XXXX -mediated signaling induces @entity2071 and Fas on rheumatoid synovial cells and Fas-mediated apoptosis.

@entity2667 @entity4404 @entity8652 @entity12 @entity3818 @entity2393 @entity2071 @entity669 @entity309
OBJECTIVE: @entity309 ( @entity309 ) synovial cells interact with inflammatory cells, as well as extracellular matrices, through integrins. However, the relevance of @entity2393 to inflammatory processes in @entity309 remains unclear. We examined the role of @entity2393 -mediated signaling in @entity309 . METHODS: Expression of cell-surface molecules was assessed by FACScan. Engagement of @entity8652 integrins was performed by crosslinking using a specific monoclonal antibody (mAb) and ligand matrices such as fibronectin or collagen. To determine the involvement of @entity669 kinases in @entity2393 -mediated signaling, the cells were pretreated with various inhibitors of intracytoplasmic signaling or were transfected with a wild-type @entity3818 ( @entity3818 ) or a dominant negative truncation of the @entity3818 expression plasmid via cationic liposome-mediated transfection. Apoptosis of synovial cells was detected by double staining with @entity2667 and @entity4404 . RESULTS: @entity2393 was highly expressed on @entity309 synovial cells. Engagement of @entity8652 integrins by crosslinking as well as by ligand matrices markedly up-regulated expression of @entity2071 ( @entity2071 ) and Fas. Up-regulation of @entity2071 and Fas induced by @entity2393 was mediated by the @entity669 kinase signaling pathway, especially involving @entity3818 . Fas-mediated early apoptotic change in the cells was amplified by @entity8652 crosslinking. CONCLUSION: Our results suggest that interaction of @entity8652 integrins with extracellular matrix augments expression of @entity2071 and Fas on @entity309 synovial cells, as well as Fas-mediated apoptosis of synovial cells. This might lead to the spontaneous growth arrest through the Fas/ @entity12 pathway observed in @entity309 .
