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Cartilage destruction in rheumatoid arthritis

WHO Collaborating Center for Molecular Biology and Novel Therapeutic Strategies for Rheumatic Diseases, Department of Rheumatology, University Hospital, Gloriastrasse 25, CH-8091 Zurich, Switzerland

Correspondence to:
Correspondence to:
Steffen.Gay@ruz.usz.ch

Keywords: cartilage destruction; rheumatoid arthritis

The first 150 words of the full text of this article appear below.

Synovial fibroblasts represent an important source of matrix degrading enzymes mediating joint destruction in rheumatoid arthritis.¹ In our search for new pathways for the activation of synovial fibroblasts we have detected endogenous retroviral sequences, like the line 1 element (L1).²

To study the functional role of L1 we transduced synovial fibroblasts with L1 constructs and showed that L1 induces a number of crucial transcription factors for the activation of these cells. Most significant was the induction of p38 . At present p38 has not been explored in detail, although several interesting pathways have been examined. The fact that p38 phosphorylates various transcription factors, including ATF-2, Elk-1, and SAP-1, and that it could be shown that the ATF-2 pathway is potentially linked to the induction of certain oncogenes as well as to the production of matrix degrading metalloproteinases³ has put this molecule at the focus of our interest.

Because inhibition of . . . [Full text of this article]

This article has been cited by other articles:

				M Neidhart, F Zaucke, R von Knoch, A Jungel, B A Michel, R E Gay, and S Gay Galectin-3 is induced in rheumatoid arthritis synovial fibroblasts after adhesion to cartilage oligomeric matrix protein Ann Rheum Dis, March 1, 2005; 64(3): 419 - 424. [Abstract] [Full Text] [PDF]