Department of orthopedics, Zhangjiagang Hospital of Traditional Chinese Medicine, Zhangjiagang, Jiangsu 215600, China.
Department of orthopedics, Zhangjiagang Hospital of Traditional Chinese Medicine, Zhangjiagang, Jiangsu 215600, China.
Pathol Res Pract. 2019 Jul;215(7):152442. doi: 10.1016/j.prp.2019.152442. Epub 2019 May 6.
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.
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-1β. 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.
SOX11 was upregulated in patients with OA and in IL-1β treated cells. IL-1β 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-1β-induced apoptosis in CHON-001 cells. Meanwhile, IL-1β 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-1β treated cell supernatant.
Inhibition of SOX11 could improve IL-1β-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.
骨关节炎（OA）是一种退行性疾病，其发病机制尚不清楚。转录因子 SOX11 已被证明参与了 OA 的发展进程。本研究旨在评估 SOX11 在 OA 发展过程中的潜在功能。
采用 qRT-PCR 检测 OA 患者和健康供体的 SOX11 表达。随后，用 IL-1β 处理软骨细胞 CHON-001 建立体外 OA 模型。接下来，我们使用 siRNA 验证 SOX11 在体外 OA 模型中的功能。最后，探讨了 SOX11 与 TNF-α 的关系。
SOX11 在 OA 患者和 IL-1β 处理的细胞中均上调。IL-1β 显著增加了 CHON-001 细胞中 MMP13 和 cleaved caspase 3 的 mRNA 和蛋白水平，同时降低了胶原 II 和聚集蛋白聚糖。此外，SOX11 的敲低可显著减少 CHON-001 细胞中由 IL-1β 诱导的细胞凋亡。同时，siRNA 干扰显著逆转了 IL-1β 诱导的 OA 样现象。此外，抑制 SOX11 降低了 OA 患者和 IL-1β 处理的细胞上清液中 TNF-α 的水平。
抑制 SOX11 可改善 CHON-001 细胞中由 IL-1β 诱导的 OA 样现象，这表明 SOX11 在 OA 的发病机制中起重要作用。因此，我们假设 SOX11 可能是治疗 OA 患者的潜在靶点。
