Knockdown of long non-coding RNA AK094629 attenuates the interleukin-1β induced expression of interleukin-6 in synovium-derived mesenchymal stem cells from the temporomandibular joint

Abstract

Interleukin (H) - 1 β 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 I L - 1 β has been reported to impede the differentiation by upregulating the secretion of IL-6, an important inflammatory factor. Long non-coding RNAs (lncRNAs) regulate a number of physi¬ ological and pathological processes, but whether lncRNA AK094629 contributes to the I L - 1 β mediated induction of inflammation remains unclear. Therefore, the aim of the present study was to investigate the effect of AK094629 on I L - 1 β -induced IL-6 expression in synovial-derived 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 IL-1β. In addition, I L - 1 β upregulated the expression of AK094629 in the SMScs in vitro, and AK094629 knockdown inhibited the I L - 1 β mediated upregulation of IL-6. The present study also demonstrated that AK094629 knockdown downregulated the expression of the mitogen-activated protein kinase kinase kinase 4 (MAP3K4), which is upregulated by IL-1β, whereas knockdown of MAP3K4 did not affect the expression of AK094629, but reversed the upregulation of IL-6 in SMScs. In conclusion, AK094629 knockdown attenuated the expression of IL-1β-regulated IL-6 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.