| pubmed-article:9199336 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C0302600 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C0079633 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C0380603 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C1171892 | lld:lifeskim |
| pubmed-article:9199336 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:9199336 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:9199336 | pubmed:dateCreated | 1997-7-24 | lld:pubmed |
| pubmed-article:9199336 | pubmed:abstractText | Tumor necrosis factor alpha (TNF-alpha) is a macrophage/monocyte-derived polypeptide which modulates the expression of various genes in vascular endothelial cells and induces angiogenesis. However, the underlying mechanism by which TNF-alpha mediates angiogenesis is not completely understood. In this study, we assessed whether TNF-alpha-induced angiogenesis is mediated through TNF-alpha itself or indirectly through other TNF-alpha-induced angiogenesis-promoting factors. Cellular mRNA levels of interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors were increased after the treatment of human microvascular endothelial cells with TNF-alpha (100 U/ml). TNF-alpha-dependent tubular morphogenesis in vascular endothelial cells was inhibited by the administration of anti-IL-8, anti-VEGF, and anti-bFGF antibodies, and coadministration of all three antibodies almost completely abrogated tubular formation. Moreover, treatment with Sp1, NF-kappaB, and c-Jun antisense oligonucleotides inhibited TNF-alpha-dependent tubular morphogenesis by microvascular endothelial cells. Administration of a NF-kappaB antisense oligonucleotide almost completely inhibited TNF-alpha-dependent IL-8 production and partially abrogated TNF-alpha-dependent VEGF production, and an Sp1 antisense sequence partially inhibited TNF-alpha-dependent production of VEGF. A c-Jun antisense oligonucleotide significantly inhibited TNF-alpha-dependent bFGF production but did not affect the production of IL-8 and VEGF. Administration of an anti-IL-8 or anti-VEGF antibody also blocked TNF-alpha-induced neovascularization in the rabbit cornea in vivo. Thus, angiogenesis by TNF-alpha appears to be modulated through various angiogenic factors, both in vitro and in vivo, and this pathway is controlled through paracrine and/or autocrine mechanisms. | lld:pubmed |
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| pubmed-article:9199336 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9199336 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9199336 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9199336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9199336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9199336 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9199336 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9199336 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:9199336 | pubmed:author | pubmed-author:OnoMM | lld:pubmed |
| pubmed-article:9199336 | pubmed:author | pubmed-author:SuzukiHH | lld:pubmed |
| pubmed-article:9199336 | pubmed:author | pubmed-author:IshibashiTT | lld:pubmed |
