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Expression of galectin-3 in rheumatoid arthritis synovium


Galectins are involved in cell-cell interactions, cell adhesion to extracellular matrix, tissue remodelling, cell growth and regulation of apoptosis. Particularly, galectin-3 has antiapoptotic properties, proinflammatory and chemotactic activities. An altered expression has been associated with tumor progression. The aim of this study was to investigate the expression pattern of galectin-3 in rheumatoid arthritis (RA) synovial tissues.

Material and methods

Synovial tissues were obtained after joint replacement from patients with RA (n = 7) or osteoarthritis (OA, n = 3). Specific sequences of galectin-3 cDNA were amplified by RT-PCR and used for the generation of digoxigenin-labeled riboprobes. In situ hybridisation was performed on paraffin sections. Immunohistochemistry was applied on paraffin and snap frozen sections using mouse monoclonal anti-galectin-3 antibodies. For comparison, the macrophage marker CD68 was used.


In RA, galectin-3 was found at sites of joint destruction, as well as in the lining and sublining layers. The percentage of positive cells, however, was lower in the lining than in the sublining layer. A predominant expression of galectin-3 was found in cells with follicle-like structures and in perivascular infiltrates, whereas vessels remained negative. Synovial fibroblasts also stained positive and, at least in the sublining, the expressions of galectin-3 and CD68 appeared mutually exclusive. In contrast, in OA synovial tissues, only a few cells in the lining layer were positive for galectin-3. Similar results were obtained by in situ hybridisation and immunohistochemistry.


Taken together, theses observations suggest that galectin-3 is involved in cell-cell and cell-matrix interactions in the RA synovium and therefore may contribute to both the inflammatory and the destructive processes.

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Neidhart, M., Kuchen, S., Seemayer, C. et al. Expression of galectin-3 in rheumatoid arthritis synovium. Arthritis Res Ther 4 (Suppl 1), 30 (2002).

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