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Please add updates@feedmyinbox.com to your address book to make sure you receive these messages in the future. RegenMD Transforming growth factor beta1 and laminin-111 cooperate in the induction of interleukin-16 expression in synovial fibroblasts from patients with rheumatoid arthritis. February 2, 2010 at 3:11 PM Related Articles Transforming growth factor beta1 and laminin-111 cooperate in the induction of interleukin-16 expression in synovial fibroblasts from patients with rheumatoid arthritis. Ann Rheum Dis. 2010 Jan;69(1):270-5 Authors: Warstat K, Hoberg M, Rudert M, Tsui S, Pap T, Angres B, Essl M, Smith TJ, Cruikshank WW, Klein G, Gay S, Aicher WK OBJECTIVES: In synovial tissues of patients with rh! eumatoid arthritis (RA), strong expression of laminins and integrins co-localises with increased expression of inflammatory cytokines. Synovial fibroblasts (SF) contribute to the pathogenesis of RA through increased expression of cytokines and chemoattractant factors, one of which is interleukin-16 (IL16). A study was undertaken to investigate the regulatory pathways of IL16 in SF from patients with RA (RA-SF) and osteoarthritis (OA-SF). METHODS: SF were seeded in laminin-coated flasks and activated by the addition of cytokines. The expression of IL16 was investigated by quantitative RT-PCR, immunoblotting and ELISA; its biological activity was determined by a cell migration assay. Cell-matrix interactions were investigated by cell binding and attachment assays. Relevant intracellular signalling pathways were studied by immunoblotting and with pharmacological blocking reagents. RESULTS: Stimulation of SF with transforming growth factor beta(1)(TGF-beta(1)) and growth on lam! inin-111 (LM-111) significantly increased the expression of IL! 16. Bind ing to LM-111 induced significantly more IL16 mRNA in RA-SF than in OA-SF (p<0.05). The IL16 cytokine was detected in supernatants of TGF-beta(1)-activated and in LM-111+TGF-beta(1)-activated RA-SF (38 to 62 pg/ml), but not in supernatants of OA-SF. This IL16 regulation involved p38MAPK, ERK1/2 and SMAD2 signalling, but not NFkappaB. CONCLUSIONS: Binding of RA-SF to LM-111 in the presence of TGF-beta(1) triggers a significant IL16 response and thus may contribute to the infiltration of CD4+ lymphocytes into synovial tissues. This mode of IL16 induction represents a novel pathway leading to IL16 production in RA-SF but not in OA-SF, which operates independently of NFkappaB signalling. PMID: 19279017 [PubMed - indexed for MEDLINE]   The Latest on Changes in CIRM's Biotech Loan Program February 2, 2010 at 11:43 AM   Advisory February 2, 2010 at 10:43 AM   Fecundity, Stem Cells and the Dark Side of Prop. 71 February 1, 2010 at 11:30 PM   This email was sent to regenmd@gmail.com.  Manage Your Account Don't want to receive this feed any longer? Unsubscribe here.