• KehribarDemet YalçınDYDepartment of Internal Medicine, Faculty of Medicine, Ondokuz Mayıs University, Samsun, Turkey., Hakan Emmungil, Neşe Başak Türkmen, Osman Çiftçi, Emine Salva, and Metin Özgen.
• Department of Internal Medicine, Faculty of Medicine, Ondokuz Mayıs University, Samsun, Turkey.
• Turk J Med Sci. 2022 Aug 1; 52 (4): 135513611355-1361.

BackgroundEpidermal growth factor receptor (EGFR) family members and their associated ligands may be related to bone and joint destruction in rheumatoid arthritis. Matrix metalloproteinases are responsible for joint and bone tissue degradation. This study is intended to investigate the effect of epidermal growth factor receptor inhibition by lapatinib on the synthesis of matrix metalloproteinases in in vitro.MethodsSynovial fibroblast cell culture was obtained from a patient with rheumatoid arthritis who underwent knee arthroplasty. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were added to the cell culture to stimulate synovial fibroblast cells and create an inflammatory character. Understimulated and nonstimulated conditions, lapatinib was applied to the culture in four different concentrations of 25, 50, 100, and 200 µmol. Then, matrix metalloproteinase -1, -3, and, -13 levels were assessed.ResultsWhen stimulated with IL-1β and TNF-α, the synthesis of matrix metalloproteinases from synovial fibroblast was increased significantly. When lapatinib is added to the stimulated synovial fibroblasts, matrix metalloproteinases synthesis is significantly suppressed.DiscussionInhibition of the EGFR pathway with lapatinib suppresses matrix metalloproteinases synthesis. Our results suggest EGFR pathway inhibition may be a promising option to prevent joint destruction in the treatment of rheumatoid arthritis.

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