周围神经损伤后能否实现成功再生很大程度上取决于是否具备适合轴突生长的再生微环境，Sema3A是再生微环境中的神经营养因子家族成员，通过影响下游效应分子CRMP1的磷酸化调节轴突生长及导向。本课题组发现一个调节细胞周期进程、凋亡、分化等重要功能的分子Spy1与CRMP1相互作用。进一步研究发现，Spy1可以调节CRMP1的磷酸化，并影响神经元突起生长。鉴于此，提出Spy1通过影响CRMP1的磷酸化修饰，从而参与Sema3A信号通路对周围神经轴突再生调节的假说。本课题拟首先研究Spy1和CRMP1与周围神经损伤再生的关系，接着在体外探讨Spy1对CRMP1的调节机制，以及该调节通路在神经元突起生长、生长锥塌陷中的作用，最后回到整体模型，分析Spy1/CRMP1调控通路在周围神经再生中的意义。本课题从再生微环境信号通路调节的角度，探讨周围神经损伤再生的分子机制，为寻找新药物治疗靶点提供理论依据。

Whether the injuried nerves could regenerate or not mainly dependens on the regenerate microenvironment they are living in. Sema3A is a member of neurotrophic factor family existing in regeneration microenvironment. Sema3A could induce the effect of axon guidance and the development of dendritic ridge, which play an important role in the formation of the connections between the neurons.CRMP1 is main downstream effector molecule in Sema3A signaling pathways. Spy1 is considered to be one of the important function genes and plays a role in the process of cell cycle regulation, apoptosis, differentiation and other envents. Our early research found that Spy1 could interact with CRMP1 and regulate the phosphorylation of CRMP1, which is involved in the regulation of repaired and developed nervous system. So our study will would concentrate on the mechanism of Spy1 regulating the phosphorylation of CRMP1, searching for the kinase participating in it and further exploring its function in the repair of peripheral nerve injury. Our study aims at exploring the molecular mechanism of regeneration of peripheral nerve injury from the view of signal pathway transduction in regenerate microenvironment and further could provid new theoretical basis for the looking for specific drug therapeutic targets.