EXPRESSION OF BASIC FIBROBLAST GROWTH-FACTOR IN SYNOVIAL TISSUE FROM PATIENTS WITH RHEUMATOID-ARTHRITIS AND DEGENERATIVE JOINT DISEASE

BACKGROUND: Recent studies have implicated polypeptide growth factors in the development of rheumatoid arthritis (RA), which is characterize d by synoviocyte hyperplasia and neovascularization. One such polypept ide, basic fibroblast growth factor (bFGF), is of particular interest because of its potent mitogenic and angiogenic activities. We have pre viously reported that cultured human synoviocytes synthesize and bind bFGF and also proliferate in response to it (1). Recently, we found a close association between increased bFGF expression and destructive ch anges in arthritic joints from rats (2). Now we extend our study by de tecting in vivo expression of bFGF in human synovial tissues obtained from patients with RA. EXPERIMENTAL DESIGN: Human synovial tissues fro m patients with RA, degenerative joint disease (DJD), and trauma were collected during joint surgery. The expression of bFGF protein and mRN A by the synovia was examined by immunolocalization, Western blot, Nor thern blot, and RNase protection assays. Synovium from patients with D JD and trauma was used to compare with rheumatoid synovium. Double imm unostaining with cell type-specific antibodies was carried out to iden tify cellular sources of bFGF. RESULTS: Both polypeptide and mRNA for bFGF were detected in the synovial samples examined. Increased bFGF st aining was found in synovium-cartilage interface where joint destructi on occurred and in hyperplastic synoviocytes of a subset of rheumatoid synovium. Strong cytoplasmic bFGF staining was localized in the major ity of mast cells and vascular cells. CONCLUSIONS: Synovial tissue fro m patients with RA, DJD, and trauma express bFGF. Increased bFGF stain ing in the hyperplastic lining synoviocytes and at the pannus-cartilag e interface suggests that bFGF may play a role in synovial hyperplasia and joint destruction. Strong cytoplasmic bFGF staining found in mast cells and vascular cells indicates that these cells are the major sou rces of tissue bFGF.