The expression of m-calpain in human synovial fibroblasts and chondrocytes.

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Calpain is generally believed to function only in the cytoplasm. However, m-calpain has recently been detected in the extracellular spaces of arthritic joint tissues. We attempted to examine the expression and secretion of m-calpain in a human chondrocytic cell line, HCS2/8 stimulated by TNF-α Cells were stimulated by TNF-α, and the expression of m-calpian in the cells and culture medium was analyzed by Western blotting. The effects of NSAIDs on the expression of m-calpain were also examined.TNF-α increased the level of m-calpain in the culture medium in a dose-and time-dependent manner.Intracellular m-calpain increased at 24 h and thereafter gradually to decreased to 48 h. NSAIDs, aspirin, diclofenac sodium, loxoprofen-SRS and NS398 significantly inhibited TNF-α-induced increase of m-calpain in the medium and cells. Prostaglandin E_2 stimulated the effect of low concentrations of TNF-α on m-calpain expression. In contrast, prostanoid-receptor antagonists inhibited the effects of TNF-α.Increase of m-calpain in the culture medium suggests that this Ca^<2+>-dependent protease may play a role in the promotion of degradation of cartilage extra-cellular matrix during arthritis. NSAIDs have protective effects, at least in part, through the inhibition of the expression and secretion of m-calpain.