pubmed-article:8132765 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0221464 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0439851 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0600210 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C1552596 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C1947931 | lld:lifeskim |
pubmed-article:8132765 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
pubmed-article:8132765 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:8132765 | pubmed:dateCreated | 1994-4-21 | lld:pubmed |
pubmed-article:8132765 | pubmed:abstractText | Directed migration or chemotaxis of arterial smooth muscle cells (SMC) contributes to intimal SMC accumulation, a key event in the development of atherosclerotic lesions and in restenosis after angioplasty. The present study compares and contrasts insulin-like growth factor I (IGF-I) and platelet-derived growth factor (PDGF-BB) as chemoattractants and mitogens for human arterial SMC. Compared with PDGF-BB, IGF-I is a weaker SMC mitogen. Thus, PDGF-BB, but not IGF-I, evokes a strong and rapid activation of mitogen-activated protein (MAP) kinase kinase and MAP kinase. However, IGF-I is a potent stimulator of directed migration of human arterial SMC, as measured in a Boyden chamber assay. The half-maximal concentration for migration is similar to the Kd for IGF-I receptor interaction. An IGF-I receptor-blocking antibody blocks the effects of IGF-I, IGF-II, and insulin, indicating that the effects are indeed mediated through the IGF-I receptor. The maximal effect of IGF-I on directed migration ranges between 50% and 100% of the effect of PDGF-BB, the strongest known chemoattractant for SMC. The ability of IGF-I and PDGF-BB to induce chemotaxis coincides with their ability to stimulate phosphatidylinositol turnover, diacylglycerol formation, and intracellular Ca2+ flux and suggests that these signaling pathways, but not activation of the MAP kinase cascade, are required for chemotaxis of human arterial SMC. | lld:pubmed |
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pubmed-article:8132765 | pubmed:language | eng | lld:pubmed |
pubmed-article:8132765 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8132765 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:8132765 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8132765 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8132765 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8132765 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8132765 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8132765 | pubmed:month | Mar | lld:pubmed |
pubmed-article:8132765 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:KrebsE GEG | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:RossRR | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:NakanoTT | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:GravesL MLM | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:RainesE WEW | lld:pubmed |
pubmed-article:8132765 | pubmed:author | pubmed-author:BornfeldtK... | lld:pubmed |
pubmed-article:8132765 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8132765 | pubmed:volume | 93 | lld:pubmed |
pubmed-article:8132765 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8132765 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8132765 | pubmed:pagination | 1266-74 | lld:pubmed |
pubmed-article:8132765 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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