pubmed-article:17302909 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17302909 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
pubmed-article:17302909 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:17302909 | lifeskim:mentions | umls-concept:C1550315 | lld:lifeskim |
pubmed-article:17302909 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:17302909 | lifeskim:mentions | umls-concept:C2611870 | lld:lifeskim |
pubmed-article:17302909 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:17302909 | pubmed:dateCreated | 2007-2-16 | lld:pubmed |
pubmed-article:17302909 | pubmed:abstractText | Interleukin (IL)-4 has been demonstrated to have anti-inflammatory and anti-tumour activity. Because aberrant angiogenesis is a significant pathogenic component of tumour growth and chronic inflammation, we investigated the effect of IL-4 on the production of vascular endothelial growth factor (VEGF) by synovial fibroblasts derived from patients with rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLS) were prepared from synovial tissues of RA and incubated with different concentrations of IL-4 in the presence or absence of transforming growth factor (TGF)-beta. VEGF level was measured by enzyme-linked immunosorbent assay and semiquantitative reverse transcription--polymerase chain reaction. Treatment of FLS with IL-4 alone caused a dose-dependent increase in VEGF levels. In contrast, IL-4 exhibited the inhibitory effect on VEGF production when FLS were stimulated with TGF-beta. Combined treatment of IL-4 and IL-10 inhibited TGF-beta-induced VEGF production in an additive fashion. TGF-beta increased the induction of cyclooxygenase-2 mRNA, which was inhibited significantly by the treatment of IL-4. NS-398, a COX-2 inhibitor, inhibited TGF-beta-induced VEGF production in a dose-dependent manner. Furthermore, exogenous addition of prostaglandin E2 (PGE2) restored IL-4 inhibition on TGF-beta induced VEGF production. Collectively, our results suggest that IL-4 have an anti-angiogenic effect, especially in the inflammatory milieu of RA by inhibiting the VEGF production in synovial fibroblasts. | lld:pubmed |
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pubmed-article:17302909 | pubmed:language | eng | lld:pubmed |
pubmed-article:17302909 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17302909 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17302909 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17302909 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17302909 | pubmed:month | Mar | lld:pubmed |
pubmed-article:17302909 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:CoxJ WJW | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:KoGG | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:DarM FMF | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:SiskE AEA | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:ShihY-LYL | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:HongK-HKH | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:ChoiJ-JJJ | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:PEIY QYQ | lld:pubmed |
pubmed-article:17302909 | pubmed:author | pubmed-author:KimW-UWU | lld:pubmed |
pubmed-article:17302909 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17302909 | pubmed:volume | 147 | lld:pubmed |
pubmed-article:17302909 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17302909 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17302909 | pubmed:pagination | 573-9 | lld:pubmed |
pubmed-article:17302909 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17302909 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17302909 | pubmed:articleTitle | Effect of interleukin-4 on vascular endothelial growth factor production in rheumatoid synovial fibroblasts. | lld:pubmed |
pubmed-article:17302909 | pubmed:affiliation | Department of Medicine, Division of Rheumatology, St Mary's Hospital, Research Institute of Immunobiology, Catholic University of Korea, Seoul, Korea. | lld:pubmed |