MicroRNA-103 contributes to osteoarthritis development by targeting Sox6
MicroRNA-103 contributes to osteoarthritis development by targeting Sox6
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MicroRNA-103 通过靶向 Sox6 促进骨关节炎的发展
DOI：
10.1016/j.biopha.2019.109186
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发表时间：
2019-10-01
影响因子：
7.5
通讯作者：
Wu, Xing
中科院分区：
文献类型：
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作者：
Chen, Jian;Wu, Xing
骨关节炎是一种世界范围内的退行性关节疾病，其潜在的分子机制仍知之甚少。 MicroRNA 是包括骨关节炎在内的多种生物过程的重要调节因子。在这项研究中，我们发现骨关节炎患者中 miR-103 失调。我们进行了 CCK8 和集落形成测定，发现 miR-103 抑制软骨细胞增殖。我们还通过 RT-PCR、蛋白质印迹和免疫细胞化学发现 miR-103 抑制软骨细胞的形成和成熟。抑制 miR-103 可抑制软骨细胞中由 IL-15 诱导的分解代谢因子和促炎细胞因子的产生。最后，我们发现Sox6是miR-103的直接靶标并参与骨关节炎的发展。总之，我们证明 miR-103 通过直接靶向和抑制 Sox6 的表达而促进骨关节炎的发展。调节人软骨细胞中 miR-103 的表达可能是骨关节炎的有效治疗方法。
Osteoarthritis is a degenerative joint disease, worldwide, and its underlying molecular mechanisms are still poorly understood. MicroRNAs are important regulators of diverse biological processes, including osteoarthritis. In this study, we showed that miR-103 was deregulated in osteoarthritis patients. We performed CCK8 and colony formation assay and found that miR-103 inhibited chondrocyte proliferation. We also found that miR-103 inhibited chondrocyte formation and maturation by RT-PCR, western blotting, and immunocytochemistry. Inhibition of miR-103 suppressed production of the catabolic factors and pro-inflammatory cytokines induced by IL-15 in chondrocytes. Finally, we found that Sox6 was a direct target of miR-103 and participated in osteoarthritis development. In summary, we demonstrated that miR-103 contributed to osteoarthritis development by directly targeting and inhibiting the expression of Sox6. Regulation of miR-103 expression in human chondrocytes may be an effective treatment for osteoarthritis.