MiR-217 promotes cell proliferation and osteogenic differentiation of BMSCs by targeting DKK1 in steroid-associated osteonecrosis

Biomedicine & Pharmacotherapy

卷:109

Jia Zheng¹  Zhipeng Dai²  Yi Jin²  Shanfeng Zhang²  Ke Liu²  Jiajun Zhao²  Zhibo Sun³  Fei Wu⁴ 

[1] Corresponding author.;

[2] Department of Orthopedics, Henan Provincial People’s Hospital, Zhengzhou, Henan, China;

[3] Department of Orthopedics, Renmin Hospital, Wuhan University, Wuhan, Hubei, China;

[4] Department of Orthopedics, Wuhan Fourth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China;

关键词: MiR-217;    DKK1;    Mesenchymal stem cells;    Osteonecrosis;   

DOI  :  

来源: DOAJ

【 摘 要 】

MicroRNAs (miRNAs) have recently been recognized to play an important role in bone-associated diseases. This study aims to explore the expression profile and biological function of miR-217, which is known to be related to tumor cell proliferation and migration, to the proliferation and osteogenic differentiation of MSCs from the patients with steroid-associated osteonecrosis (ONFH). Bone marrow was obtained from the proximal femur of 10 patients with ONFH and 10 patients with femoral neck fractures. Bone marrow-derived mesenchymal stem cells (MSCs) were isolated and cultured. The expression profile, biological function of miR-217 and the interaction between miR-217 and DKK1 were assayed using cell viability measurement, western blot, Real-time PCR, luciferase reporter assay, Alizarin Red S (ARS) staining. We noted that the expression level of miR-217 was significantly decreased in the ONFH samples compared to the control samples (P < 0.0001). By targeting DKK1, miR-217 promoted nuclear translocation of β-catenin, increased expression of RUNX2, COL1A1 and obviously promoted the proliferation and differentiation of MSCs. Restoring the expression of DKK1 in the MSCs partially reversed the role of miR-217. These findings suggest that miR-217 promotes cell proliferation and osteogenic differentiation by inhibiting DKK1 during the development of steroid-associated osteonecrosis.

【 授权许可】

Unknown