Modulation of receptor bound urokinase-type plasminogen activator on human monocytes by non-steroidal...

It has been shown previously that cell surface bound fibrinolytic activity on human monocytes is significantly increased in patients with rheumatoid arthritis (RA) as compared to monocytes from healthy volunteers. Studies on the modulation of receptor-bound urokinase type plasminogen activator on peripheral blood monocytes of patients with RA showed that tenoxicam, a non-steroidal antiinflammatory drug with long half life and good tissue permeability, is able to downregulate the total number of urokinase receptors. Furthermore the degree of endogenous occupation of the urokinase receptor was significantly decreased in post-treatment monocytes. These data provide evidence that the non-steroidal antiinflammatory drug tenoxicam is able to downregulate cell bound fibrinolytic activity, known to contribute to pronounced degradation of cartilage and connective tissue in patients with RA.