Orthopaedic Department of 3rd Medical Center, Chinese PLA General Hospital, Beijing 100039, China.
Urology Department of 3rd Medical Center, Chinese PLA General Hospital, Beijing 100039, China.
Cell Mol Biol (Noisy-le-grand). 2022 Feb 4;67(5):123-130. doi: 10.14715/cmb/2021.67.5.17.
In this study, the expression of miR-182 in secondary bone degeneration was investigated, and the effect of its antagonist on glucocorticoid-induced osteoclast differentiation and its mechanism was studied. For this purpose, PBMC cell lines were selected for cultivation, and the changes were observed by hematoxylin-eosin (HE) staining. Real-time fluorescence quantitative (qRT-PCR) was used to detect mRNA expression. The protein expressions of RANKL, OPG and CXCL10 were detected by Western blot. CCK-8 and flow cytometry was used to detect cell proliferation and apoptosis. The results showed that protein expression levels of RANKL, OPG and CXCL10 in the miR-182 group were significantly higher than those in other groups (P>0.01). The miR-182 can promote RANK signal transduction in osteoclasts by regulating RANKL/NFκB signaling pathway, accelerating osteoclast proliferation and differentiation, and slowing down the process by miR-182 inhibitor. In general, miR-182 alleviates OP by inhibiting the activity of osteoclast via RANKL/NFκB signaling.
在这项研究中，研究了 miR-182 在继发性骨退变中的表达，并研究了其拮抗剂对糖皮质激素诱导的破骨细胞分化的影响及其机制。为此，选择 PBMC 细胞系进行培养，并通过苏木精-伊红（HE）染色观察变化。实时荧光定量（qRT-PCR）用于检测 mRNA 表达。Western blot 用于检测 RANKL、OPG 和 CXCL10 的蛋白表达。CCK-8 和流式细胞术用于检测细胞增殖和凋亡。结果表明，miR-182 组 RANKL、OPG 和 CXCL10 的蛋白表达水平明显高于其他组（P>0.01）。miR-182 可以通过调节 RANKL/NFκB 信号通路促进破骨细胞中 RANK 信号转导，加速破骨细胞增殖和分化，而 miR-182 抑制剂则减缓这一过程。总之，miR-182 通过 RANKL/NFκB 信号抑制破骨细胞的活性来减轻 OP。
