z-logo
Premium
Production of the chemokine eotaxin‐1 in osteoarthritis and its role in cartilage degradation
Author(s) -
Hsu YiHsin,
Hsieh MingShium,
Liang YuChih,
Li ChaoYi,
Sheu MingThau,
Chou DerTsay,
Chen TzengFu,
Chen ChienHo
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20239
Subject(s) - eotaxin , ccr3 , chemokine , chemistry , cartilage , chemokine receptor , autocrine signalling , chondrocyte , matrix metalloproteinase , cytokine , receptor , immunology , microbiology and biotechnology , medicine , biology , biochemistry , anatomy
The expression of the chemokine, eotaxin‐1, and its receptors in normal and osteoarthritic human chondrocytes was examined, and its role in cartilage degradation was elucidated in this study. Results indicated that plasma concentrations of eotaxin‐1 as well as the chemokines, RANTES, and MCP‐1α, were higher in patients with osteoarthritis (OA) than those in normal humans. Stimulation of chondrocytes with IL‐1β or TNF‐α significantly induced eotaxin‐1 expression. The production of eotaxin‐1 induced expression of its own receptor of CCR3 and CCR5 on the cell surface of chondrosarcomas, suggesting that an autocrine/paracrine pathway is involved in eotaxin‐1's action. In addition, eotaxin‐1 markedly increased the expressions of MMP‐3 and MMP‐13 mRNA, but had no effect on TIMP‐1 expression in chondrocytes. However, pretreatment of anti‐eotaxin‐1 antibody significantly decreased the MMP‐3 expression induced by IL‐1β. These results first demonstrate that human chondrocytes express the chemokine, eotaxin‐1, and that its expression is induced by treatment with IL‐1β and TNF‐α. The cytokine‐triggered induction of eotaxin‐1 further results in enhanced expressions of its own receptor of CCR3, CCR5, and MMPs, suggesting that eotaxin‐1 plays an important role in cartilage degradation in OA. © 2004 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here