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Glucosamine modulates IL‐1‐induced activation of rat chondrocytes at a receptor level, and by inhibiting the NF‐κB pathway
Author(s) -
Gouze J.N.,
Bianchi A.,
Bécuwe P.,
Dauça M.,
Netter P.,
Magdalou J.,
Terlain B.,
Bordji K.
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03255-0
Subject(s) - glucosamine , chemistry , activator (genetics) , receptor , signal transduction , proteoglycan , beta (programming language) , microbiology and biotechnology , biochemistry , biology , extracellular matrix , computer science , programming language
We recently reported that glucosamine reversed the decrease in proteoglycan synthesis and in UDP‐glucuronosyltransferase I mRNA expression induced by interleukin‐1β (IL‐1β) [Arthritis Rheum. 44 (2001) 351–360]. In the present work, we show that glucosamine does not exert the same effects when chondrocytes were stimulated with reactive oxygen species (ROS). In order to better understand its mechanism of action, we determined if glucosamine could prevent the binding of IL‐1β to its cellular receptors or could interfere with its signaling pathway at a post‐receptor level. Addition of glucosamine to rat chondrocytes treated with IL‐1β or with ROS decreased the activation of the nuclear factor κB, but not the activator protein‐1. After treatment with IL‐1β, glucosamine increased the expression of mRNA encoding the type II IL‐1β receptor. These results emphasize the potential role of two regulating proteins of the IL‐1β signaling pathway that could account for the beneficial effect of glucosamine in osteoarthritis.