在张应力作用下，牙周膜细胞的凋亡机制研究一直是困扰大家的一个难题。我们前期已研究表明周期性张应力可以激活Rho GDIα /caspase-3/ PARP信号通路引起细胞凋亡，那么其他的Rho GTPases是否参与其中，是通过哪些不同的信号通路调节的有待进一步研究。本项目拟采用 Flexcell 细胞应力加载系统建立人牙周膜细胞体外培养－力学刺激模型，观察细胞凋亡形态和凋亡率；应用 Western blotting 检测Rho GTPases ( RhoA, Rac, Cdc42等)及下游可能的作用蛋白(MEK1/2/ERK1/2, MEK5/ERK5, Bad, Bim, caspases-3, caspases-8等)的表达；应用RNA干扰和构建高表达载体质粒转染技术，探讨Rho GTPases调节周期性张应力诱导牙周膜细胞凋亡的信号机制，具有学科交叉的特色与创新。

Under stress, the study of the mechanism of apoptosis of periodontal ligament cells is always a difficult problem for everyone. Our previous studies showed that cyclic strain can induce apoptosis through Rho GDIα /caspase-3/ PARP signaling pathway, then whether other Rho GTPases involved, through which different signaling pathways remained to be further studied. This project using Flexcell strain loading system, intends to establish mechanical stimulation models of periodontal ligament cells in vitro to observe the morphological changes of apoptotic cells and apoptotic rate. Western blotting will be used to detect Rho GTPases expression(RhoA, Rac, Cdc42, etc.) and downstream possible role protein expression(MEK1/2/ERK1/2, MEK5/ERK5, Bad, Bim, caspases-3, caspases-8, etc.); RNA interference and the construction of high expression vector plasmid transfection technology will be used to investigate the signaling mechanism of Rho GTPases in regulation of apoptosis of periodontal ligament cells induced by cyclic strain with the characteristic and innovation of interdisciplinary.