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| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C0038836 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1419227 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:12606638 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:12606638 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12606638 | pubmed:dateCreated | 2003-4-21 | lld:pubmed |
| pubmed-article:12606638 | pubmed:abstractText | Oxidative signals play an important role in the regulation of endothelial cell adhesion molecule expression. Small GTP-binding protein Rac1 is activated by various proinflammatory substances and regulates superoxide generation in endothelial cells. In the present study, we demonstrate that adenoviral-mediated expression of dominant negative N17Rac1 (Ad.N17Rac1) suppresses tumor necrosis factor-alpha (TNF-alpha)-induced vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin gene expression in a dose-dependent manner. Ad.N17Rac1 did not inhibit TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB) binding activity or inhibitor of NF-kappaB-alpha degradation. In contrast, Ad.N17Rac1 inhibited TNF-alpha-induced NF-kappaB-driven HIV(kappaB)(4)-CAT and p288VCAM-Luc promoter activity, suggesting that N17Rac1 inhibits TNF-alpha-induced VCAM-1, E-selectin, and ICAM-1 through suppressing NF-kappaB-mediated transactivation. In addition, expression of superoxide dismutase by adenovirus suppressed TNF-alpha-induced VCAM-1, E-selectin, and ICAM-1 mRNA accumulation. However, adenoviral-mediated expression of catalase only partially inhibited TNF-alpha-induced E-selectin gene expression and had no effect on VCAM-1 and ICAM-1 gene expression. These data suggest that Rac1 and superoxide play crucial roles in the regulation of expression of cell adhesion molecules in endothelial cells. | lld:pubmed |
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| pubmed-article:12606638 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12606638 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12606638 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12606638 | pubmed:month | May | lld:pubmed |
| pubmed-article:12606638 | pubmed:issn | 0022-3565 | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:ZhangQiangQ | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:DingXiaoyuX | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:ChenXi-LinXL | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:MedfordRussel... | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:ZhaoRuozhiR | lld:pubmed |
| pubmed-article:12606638 | pubmed:author | pubmed-author:TummalaPradyu... | lld:pubmed |
| pubmed-article:12606638 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12606638 | pubmed:volume | 305 | lld:pubmed |
| pubmed-article:12606638 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12606638 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12606638 | pubmed:pagination | 573-80 | lld:pubmed |
| pubmed-article:12606638 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:12606638 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12606638 | pubmed:articleTitle | Rac1 and superoxide are required for the expression of cell adhesion molecules induced by tumor necrosis factor-alpha in endothelial cells. | lld:pubmed |
| pubmed-article:12606638 | pubmed:affiliation | Discovery Research, AtheroGenics, Inc., 8995 Westside Parkway, Alpharetta, GA 30004, USA. xchen@atherogenics.com | lld:pubmed |
| pubmed-article:12606638 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12606638 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12606638 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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