内皮祖细胞(EPCs)可分泌多种细胞因子募集和分化破骨细胞前体(OPC)，加速组织工程骨（TEB）髓腔再通，促进新生骨改建塑形。前期实验发现，体外与EPCs共培养时，OPC高表达Talin-1，而Talin-1作为趋化细胞骨架蛋白已被证实对破骨细胞粘附、聚集、破骨功能至关重要。干扰EPCs的TGF-β1表达则不能有效诱导破骨细胞募集分化。推测EPCs通过TGF-β1调控宿主OPC高表达Talin-1在修复区募集分化，加速骨愈合过程髓腔再通。基于此，课题组拟模拟体内环境，将TGF-β1不同表达状态的EPCs与宿主单核巨噬细胞共培养，检测其信号通路变化及Talin-1表达情况；利用在体TEB模型，观察对破骨相关细胞向TEB迁移的影响；探索TGF-β1信号对所募集破骨细胞前体Talin-1表达的作用机制。可望通过本研究验证上述假说，为EPCs更好地在TEB中应用提供理论基础。

Endothelial progenitor cells (EPCs) secret a variety of cytokines to regulate recruitment and differentiation of osteoclast precursors (OPC), which can accelerate recanalization of the marrow cavity of tissue engineered bone (TEB), promoting the new bone's restruction. It has been confirmed that Talin-1 is Critical for osteoclast adhesion, aggregation, and resorption. In preliminary experiments, we found that Talin-1 high expression in OPC when co-cultured with EPCs in vitro. Interference EPCs TGF-β1 expression can not be effectively induce osteoclast recruitment and differentiation. Therefore, we speculate that EPCs regulate Talin-1 of the host OPC hight expression to promote OPC recruition and differentiation in bone repair area, accelerate osteolytic in the front end of healing bone and medullary cavity recanalization .Based on this hypothesis, we plan to simulate the environment in vivo, mononuclear-macrophages co-culture with EPCs, which's TGF-β1 expression is different. Then, detect the changes of Talin-1 expression and the signal path in macrophages. In vivo，using TEB model to observate the variations of osteoclasts migration. Try to analyze the mechanisms in the signal pathway of TGF-β1 regulating OPC expression Talin-1. We hope that this study would verify the hypothesis, broaden EPCs biology research，provide the theory for applications of EPCs in TEB better.