pubmed-article:10024304 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0007272 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0128897 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0008013 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C0020507 | lld:lifeskim |
pubmed-article:10024304 | lifeskim:mentions | umls-concept:C1337092 | lld:lifeskim |
pubmed-article:10024304 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:10024304 | pubmed:dateCreated | 1999-3-12 | lld:pubmed |
pubmed-article:10024304 | pubmed:abstractText | Monocyte 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:10024304 | pubmed:language | eng | lld:pubmed |
pubmed-article:10024304 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10024304 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10024304 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10024304 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10024304 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10024304 | pubmed:month | Feb | lld:pubmed |
pubmed-article:10024304 | pubmed:issn | 0009-7330 | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:OnoKK | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:FurukawaYY | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:HaradaAA | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:MatsushimaKK | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:SasayamaSS | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:MatsumoriAA | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:OhashiNN | lld:pubmed |
pubmed-article:10024304 | pubmed:author | pubmed-author:ShioiTT | lld:pubmed |
pubmed-article:10024304 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10024304 | pubmed:day | 19 | lld:pubmed |
pubmed-article:10024304 | pubmed:volume | 84 | lld:pubmed |
pubmed-article:10024304 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10024304 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10024304 | pubmed:pagination | 306-14 | lld:pubmed |
pubmed-article:10024304 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:10024304 | pubmed:meshHeading | pubmed-meshheading:10024304... | lld:pubmed |
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pubmed-article:10024304 | pubmed:meshHeading | pubmed-meshheading:10024304... | lld:pubmed |
pubmed-article:10024304 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10024304 | pubmed:articleTitle | Anti-monocyte chemoattractant protein-1/monocyte chemotactic and activating factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries. | lld:pubmed |
pubmed-article:10024304 | pubmed:affiliation | Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. | lld:pubmed |
pubmed-article:10024304 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10024304 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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