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Midkine as a molecular target: comparison of effects of chondroitin sulfate E and siRNA.

Yamamoto H, Muramatsu H, Nakanishi T, Natori Y, Sakuma S, Ishiguro N, Muramatsu T

Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Intraperitoneally administered chondroitin sulfate E inhibited the development of antibody-induced arthritis, a model of rheumatoid arthritis, while chondroitin 4-sulfate showed no effects. Chondroitin sulfate E inhibited in vitro differentiation of osteoclasts, which play key roles in the etiology of rheumatoid arthritis. One of the targets of chondroitin sulfate E is midkine, a heparin-binding growth factor or cytokine. Indeed, a chimeric-type siRNA for midkine inhibited the development of antibody-induced arthritis and adhesion of the omentum to the injured abdominal wall. These results indicate the significance of midkine as a molecular target to treat or prevent rheumatoid arthritis and adhesion after surgery, and the utility of chondroitin sulfate E to inhibit midkine in vivo.

Published 19 November 2006 in Biochem Biophys Res Commun, 351(4): 915-9.
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