IL-1 beta increases uPA and uPA receptor expression in human gingival fibroblasts

The binding of urokinase-type plasminogen activator (uPA) to its receptor ( uPAR) in various cell types has been proposed as an important feature of ma ny cellular processes requiring extracellular proteolysis, cell adhesion, m otility, and invasion. uPAR attaches to the cell surface with a glycosylpho phatidylinositol (GPI) anchor, and serves to localize and accelerate the pr oteolysis cascade. In this study, we examined both uPA and uPAR levels in h uman gingival fibroblasts treated with an inflammatory cytokine, interleuki n-1 beta (IL-1 beta). PA activity in the cell lysate was increased by treat ment with IL-1 beta. Further, PA activity released by phosphatidylinositol- specific phospholipase C, which detaches the GPI anchor, was also increased by IL-1 beta. The activity was inhibited by amiloride, a specific inhibito r of uPA. In addition, IL-1 beta increased the protein and mRNA levels of b oth uPA and uPAR in gingival fibroblasts. These findings suggest that the e nhancement of uPA and uPAR levels by IL-1 beta may play an important role i n the progression of periodontal diseases through pericellular proteolysis, and subsequent cellular behavior.