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Rheumatology Advance Access originally published online on June 22, 2004
Rheumatology 2004 43(9):1116-1120; doi:10.1093/rheumatology/keh274
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Rheumatology Vol. 43 No. 9 © British Society for Rheumatology 2004; all rights reserved

Paper

COOH-terminal heparin-binding fibronectin fragment induces nitric oxide production in rheumatoid cartilage through CD44

T. Yasuda1,2, T. Kakinuma1, S. M. Julovi1, M. Yoshida1, T. Hiramitsu1, M. Akiyoshi1 and T. Nakamura1

1 Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507 and 2 Department of Sports Medicine, Faculty of Health, Budo, and Sports Studies, Tenri University, 80 Tainosho-cho, Tenri, Nara 632-0071, Japan.

Correspondence to: T. Yasuda, Department of Sports Medicine, Faculty of Health, Budo, and Sports Studies, Tenri University, 80 Tainosho-cho, Tenri, Nara 632-0071, Japan. E-mail: tyasuda-jsb{at}umin.ac.jp

Objectives. To examine the mechanism of nitric oxide (NO) production by a COOH-terminal heparin-binding fibronectin fragment (HBFN-f) in rheumatoid arthritis (RA) cartilage.

Methods. Articular cartilage slices from RA knee joints and normal hip joints were cultured with HBFN-f. Secreted NO levels in conditioned media were determined. Cultures were pretreated with anti-CD44 antibody or HBFN-f-derived synthetic peptide (peptide V; WQPPRARI) to evaluate the role of CD44 in HBFN-f action. Immunofluorescence histochemistry was performed using fluorescein isothiocyanate-conjugated anti-CD44 antibody.

Results. HBFN-f stimulated NO production in a dose-dependent manner. Whereas CD44 expression was up-regulated in RA cartilage, anti-CD44 antibody blocked HBFN-f-stimulated NO production. Peptide V with heparin-binding ability significantly reduced NO levels elevated by HBFN-f. Compared with normal cartilage, cartilage response to HBFN-f and the blocking effects of anti-CD44 antibody on HBFN-f action were stronger in RA cartilage.

Conclusions. The present study clearly demonstrated that HBFN-f stimulated NO production through CD44 in RA cartilage. Increased expression of CD44 in RA cartilage may play a pathological role in joint destruction through enhanced NO production by binding to fibronectin fragments such as HBFN-f.

KEY WORDS: Fibronectin fragment, Nitric oxide, Inducible nitric oxide synthase, Rheumatoid arthritis, Cartilage, CD44


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X. Chang, R. Yamada, A. Suzuki, Y. Kochi, T. Sawada, and K. Yamamoto
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