関節リウマチとオステオポンチン

抄録

We review here regarding the observations that expression of osteopontin (OPN) was enhanced in the joints of rheumatoid arthritis patients. OPN in arthritic joints had not been clear previously. We published in 2002 that joint destruction in the arthritis model induced by a mixture of anti-type II collagen monoclonal antibodies and LPS (mAbs/LPS) injection was suppressed in the OPN-deficient mice. OPN is a phosphorylated glycoprotein interacts with integrins and CD44, promote the cell attachment and migration. OPN is highly expressed in bone, kidney and ovary and also produced by osteoclasts, endotherial cells, activated T cells and macrophages. One of the functions of OPN in the inflammatory condition is to bring inflammatory cells to the sites of injury and OPN is also a survival factor for the endotherial cells and enhances angiogenesis by promoting the vascular tube formation. Infiltration of inflammatory cells and angiogenesis in synovium in the arthritis model was suppressed in OPN-deficient mice. Additionally, apoptosis of chondrocytes in articular cartilage was reduced and destruction of articular cartilage was suppressed in the arthritis model in OPN-deficient mice. These data suggested that OPN might be a new target for the treatment of rheumatoid arthritis.