IL23 in rheumatoid arthritis synovial fibroblasts the role of RANKL expression.docVIP

 PAGE \* MERGEFORMAT 11 IL23 in rheumatoid arthritis synovial fibroblasts the role of RANKL expression Abstract Objective To investigate the IL 23 in rheumatoid arthritis (RA) synovial fibroblast nuclear factor B (NF B) ligand receptor activator (RANKL) expression in the role; and analysis of RANKL expression induced by IL 23 signaling pathways. Isolated RA and osteoarthritis (OA) synovial fibroblasts were added to different concentrations of IL 23 (1,5 and 10 ng / ml), 72 h, the real-time fluorescence quantitative PCR (FQ PCR) RANKL mRNA expression was detected. In order to study the expression of RANKL signaling pathways in fibroblasts were added PD98059, Ly294002, AG490, and Pathenolide incubated 1 h, then stimulated by adding IL 23 72 h, FQ PCR detected the expression of RANKL mRNA levels of RA patients. Results IL 23 to RA synovial fibroblasts upregulated RANKL expression; In contrast, IL 23 OA patients with almost no fibroblasts induced RANKL expression. Adding PD98059, Pathenolide and after AG490, IL 23 induced RA synovial fibroblasts significantly inhibited the expression of RANKL. Conclusion IL 23 possibly through MEK1 / 2, NF B and STAT3 signaling pathways induced by RA synovial fibroblasts express RANKL. Keywords: Rheumatoid arthritis; RANKL; IL 23; fibroblasts; signal transduction Rheumatoid arthritis (RA) is a characterized by chronic synovitis systemic autoimmune diseases. Persistent recurrent synovitis can lead to destruction of articular cartilage and bone, and ultimately lead to joint dysfunction or disability. Although damage to the cartilage and bone destruction in RA pathogenesis is not fully understood, but a large number of relevant tests showed that the osteoclasts in bone destruction in the pathogenesis of RA play a key role in 1; and nuclear factor B (NF B) receptor activator ligand (RANKL) is the osteoclast formation and differentiation of the necessary factors 2. RANKL expression is regulated by many cyt