-1 in early neointimal lesion formation. However, recombinant MCP-1 did not stimulate chemotaxis of vascular smooth muscle cells in an in vitro migration assay. These results suggest that MCP-1 promotes neointimal hyperplasia in early neointimal lesion formation and that neutralization of MCP-1 before, and immediately after, arterial injury may be effective in preventing restenosis after angioplasty. Further studies are needed to clarify the mechanism underlying the promotion of neointimal hyperplasia by MCP-1.lld:pubmed
pubmed-article:10024304pubmed:languageenglld:pubmed
pubmed-article:10024304pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10024304pubmed:citationSubsetIMlld:pubmed
pubmed-article:10024304pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10024304pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10024304pubmed:statusMEDLINElld:pubmed
pubmed-article:10024304pubmed:monthFeblld:pubmed
pubmed-article:10024304pubmed:issn0009-7330lld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:OnoKKlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:FurukawaYYlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:HaradaAAlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:MatsushimaKKlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:SasayamaSSlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:MatsumoriAAlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:OhashiNNlld:pubmed
pubmed-article:10024304pubmed:authorpubmed-author:ShioiTTlld:pubmed
pubmed-article:10024304pubmed:issnTypePrintlld:pubmed
pubmed-article:10024304pubmed:day19lld:pubmed
pubmed-article:10024304pubmed:volume84lld:pubmed
pubmed-article:10024304pubmed:ownerNLMlld:pubmed
pubmed-article:10024304pubmed:authorsCompleteYlld:pubmed
pubmed-article:10024304pubmed:pagination306-14lld:pubmed
pubmed-article:10024304pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:meshHeadingpubmed-meshheading:10024304...lld:pubmed
pubmed-article:10024304pubmed:year1999lld:pubmed
pubmed-article:10024304pubmed:articleTitleAnti-monocyte chemoattractant protein-1/monocyte chemotactic and activating factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries.lld:pubmed
pubmed-article:10024304pubmed:affiliationDepartment of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.lld:pubmed
pubmed-article:10024304pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10024304pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:10024304lld:pubmed