Fibroblast-like synoviocytes from rheumatoid arthritis patients express less flice-inhibitory protein than FLS from osteoarthritis, trauma and prosthesis loosening patie

Rheumatoid arthritis (RA) is characterized by hyperplasia of the synovium and degradation of cartilage by fibroblast-like synoviocytes (FLS). The hyperplasia is thought to be a result of an imbalance between proliferation and apoptosis. Proliferation and apoptosis can be regulated by death receptors like TNF receptor and Fas. TNF is abundantly expressed in the rheumatoid synovium and could contribute to the hyperplasia by promoting proliferation and/or inhibition of apoptosis. In this study it was investigated whether overexpression of flice inhibitory protein (FLIP), a protein that inhibits death receptor mediated apoptosis, could potentially be involved in the hyperplasia of FLS. Epression of FLIP was investigated using a western blot and was seen in all samples tested, but most expression was seen in two trauma patients (n = 3), one OA patient (n = 2) and two patients with prosthesis loosening (n = 3). RA patients (n = 3) showed the least expression of FLIP (see figure 1). Thus, in RAFLS no overexpression of FLIP was observed, therefore it is unlikely that FLIP contributes to resistance to apoptosis of FLS and hyperplasia in the rheumatoid synovium.

Figure 1

Western blot showing expression of human FLIP in several patients. #, Trauma patients; RA, rheumatoid arthritis; PL, prosthesis lossening patients.