Regulatory mechanism of transforming growth factor beta receptor type II degradation by interleukin-1 in primary chondrocytes

被引:16
作者
Bauge, Catherine [1 ]
Girard, Nicolas
Leclercq, Sylvain [2 ]
Galera, Philippe
Boumediene, Karim
机构
[1] Univ Caen Basse Normandie, Microenvironm Cellulaire & Pathol MILPAT EA4652, UFR Med, F-14032 Caen, France
[2] Clin St Martin, Dept Chirurg Orthoped, Caen, France
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2012年 / 1823卷 / 05期
关键词
TGF beta receptor; Interleukin-1; Turnover regulation; Caveolin-1; Proteasome; Osteoarthritis; OSTEOARTHRITIS; INHIBITION; MEMBRANE; SMURF2; TRANSFORMING-GROWTH-FACTOR-BETA-1; COMPARTMENTALIZATION; EXPRESSION; CAVEOLIN-1; INDUCTION; CARTILAGE;
D O I
10.1016/j.bbamcr.2012.02.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-1 beta (IL-1 beta), a key-cytokine in osteoarthritis, impairs TGF beta signaling through T beta RII down-regulation by increasing its degradation. Here, we investigated the molecular mechanism that controls T beta RII fate in IL-1 beta treated cells. Chondrocytes were treated with IL-1 beta in the presence of different inhibitors. T beta RII and Cav-1 expression were assayed by Western blot and RT-PCR. We showed that IL-1 beta-induced degradation of T beta RII is dependent on proteasome and on its internalization in caveolae. In addition, IL-1 beta enhances Cav-1 expression, a major constituent of lipid raft. In conclusion, we enlighten a new mechanism by which IL-1 beta antagonizes TGF beta pathway and propose a model of T beta RII turnover regulation upon IL-1 beta treatment (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:983 / 986
页数:4
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