Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, China; Medical College of Zhejiang University, Hangzhou, China.
Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, China.
Biochem Biophys Res Commun. 2020 Jan 29;522(1):74-80. doi: 10.1016/j.bbrc.2019.11.043. Epub 2019 Nov 15.
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.
骨质疏松症是一种骨代谢疾病，其特征是骨密度丧失导致骨折。它的发病率随着年龄的增长而增加，并影响患者的生活质量。虽然破骨细胞在骨质疏松症中起着重要作用，但它们的潜在调节机制尚不清楚。在这项研究中，我们发现 microRNA（miR）-25-3p 通过核因子 I X（NFIX）负调控破骨细胞功能。NFIX 的过表达促进破骨细胞增殖，并增加破骨细胞分化和活性标志物抗酒石酸酸性磷酸酶和组织蛋白酶 K 的表达。miR-25-3p 转染抑制 NFIX 的表达，进而抑制破骨细胞的增殖。总之，我们的结果表明，miR-25-3p 通过调节 NFIX 的表达促进破骨细胞的活性。因此，针对破骨细胞中的 miR-25-3p 可能是治疗涉及骨形成减少的骨骼疾病的一种有前途的策略。
