Abstract
BackgroundRheumatoid arthritis (RA) is a chronic and refractory autoimmune joint disease. Fibroblast-like synoviocytes (FLS) produce inflammatory cytokines and are involved in the migration and invasion of panuus tissue, which leads to the destruction of joints in RA. Receptor for hyaluronan mediated motility (RHAMM), is known to be one of the important receptors for hyaluronic acid. It has the ability to regulate migration of fibrocytes and infiltration of inflammatory cells. Here,we explored the mechanisms of RHAMM in RAFs.MethodsQuantitative PCR and western blot were performed to test the expression of RHAMM in synoviocytes of RA patients and osteoarthritis (OA) controls. Collagen antibody-induced arthritis (CAIA) was used to investigate the RHAMM expression in mouse synovial issues. RHAMM siRNA was used to detect the function of RHAMM in FLS.ResultsRA-FLS has a significantly higher expression of RHAMM than OA-FLS. Expression of RHAMM in joint synovial tissue was markedly increased in the CAIA mice compared with the controls. RHAMM silencing using SiRNA was not only decreased the production of IL-6 and IL-8, but also inhibited the migration and invasion of RA-FLS.ConclusionsRHAMM has an important role in the FLS induced modulation of inflammation and destruction of joints in RA.
Highlights
Rheumatoid arthritis (RA) is a chronic and refractory autoimmune joint disease
Destruction of the cartilage and bone, synovial hyperplasia, visible articular cartilage surface roughness, local infiltration of inflammatory cells, synovial hyperplasia were observed in the Collagen antibody-induced arthritis (CAIA) mice (Fig. 3 A: c and d)
Immunohistochemical analysis of the ankles exhibited increased expression of Receptor for hyaluronan mediated motility (RHAMM) in the CAIA mice compared with the control mice, especially in the cartilage, bone and synovial membrane (Fig. 3 A: e, f and g, h).Expression of RHAMM was different in joints tissues, in synovial tissues both in CAIA induced and control mice
Summary
Rheumatoid arthritis (RA) is a chronic and refractory autoimmune joint disease. Fibroblast-like synoviocytes (FLS) produce inflammatory cytokines and are involved in the migration and invasion of panuus tissue, which leads to the destruction of joints in RA. Here,we explored the mechanisms of RHAMM in RAFs. Rheumatoid arthritis (RA) is an immune-mediated disorder induced by chronic and refractory autoimmunity in the synovial joints, which leads to the damage of the cartilage and bone. RA affects approximately 1% of the population globally, its complex pathogenesis is not fully understood.[1, 2] The fibroblast-like synoviocytes (FLS) play a critical role in the progression of RA. These cells normally line the synovium, but in RA they proliferate in an uncontrolled manner and form the pannus tissue, a tumor-like structure that causes significant damage to the joints [3, 4].
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