MicroRNA-25-3p regulates osteoclasts through nuclear factor I X
MicroRNA-25-3p regulates osteoclasts through nuclear factor I X
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MicroRNA-25-3p通过核因子I X调节破骨细胞
DOI：
10.1016/j.bbrc.2019.11.043
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发表时间：
2020-01-29
影响因子：
3.1
通讯作者：
Ma, Jianjun
中科院分区：
文献类型：
--
作者：
Huang, Yizhen;Ren, Keyi;Ma, Jianjun
骨质疏松症是一种骨代谢疾病，其特征是骨密度降低导致骨折。其发病率随年龄增长而增加，并影响患者的生活质量。尽管破骨细胞在骨质疏松症中发挥着重要作用，但其潜在的调控机制仍不清楚。在本研究中，我们发现microRNA(MiR)-25-3p通过核因子I X(NFIX)负向调节破骨细胞的功能。NFIX的过表达促进了破骨细胞的增殖，增加了破骨细胞分化和活性标志物酒石酸抗性酸性磷酸酶和组织蛋白酶K的表达，Mir-25-3p的过表达抑制了NFIX的表达，进而抑制了破骨细胞的增殖。总之，我们的结果表明miR-25-3p通过调节NFIX的表达来促进破骨细胞的活性。因此，在破骨细胞中靶向miR-25-3p可能是治疗骨形成减少的骨骼疾病的一种有前途的策略。(C)2019年提交人。由爱思唯尔公司出版。
Osteoporosis is a bone metabolic disease, characterized by loss of bone density leading to fractures. Its incidence increases with age and affects patient quality of life. Although osteoclasts play a significant role in osteoporosis, their underlying regulatory mechanisms remain unclear. In this study, we found that microRNA (miR)-25-3p negatively regulates osteoclast function through nuclear factor I X (NFIX). Overexpression of NFIX promoted osteoclast proliferation and increased the expression of the osteoclast differentiation and activity markers tartrate-resistant acid phosphatase and cathepsin K. MiR-25-3p transfection inhibited NFIX expression, which in turn inhibited osteoclast proliferation. Collectively, our results suggest that miR-25-3p promotes osteoclast activity by regulating the expression of NFIX. Therefore, targeting miR-25-3p in osteoclasts could be a promising strategy for treating skeletal disorders involving reduced bone formation. (C) 2019 The Authors. Published by Elsevier Inc.