RESUMO
Interleukin (IL)1ß is a key promotor in the pathogenesis of temporomandibular joint osteoarthritis. Differentiation of stem cells to cartilage is a crucial repair mechanism of articular cartilage damage, and IL1ß has been reported to impede the differentiation by upregulating the secretion of IL6, an important inflammatory factor. Long noncoding RNAs (lncRNAs) regulate a number of physiological and pathological processes, but whether lncRNA AK094629 contributes to the IL1ß mediated induction of inflammation remains unclear. Therefore, the aim of the present study was to investigate the effect of AK094629 on IL1ßinduced IL6 expression in synovialderived mesenchymal stem cells (SMSCs) of the temporomandibular joints. The results of the present study demonstrated that the expression of AK094629 in the synovial tissue of patients with osteoarthritis was positively correlated with IL1ß. In addition, IL1ß upregulated the expression of AK094629 in the SMSCs in vitro, and AK094629 knockdown inhibited the IL1ß mediated upregulation of IL6. The present study also demonstrated that AK094629 knockdown downregulated the expression of the mitogenactivated protein kinase kinase kinase 4 (MAP3K4), which is upregulated by IL1ß, whereas knockdown of MAP3K4 did not affect the expression of AK094629, but reversed the upregulation of IL6 in SMSCs. In conclusion, AK094629 knockdown attenuated the expression of IL1ßregulated IL6 in the SMSCs of the temporomandibular joint by inhibiting MAP3K4. Therefore, AK094629 may be a potential novel therapeutic target for the treatment of temporomandibular joint osteoarthritis.
