Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Originally published in Science Express on 25 January 2007
Science 16 February 2007:
Vol. 315. no. 5814, pp. 1006 - 1010
DOI: 10.1126/science.1137306
Prev | Table of Contents | Next

Reports

Cadherin-11 in Synovial Lining Formation and Pathology in Arthritis

David M. Lee,1 Hans P. Kiener,1 Sandeep K. Agarwal,1* Erika H. Noss,1* Gerald F. M. Watts,1* Osamu Chisaka,2 Masatoshi Takeichi,3 Michael B. Brenner1{dagger}

The normal synovium forms a membrane at the edges of joints and provides lubrication and nutrients for the cartilage. In rheumatoid arthritis, the synovium is the site of inflammation, and it participates in an organized tissue response that damages cartilage and bone. We identified cadherin-11 as essential for the development of the synovium. Cadherin-11–deficient mice have a hypoplastic synovial lining, display a disorganized synovial reaction to inflammation, and are resistant to inflammatory arthritis. Cadherin-11 therapeutics prevent and reduce arthritis in mouse models. Thus, synovial cadherin-11 determines the behavior of synovial cells in their proinflammatory and destructive tissue response in inflammatory arthritis.

1 Department of Medicine and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, 1 Jimmy Fund Way, Boston, MA 02115, USA.
2 Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Yoshida-honmachi, Kyoto 606-8501, Japan.
3 RIKEN Center for Developmental Biology, Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan.

* These authors contributed equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: mbrenner{at}rics.bwh.harvard.edu

Read the Full Text

Find additional patient-related information at:

A New Treatment Possibility for RA

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Synoviocyte Stimulation by the LFA-1-Intercellular Adhesion Molecule-2-Ezrin-Akt Pathway in Rheumatoid Arthritis.
K. Singh, I. Colmegna, X. He, C. M. Weyand, and J. J. Goronzy (2008)
J. Immunol. 180, 1971-1978
   Abstract »    Full Text »    PDF »
Actin cytoskeleton dynamics linked to synovial fibroblast activation as a novel pathogenic principle in TNF-driven arthritis.
Y Vasilopoulos, V Gkretsi, M Armaka, V Aidinis, and G Kollias (2007)
Ann Rheum Dis 66, iii23-iii28
   Abstract »    Full Text »    PDF »
Tendon Development Requires Regulation of Cell Condensation and Cell Shape via Cadherin-11-Mediated Cell-Cell Junctions.
S. H. Richardson, T. Starborg, Y. Lu, S. M. Humphries, R. S. Meadows, and K. E. Kadler (2007)
Mol. Cell. Biol. 27, 6218-6228
   Abstract »    Full Text »    PDF »
Why Does Rheumatoid Arthritis Involve the Joints?.
P. E. Lipsky (2007)
N. Engl. J. Med. 356, 2419-2420
   Full Text »    PDF »
Identification of a Molecular Key to Rheumatoid Arthritis.
(2007)
Journal Watch (General) 2007, 4
   Full Text »


ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)