经典的组织工程骨（TEB）为大段骨缺损修复带来希望，但受种子细胞扩增周期长、伦理等限制；选择性细胞滞留（SCR）技术可将种子细胞、支架、生长因子等关键成份快速整合，实现TEB快速构建。内源性MSC募集和归巢是受损组织修复的重要机制，而其如何被募集到TEB是研究的关键。前期研究发现，PDGF-BB与MSC的PKC、核受体NR4A1、转录因子SP1的表达高度相关。提出，PDGF-BB可能结合MSC膜β受体后，致胞浆Ca2+ 升高，激活的PKC通过NR4A1/SP1调控细胞骨架 F-actin，调动MSC向锚着点迁移，促进骨修复。藉此，可望通过靶分子激活/阻断等明确通路的关键环节；拟采用siRNA技术验证复合体对MSC迁移的直接作用；在体内用免疫印迹等印证通路关键分子的表达，并观察对成骨效果的影响。本项目通过阐明外源性PDGF-BB激活内源性MSC迁移的信号通路，为TEB的快速构建提供实验基础。

Classic tissue engineered-bone (TEB) brings the hope for the repair of large bone defect, however, it is restricted due to the long amplification cycle of seed cells and Ethics. Selective cell retention (SCR) technology can construct TEB rapidly for its integration of components including of the seed cells, scaffolds, and growth factors and so on. The recruitment and homing of endogenous MSCs play an important role for damaged tissue, however, the key of research is, how they are recruited to TEB? Our preliminary study found that the high relevance of exogenous PDGF-BB among PKC, nuclear receptor NR4A1, transcription factor SP1 for MSCs migration. According to the study of the professional fields, we propose that PDGF-BB could bind to receptors β in the membrane surface of MSCs, increasing the Ca2+ concentration of cytosolic, and activation of PKC regulate the cytoskeletal F-actin of MSCs through NR4A1/SP1 complex, and mobilize the migration of MSCs to the anchor area for ossification. In this way, we will identify the key bit of signal pathway by the activation and inhibition of target molecule, and validate the direct regulation of NR4A1/SP1 complex for migration of MSCs by siRNA technology, and confirm the expression of key molecules in the signal pathway in vivo by Western blot and other methods, and further observe its efficacy on post-osteogenic. This research will provide experimental basis for the rapid construction of TEB by the signal pathways of PDGF-BB activated migration for endogenous MSCs.