Hou Qiuke, Huang Yongquan, Luo Yiwen, Wang Bin, Liu Yamei, Deng Rudong, Zhang Saixia, Liu Fengbin, Chen Dongfeng
Department of Anatomy, The Research Centre of Integrative Medicine, Guangzhou University of Traditional Chinese MedicineGuangzhou 510000, Guangdong, P.R. China.
The First Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou 510000, Guangdong, P.R. China.
Am J Transl Res. 2017 Nov 15;9(11):4963-4973. eCollection 2017.
Our previous reports indicated that (+)-cholesten-3-one induces osteogenic differentiation of bone marrow mesenchymal stem cells (MSCs) by activating vitamin D receptor (VDR). However, whether and how miRNAs modulate osteogenic differentiation induced by (+)-cholesten-3-one have not been explored. In this study, miRNA array profiling and further validation by quantitative real-time PCR revealed that miR-351 was downregulated during (+)-cholesten-3-one-induced osteogenic differentiation of MSCs. Overexpression of miR-351 by miR-351 precursor transfection markedly inhibited the expression of osteoblast-specific genes, such as alkaline phosphatase (ALP), collagen type II, osteopontin (OPN), and runt-related transcription factor 2 (RUNX2), which consequently decreased a number of calcium mineralized nodules. Inhibition of miR-351 function by anti-miR-351 promoted expression of osteoblast-specific genes. Our results suggest that miR-351 is a negative regulator of osteoblast differentiation of MSCs induced by (+)-cholesten-3-one. Target prediction analysis tools and experimental validation by luciferase 3'UTR reporter assay identified VDR as a direct target of miR-351. miR-351 inhibited the expression of the VDR, which played a critical role in the control of osteogenic differentiation of MSCs. Importantly, overexpression of VDR significantly abolished the inhibitory effect of miR-351 on (+)-cholesten-3-one induced osteogenic differentiation. Taken together, our results demonstrate that miR-351 negatively regulates osteoblast differentiation of MSCs induced by (+)-cholesten-3-one through targeting VDR. These findings provid evidence that miR-351 can bea possible therapeutic target for bone repair and regeneration.
我们之前的报告表明,(+)-胆甾-3-酮通过激活维生素D受体(VDR)诱导骨髓间充质干细胞(MSC)的成骨分化。然而,miRNA是否以及如何调节(+)-胆甾-3-酮诱导的成骨分化尚未得到研究。在本研究中,通过miRNA芯片分析和定量实时PCR进一步验证发现,在(+)-胆甾-3-酮诱导的MSC成骨分化过程中,miR-351表达下调。通过转染miR-351前体过表达miR-351显著抑制了成骨细胞特异性基因的表达,如碱性磷酸酶(ALP)、II型胶原、骨桥蛋白(OPN)和 runt相关转录因子2(RUNX2),从而减少了钙矿化结节的数量。抗miR-351抑制miR-351功能促进了成骨细胞特异性基因的表达。我们的结果表明,miR-351是(+)-胆甾-3-酮诱导的MSC成骨细胞分化的负调节因子。通过荧光素酶3'UTR报告基因检测的靶标预测分析工具和实验验证确定VDR是miR-351的直接靶标。miR-351抑制VDR的表达,而VDR在MSC成骨分化的控制中起关键作用。重要的是,VDR的过表达显著消除了miR-351对(+)-胆甾-3-酮诱导的成骨分化的抑制作用。综上所述,我们的结果表明,miR-351通过靶向VDR负调节(+)-胆甾-3-酮诱导的MSC成骨细胞分化。这些发现提供了证据表明,miR-351可能成为骨修复和再生的治疗靶点。