Park J, Wada S, Ushida T, Akimoto T
Division of Regenerative Medical Engineering, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo, Japan.
Physiol Res. 2015;64(5):711-9. doi: 10.33549/physiolres.932901. Epub 2015 Mar 24.
Recent studies have demonstrated that some microRNAs (miRNAs) inhibit bone formation by inhibiting the translation of specific genes. Several in vitro studies have suggested that miR-23a inhibits osteogenic differentiation by suppressing the translation of Runx2, a transcription factor essential for osteoblastogenesis, and of Satb2, a member of the special AT-rich binding protein family. In the present study, we used a gain-of-function approach to determine the roles of miR-23a in bone formation and homeostasis in vivo. The miR-23a transgenic (Tg) mice grew normally and their body size and weight were similar to those of wild-type (WT) littermates. Bone structure and morphology were similar in Tg and WT mice. Furthermore, the numbers of osteoblasts and osteoclasts, as well as their activities in bone were similar between Tg and WT mice. Our results indicate that miR-23 has limited roles in bone formation and maintenance in vivo in mice.
近期研究表明,一些微小RNA(miRNA)通过抑制特定基因的翻译来抑制骨形成。多项体外研究提示,miR-23a通过抑制Runx2(成骨细胞生成所必需的转录因子)和Satb2(富含AT的特殊结合蛋白家族成员)的翻译来抑制成骨分化。在本研究中,我们采用功能获得性方法来确定miR-23a在体内骨形成和骨稳态中的作用。miR-23a转基因(Tg)小鼠生长正常,其体型和体重与野生型(WT)同窝小鼠相似。Tg小鼠和WT小鼠的骨结构和形态相似。此外,Tg小鼠和WT小鼠之间的成骨细胞和破骨细胞数量及其在骨中的活性也相似。我们的结果表明,miR-23在小鼠体内骨形成和维持中的作用有限。