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IL‐1β Increases uPA and uPA Receptor Expression in Human Gingival Fibroblasts
Author(s) -
Ogura Naomi,
Tobe Makiko,
Tamaki Hiroyuki,
Nagura Hideaki,
Abiko Yoshimitsu
Publication year - 2001
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/152165401753366159
Subject(s) - chemistry , receptor , cancer research , microbiology and biotechnology , biology , biochemistry
The binding of urokinase‐type plasminogen activator (uPA) to its receptor (uPAR) in various cell types has been proposed as an important feature of many cellular processes requiring extracellular proteolysis, cell adhesion, motility, and invasion. uPAR attaches to the cell surface with a glycosylphophatidylinositol (GPI) anchor, and serves to localize and accelerate the proteolysis cascade. In this study, we examined both uPA and uPAR levels in human gingival fibroblasts treated with an inflammatory cytokine, interleukin‐1 β(IL‐1 β). PA activity in the cell lysate was increased by treatment with IL‐1 β. Further, PA activity released by phosphatidylinositol‐specific phospholipase C, which detaches the GPI anchor, was also increased by IL‐1 β. The activity was inhibited by amiloride, a specific inhibitor of uPA. In addition, IL‐1 βincreased the protein and mRNA levels of both uPA and uPAR in gingival fibroblasts. These findings suggest that the enhancement of uPA and uPAR levels by IL‐1 βmay play an important role in the progression of periodontal diseases through pericellular proteolysis, and subsequent cellular behavior.