Recent studies have implicated polypeptide growth factors in the development of rheumatoid arthritis (RA), which is characterized by synoviocyte hyperplasia and neovascularization. One such polypeptide, basic fibroblast growth factor (bFGF), is of particular interest because of its potent mitogenic and angiogenic activities. We have previously 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 changes in arthritic joints from rats (2). Now we extend our study by detecting in vivo expression of bFGF in human synovial tissues obtained from patients with RA.
Human synovial tissues from patients with RA, degenerative joint disease (DJD), and trauma were collected during joint surgery. The expression of bFGF protein and mRNA by the synovia was examined by immunolocalization, Western blot, Northern blot, and RNase protection assays. Synovium from patients with DJD and trauma was used to compare with rheumatoid synovium. Double immunostaining with cell type-specific antibodies was carried out to identify cellular sources of bFGF.
Both polypeptide and mRNA for bFGF were detected in the synovial samples examined. Increased bFGF staining was found in synovium-cartilage interface where joint destruction occurred and in hyperplastic synoviocytes of a subset of rheumatoid synovium. Strong cytoplasmic bFGF staining was localized in the majority of mast cells and vascular cells.
Synovial tissue from patients with RA, DJD, and trauma express bFGF. Increased bFGF staining in the hyperplastic lining synoviocytes and at the pannus-cartilage 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 sources of tissue bFGF.