Zhang Liang, Zhao Weidong, Bao Dongmei, Sun Kening, Li Peng, Gao Zhihui, Lu Zhidong
Department of Orthoped, General Hospital of Ningxia Medical University, No. 804 Shengli South Street, Xingqing District, Yinchuan, 750004 Ningxia Province China.
3 Biotech. 2021 Jun;11(6):258. doi: 10.1007/s13205-021-02814-8. Epub 2021 May 9.
To explore the potential function of miR-9-5p in wear-particle-induced osteoclastogenesis, we examined the expression of SIRT1 and miR-9-5p in particle-induced osteolysis (PIO) mice calvariae and polyethylene (PE)-induced RAW 264.7 cells and found that SIRT1 expression was downregulated while miR-9-5p expression was upregulated in both models. We then verified that miR-9-5p targets SIRT1. miR-9-5p was found to promote PE-induced osteoclast formation from RAW 264.7 cells by staining and detection of osteoclast markers, and miR-9-5p activation of the SIRT1/NF-kB signaling pathway was found in cells by detecting the expression of SIRT1/NF-kB pathway-related proteins and rescue assays. In conclusion, we found that miR-9-5p activated the SIRT1/NF-κB pathway to promote wear-particle-induced osteoclastogenesis. miR-9-5p may be a useful therapeutic target for PIO remission and treatment.
为了探究miR-9-5p在磨损颗粒诱导的破骨细胞生成中的潜在作用，我们检测了颗粒诱导性骨溶解（PIO）小鼠颅骨和聚乙烯（PE）诱导的RAW 264.7细胞中SIRT1和miR-9-5p的表达，发现在这两种模型中SIRT1表达下调而miR-9-5p表达上调。然后我们证实miR-9-5p靶向SIRT1。通过对破骨细胞标志物进行染色和检测，发现miR-9-5p可促进RAW 264.7细胞形成PE诱导的破骨细胞，并且通过检测SIRT1/NF-κB信号通路相关蛋白的表达和拯救实验，在细胞中发现了miR-9-5p对SIRT1/NF-κB信号通路的激活作用。总之，我们发现miR-9-5p激活SIRT1/NF-κB通路以促进磨损颗粒诱导的破骨细胞生成。miR-9-5p可能是PIO缓解和治疗的一个有用的治疗靶点。
