本课题以促进下颌骨牵张成骨（DO）新骨形成为研究目标，以明确microRNA-26a-5p (miR-26a-5p)在牵张成骨中的力学信号作用机制为研究核心，建立下颌骨牵张成骨动物模型，将调节miR-26a-5p功能的慢病毒载体转染入 BMSCs后分别导入牵张区，研究上调和下调miR-26a-5p后Wnt5a、非经典Wnt途径关键分子及成骨特异基因在DO成骨进程中的表达变化，从而明确miR-26a-5p对新骨形成的影响及其参与成骨的力学转导模式。此外，本研究建立了体外模拟DO应力环境的细胞力学刺激系统，将转染miR-26a-5p后的BMSCs置于该系统中进行张应力刺激，探讨miR-26a-5p在外施加力学刺激中对BMSCs骨向分化的分子调控机制，研究其力学信号传导作用机制，并对上述动物实验的结果进行验证，同时为深入认识miR-26a-5p在牵张成骨治疗中的促成骨作用奠定细胞力学实验基础。

The aim of this project is to promote the new bone formation in mandibular distraction osteogenesis(DO), and the key research point in this study is to investigate the mechanism of microRNA-26a-5p(miR-26a-5p) as mechanical signal transmission molecular in DO. Based on our previous works, the animal models of DO is established, and we transfect Lv-miR-26a-5p、Lv-miR-NC、Lv-ASO-26a-5p or Lv-ASO-NC into BMSCs respectively in vitro, and then we deliver these BMSCs into distraction gap respectively. After down-regulated or up-regulated the expression of miR-26a-5p,we investigate the expressions of Wnt5a、 representative molecules of non-canonical Wnt and osteogenic genes during distraction osteogenesis, and we want to understand the definite mechanical signal transmission mechanisms of miR-26a-5p in distraction osteogenesis through above works. In addition, in this study, a cellular mechanical stimulation apparatus which could simulate biomechanic environment of DO is established. The miR-26a-5p transfected BMSCs are loaded respectively by tension in this cellular mechanical stimulation apparatus , and the miR-26a-5p、Wnt5a and its downstream genes are investigated too, we hope that the results of the cell biomechanic test could verify that of animal experiment. In general, in this project, all the above works help us to understand the effects on new bone formation and the roles in mechanical signal transmission of miR-26a-5p targeting Wnt5a during distraction osteogenesis process.