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Overexpression of Proto-oncogene bd-2 in Rheumatoid Synovium SIR—Synovial lining thickening is one of the main histopathological features of rheumatoid synovium. The increased lining layer cellularity has been viewed as a consequence of increased recruitment of bone marrow-derived macrophages and in situ proliferation of synoviocytes [1,2]. Alternatively, the increased cellularity could reflect a decreased frequency of cell death. We propose that prolonged survival of lining cells may also play a role in the increased cellularity in rheumatoid synovium. It has been demonstrated that the proto-oncogene bcl-2 is involved in the control of apoptosis in many types of tissue cells and overproduction of bcl-2 protein prevents cell death [3]. We therefore investigated the expression of bcl-2 gene by synovial cells in RA patients using in situ hybridization. Frozen sections of synovium from 10 RA patients were studied. Antisense bcl-2 riboprobes were prepared by standard procedures and labelled with digoxigenin [4]. The hybridization was detected with alkaline phosphatase-conjugated anti-DIG-Fab. The antisense riboprobe for bcl-2 hybridized strongly with the synovial sections from all 10 RA patients. The hybridization was found predominantly in the lining layer, where an average of 70% of the cells hybridized (Fig. 1). To a lesser extent, however, some cells in the sublining layers also hybridized with the bcl-2 antisense riboprobe. By contrast, the hybridization was found in only two of three OA synovial samples, and the hybridized cells scattered in the membrane and were far fewer than in RA samples. No cells hybridized for bcl-2 antisense riboprobe were detected in the normal synovial sections from one patient with trauma. bcl-2 was first identified in follicular B-cell lymphoma [5]. Its ability to block cell apoptosis has been considered to be important in autoimmunity [6]. Our results suggest that overexpression of the bcl-2 gene in rheumatoid synovial lining cells may be involved in the downregulation of apoptosis in this population with a concomitant increase in cellularity in the lining layer, bcl-2 may render these cells invasive, growth causing destruction of the adjacent cartilage and bone. It is noteworthy that recent studies have revealed that the regulation of the fine balance between cell death and survival may involve many gene products. For instance, Bax has been shown to have considerable sequence homology with bcl-2, it can form heterodimers with bcl-2 and counter bcl-2-mediated protection from apoptosis [7]. Thus, it would also be of interest to see the expression pattern of Bax in rheumatoid …

Overexpression of Proto-oncogene bcl-2 in Rheumatoid Synovium