| pubmed-article:8003632 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0012472 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0069535 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:8003632 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:8003632 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8003632 | pubmed:dateCreated | 1994-7-15 | lld:pubmed |
| pubmed-article:8003632 | pubmed:abstractText | The role of Oncostatin M (OM), a monocyte/macrophage and T-cell product, in regulating IL-6 expression in fibroblasts of lung or synovial origin was examined in vitro. Although by itself OM had a minimal effect on enhancing IL-6 production by fibroblasts, in combination with IL-1 alpha or PGE2, OM addition resulted in a dose-dependent synergistic enhancement of IL-6 production. This synergistic effect with either IL-1 alpha (5 ng/ml) or PGE2 (10(-7) M) was clearly evident at concentrations of OM of 10, 20 or 50 ng/ml. Levels of IL-6 resulting from OM and IL-1 alpha stimulation could be reduced by indomethacin (10(-6) M) and restored again by also adding PGE2. Northern blots probed for IL-6 mRNA showed cooperative enhancement of steady state levels at 18 hours of stimulation by OM and IL-1 alpha, or OM and PGE2. Probing for mRNA of the metalloproteinase inhibitor TIMP-1 showed that stimulation by OM, IL-1 alpha or PGE2 enhanced TIMP-1 levels. However, OM (alone) or PGE2 or both combined did not elevate the metalloproteinase stromelysin-1 mRNA signals. Analysis utilizing a rat IL-6 promoter-luciferase reporter gene construct showed that OM stimulation resulted in activation of transcription that synergistically enhanced IL-1-induced levels of reporter gene expression. These results show that although OM has minor effects on IL-6 production alone, the combination of OM and other mediators result in markedly enhanced IL-6 production by fibroblasts in vitro. | lld:pubmed |
| pubmed-article:8003632 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8003632 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8003632 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8003632 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8003632 | pubmed:issn | 1043-4666 | lld:pubmed |
| pubmed-article:8003632 | pubmed:author | pubmed-author:RichardsC DCD | lld:pubmed |
| pubmed-article:8003632 | pubmed:author | pubmed-author:AgroAA | lld:pubmed |
| pubmed-article:8003632 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8003632 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:8003632 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8003632 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8003632 | pubmed:pagination | 40-7 | lld:pubmed |
| pubmed-article:8003632 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8003632 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8003632 | pubmed:articleTitle | Interaction between oncostatin M, interleukin 1 and prostaglandin E2 in induction of IL-6 expression in human fibroblasts. | lld:pubmed |
| pubmed-article:8003632 | pubmed:affiliation | Department of Pathology, McMaster University, Hamilton, Ontario, Canada. | lld:pubmed |
| pubmed-article:8003632 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8003632 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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