基因沉默
骨形态发生蛋白2
间充质干细胞
骨质疏松症
小RNA
骨吸收
细胞生物学
癌症研究
化学
成骨细胞
运行x2
体外
内科学
生物
医学
基因
生物化学
作者
Ke Liu,Ying Jing,Wen Zhang,Xuejie Fu,Huan Zhao,Xichao Zhou,Yunxia Tao,Huilin Yang,Yan Zhang,Ke Zen,Chenyu Zhang,Donghai Li,Qin Shi
出处
期刊:Bone
[Elsevier BV]
日期:2017-04-01
卷期号:97: 130-138
被引量:50
标识
DOI:10.1016/j.bone.2017.01.014
摘要
Osteoporosis is a serious health problem worldwide. MicroRNA is a post-transcriptional regulator of gene expression by either promoting mRNA degradation or interfering with mRNA translation of specific target genes. It plays a significant role in the pathogenesis of osteoporosis. Here, we first demonstrated that miR-106b (miR-106b-5p) negatively regulated osteogenic differentiation of mesenchymal stem cells in vitro. Then, we found that miR-106b expression increased in C57BL/6 mice with glucocorticoid-induced osteoporosis (GIOP), and that silencing of miR-106b signaling protected mice against GIOP through promoting bone formation and inhibiting bone resorption. At last, we showed that miR-106b inhibited osteoblastic differentiation and bone formation partly through directly targeting bone morphogenetic protein 2 (BMP2) both in vitro and in the GIOP model. Together, our findings have identified the role and mechanism of miR-106b in negatively regulating osteogenesis. Inhibition of miR-106b might be a potential new strategy for treating osteoporosis and bone defects.
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