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

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• 作者：Catherine Baugé ; ^a ; ^{catherine.bauge@unicaen.fr} ; Nicolas Girard^a ; Sylvain Leclercq^a ; ^b ; Philippe Galé ; ra^a ; Karim Boumé ; diene^a
• 关键词：TGFß ; receptor ; Interleukin-1 ; Turnover regulation ; Caveolin-1 ; Proteasome ; Osteoarthritis
• 刊名：Biochimica et Biophysica Acta (BBA)/Molecular Cell Research
• 出版年：2012
• 期刊代码：20_01674889
• 类别：bio
• 出版时间：May, 2012
• 卷：1823
• 期：5
• 页码：983-986
• 文件大小：394 K

摘要

Interleukin-1尾 (IL-1尾), a key-cytokine in osteoarthritis, impairs TGF尾 signaling through T尾RII down-regulation by increasing its degradation. Here, we investigated the molecular mechanism that controls T脽RII fate in IL-1脽 treated cells.

Chondrocytes were treated with IL-1脽 in the presence of different inhibitors. T脽RII and Cav-1 expression were assayed by Western blot and RT-PCR.

We showed that IL-1脽-induced degradation of T脽RII is dependent on proteasome and on its internalization in caveolae. In addition, IL-1脽 enhances Cav-1 expression, a major constituent of lipid raft.

In conclusion, we enlighten a new mechanism by which IL-1脽 antagonizes TGF脽 pathway and propose a model of T脽RII turnover regulation upon IL-1脽 treatment.