pubmed-article:16846535 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0909868 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0234402 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:16846535 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:16846535 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:16846535 | pubmed:dateCreated | 2007-1-16 | lld:pubmed |
pubmed-article:16846535 | pubmed:abstractText | Stromal cells such as fibroblasts play an important role in defining tissue-specific responses during the resolution of inflammation. We hypothesized that this involves tissue-specific regulation of glucocorticoids, mediated via differential regulation of the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). Expression, activity and function of 11beta-HSD1 was assessed in matched fibroblasts derived from various tissues (synovium, bone marrow and skin) obtained from patients with rheumatoid arthritis or osteoarthritis. 11beta-HSD1 was expressed in fibroblasts from all tissues but mRNA levels and enzyme activity were higher in synovial fibroblasts (2-fold and 13-fold higher mRNA levels in dermal and synovial fibroblasts, respectively, relative to bone marrow). Expression and activity of the enzyme increased in all fibroblasts following treatment with tumour necrosis factor-alpha or IL-1beta (bone marrow: 8-fold and 37-fold, respectively, compared to vehicle; dermal fibroblasts: 4-fold and 14-fold; synovial fibroblasts: 7-fold and 31-fold; all P < 0.01 compared with vehicle). Treatment with IL-4 or interferon-gamma was without effect, and there was no difference in 11beta-HSD1 expression between fibroblasts (from any site) obtained from patients with rheumatoid arthritis or osteoarthritis. In the presence of 100 nmol/l cortisone, IL-6 production--a characteristic feature of synovial derived fibroblasts--was significantly reduced in synovial but not dermal or bone marrow fibroblasts. This was prevented by co-treatment with an 11beta-HSD inhibitor, emphasizing the potential for autocrine activation of glucocorticoids in synovial fibroblasts. These data indicate that differences in fibroblast-derived glucocorticoid production (via the enzyme 11beta-HSD1) between cells from distinct anatomical locations may play a key role in the predeliction of certain tissues to develop persistent inflammation. | lld:pubmed |
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pubmed-article:16846535 | pubmed:language | eng | lld:pubmed |
pubmed-article:16846535 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16846535 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16846535 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16846535 | pubmed:issn | 1478-6362 | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:RabbittElizab... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:CooperMark... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:StewartPaul... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:HewisonMartin... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:BuckleyChrist... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:ParsonageGreg... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:FilerAndrewA | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:HardieDebbie... | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:RazaKarimK | lld:pubmed |
pubmed-article:16846535 | pubmed:author | pubmed-author:HardyRowan... | lld:pubmed |
pubmed-article:16846535 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:16846535 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:16846535 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16846535 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16846535 | pubmed:pagination | R108 | lld:pubmed |
pubmed-article:16846535 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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