Rheumatoid arthritis is a chronic inflammatory disease characterized by joint destruction. It has been suggested that the extracellular matrix protein osteopontin (OPN), which is expressed by a number of different mediators of the immune response, may facilitate this destruction.
In the July 15 issue of The Journal of Clinical Investigation, Nobuchika Yamamoto and colleagues from the Fujisawa Pharmaceutical Company in Japan, provide important new evidence indicating a role for OPN in the pathogenesis of inflammatory arthritis and associated joint destruction.
OPN is abundant in bone, where it facilitates cell adhesion and modulation of the immune response. This adhesion is facilitated by interaction with a variety of cell surface molecules known as integrins. Binding of OPN to these cell surface molecules generally occurs at a specific integrin-binding motif. A second sequence, (SLAYGLR in mice and SVVYGLR in humans) within OPN has also been shown to mediate this cell adhesion. The site is the result of cleavage of human OPN by the protease thrombin and promotes the adherence of cells expressing intergrins a4 and a9.
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