MiR-217 promotes cell proliferation and osteogenic differentiation of BMSCs by targeting DKK1 in steroid-associated osteonecrosis - 09/12/18
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Graphical abstract |
Highlights |
• | The expression of miR-217 was clearly decreased in steroid-associated osteonecrosis. |
• | DKK1 is negatively regulated by miR-217 in BMSCs. |
• | MiR-217 promotes cell proliferation and osteogenic differentiation by targeting DKK1. |
• | Negative modulation of DKK1 by miR-217 results in nuclear translocation of β-catenin. |
Abstract |
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.
Le texte complet de cet article est disponible en PDF.Keywords : MiR-217, DKK1, Mesenchymal stem cells, Osteonecrosis
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Vol 109
P. 1112-1119 - janvier 2019 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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