| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1950786 | Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | 2012 | 4 Pages |
Interleukin-1β (IL-1β), a key-cytokine in osteoarthritis, impairs TGFβ signaling through TβRII down-regulation by increasing its degradation. Here, we investigated the molecular mechanism that controls TßRII fate in IL-1ß treated cells.Chondrocytes were treated with IL-1ß in the presence of different inhibitors. TßRII and Cav-1 expression were assayed by Western blot and RT-PCR.We showed that IL-1ß-induced degradation of TßRII is dependent on proteasome and on its internalization in caveolae. In addition, IL-1ß enhances Cav-1 expression, a major constituent of lipid raft.In conclusion, we enlighten a new mechanism by which IL-1ß antagonizes TGFß pathway and propose a model of TßRII turnover regulation upon IL-1ß treatment.
► IL-1ß increases degradation of TßRII. ► IL-1ß-induced degradation of TßRII is dependent on proteasome pathways. ► IL-1ß-induced degradation of TßRII is blocked by nystatin.
