Janus激酶/信号转导与转录激活子(JAK/STAT) 途径参与多种细胞的增殖、分化、凋亡以及免疫调节等过程，影响成骨、破骨细胞功能和骨组织再生，并可促进创伤局部血管生成。然而其在成骨细胞与破骨细胞相互作用中的机制尚不清楚。本项目拟通过对成骨细胞系与原代破骨细胞进行信号通路研究，明确该信号通路在成骨细胞分化中的调控机制；然后进行体外成、破骨细胞共培养，检测细胞在JAK2-STAT3信号通路介导下的细胞间相互作用及其功能改变；通过构建下颌骨骨折动物模型，利用转染后细胞移植，在体内检测通路激活条件下对骨痂内成骨、破骨细胞功能的影响。本项目应用SiRNA、非损伤微测技术和量子点等技术，多角度阐明JAK2-STAT3在成骨细胞与破骨细胞相互作用中的调控机制，为其在促进下颌骨骨折修复重建中的应用提供理论依据。

Janus kinase / signal transducer and activator of transcription (JAK / STAT) pathway is widely involved in cell proliferation, differentiation, apoptosis and immune regulation process, it plays an important roles in many different ways, such as the function of osteoclasts and osteoblasts, the bone tissue regeneration and post-trauma angiogenesis. However, the regulation mechanism of JAK2-STAT3 signaling pathway during the interaction between osteoblasts and osteoclasts remains unclear. In this project ,we want to make clear of the regulation effect of JAK2 - STAT3 signaling pathways in osteoblast differentiation and mineralization through the study of signaling pathways in osteogenesis of the preosteoblast cell line and the primary culture of osteoclasts; then through the co-culture of osteoclasts and osteoblasts to detecte the JAK2-STAT3 pathway mediated intercellular effects; then utilize the animal model of the mandibular fracture combines with the transplantation of transfected cells to detect the effects on fracture healing, osteoblasts and osteoclast functions. This research project is aimed to clarify the regulation mechanism of JAK2-STAT3 signaling pathway during the interaction between osteoblasts and osteoclasts,by applying SiRNA, non-invasive measurement techniques and micro-technologies such as quantum dots etc. To provide the theory basis for applications of mandibular fractures healing.