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• W2117370942 abstract "Objective. The hyaluronan-binding protein TSG-6 (tumor necrosis factor-stimulated gene 6) forms a stable complex with the serine protease inhibitor, inter-α-inhibitor, potentiates the inhibition of plasmin activity, and has antiinflammatory effects in vivo. This study examines the expression of TSG-6 in human articular chondrocytes and cartilage. Methods. Human articular chondrocytes and cartilage explants were stimulated with cytokines, growth factors, and other agents. TSG-6 expression was analyzed by imaging-assisted Northern and Western blotting. Results. TSG-6 messenger RNA (mRNA) expression was upregulated by cytokines and growth factors, predominantly interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), platelet-derived growth factor AA (PDGF-AA), and transforming growth factor β1 (TGFβ1). TSG-6 mRNA induction by TGFβ1 was delayed as compared with IL-1β. Treatment of the cells with the glucocorticoid dexamethasone neither induced TSG-6 mRNA nor did it affect IL-1β-induced transcript levels. TSG-6 mRNA induction may involve several signal transduction pathways. The strong transcriptional stimulation by phorbol myristate acetate suggests protein kinase C (PKC)-mediated signaling. In contrast, PKA- and Cadependent signals are only marginally involved as messengers leading to increased TSG-6 levels after IL-1β and TNFα treatment. In chondrocyte and cartilage organ cultures, both free TSG-6 (35 kd) and the complex with inter-α-inhibitor (120 kd) were present and upregulated by IL-1β, TNFα, or TGFβ1. Conclusion. Chondrocytes are a source of TSG-6 which may play a role in cartilage remodeling and joint inflammation." @default.
• W2117370942 created "2016-06-24" @default.
• W2117370942 creator A5004616732 @default.
• W2117370942 creator A5072444665 @default.
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• W2117370942 date "1996-04-01" @default.
• W2117370942 modified "2023-10-01" @default.
• W2117370942 title "TSG-6 expression in human articular chondrocytes: Possible implications in joint inflammation and cartilage degradation" @default.
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• W2117370942 doi "https://doi.org/10.1002/art.1780390403" @default.
• W2117370942 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8630102" @default.
• W2117370942 hasPublicationYear "1996" @default.
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