SOX11 promotes osteoarthritis through induction of TNF-α.

OBJECTIVE: Osteoarthritis (OA) is a degenerative disease and the molecular mechanism of OA remains unclear. Transcription factor SOX11 has been proved to be involved in the development progress of OA. The present study aimed to evaluate the potential function of SOX11 during the development of OA. METHODS: SOX11 expression in patients with OA and health donator was determined with qRT-PCR. Subsequently, in vitro OA model was established by treating the chondrocyte cells CHON-001 with IL-1ß. Next, we validated the function of SOX11 in in vitro OA model by using siRNAs. Finally, the relationship between SOX11 and TNF-α was explored. RESULTS: SOX11 was upregulated in patients with OA and in IL-1ß treated cells. IL-1ß significantly increased both the mRNA and protein levels of MMP13 and cleaved caspase 3, while decreased collagen II and aggrecan in CHON-001 cells. In addition, knockdown of SOX11 could significantly decrease IL-1ß-induced apoptosis in CHON-001 cells. Meanwhile, IL-1ß induced OA like phenomenon was significantly reversed by siRNA interference. Moreover, inhibition of SOX11 decreased the level of TNF-α in patients with OA and in IL-1ß treated cell supernatant. CONCLUSION: Inhibition of SOX11 could improve IL-1ß-induced OA like phenomenon in CHON-001 cells, which suggesting SOX11 played an important role during the pathogenesis of OA. Thus, we hypothesized that SOX11 could be a potential target for the treatment of patients with OA.