| Literature DB >> 28108317 |
Ke Liu1, Ying Jing2, Wen Zhang1, Xuejie Fu1, Huan Zhao1, Xichao Zhou1, Yunxia Tao1, Huilin Yang1, Yan Zhang3, Ke Zen2, Chenyu Zhang4, Donghai Li5, Qin Shi6.
Abstract
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.Entities:
Keywords: BMP2; Glucocorticoid-induced osteoporosis; Mesenchymal stem cells; Osteogenesis; miR-106b
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Year: 2017 PMID: 28108317 DOI: 10.1016/j.bone.2017.01.014
Source DB: PubMed Journal: Bone ISSN: 1873-2763 Impact factor: 4.398