中文摘要：

髓鞘抑制因子Nogo-A、MAG和OMgp通过共同的受体信号复合物NgR／p75^NTR（或者TROY）发挥对中枢神经纤维再生的抑制作用．新近克隆的跨膜蛋白LINGO-1是该信号途径的另一个重要组成成分和调节分子．LINGO-1特异表达于中枢神经系统，神经元上的LINGO-1被证明参与调节中枢神经再生的抑制信号，而少突胶质细胞表达的LINGO-1分子参与负调节少突胶质细胞的髓鞘化过程．为探讨LINGO-1分子在神经元凋亡过程中的作用，利用包含LINGO-1分子胞外段LRR和IgC2结构域的Fc融合蛋白作为功能性拮抗剂，研究LINGO-1对低钾诱导的小脑颗粒神经元凋亡的保护作用．利用成熟的Hoechst标记凋亡细胞的方法，观察到经LINGO-1-Fc蛋白预处理2h能够显著阻止小脑颗粒神经元的凋亡．仅包括LRR结构域的GST-LINGO-1与LINGO-1-Fc蛋白，虽同样具有与颗粒神经元的结合活性，但是GST-LINGO-1不能有效地阻止低钾诱导的细胞凋亡．这些结果提示，LINGO-1-Fc蛋白能够阻止低钾诱导的小脑颗粒神经元凋亡，并且这种作用可能是IgC2结构域依赖的．

英文摘要：

Three myelin proteins, Nogo-A, MAG and OMgp, transduce their neurite-outgrowth inhibitory signal through a common receptor complex： NgR/ p75^NTR （or TROY）. Recently, LINGO-1 is identified as another essential component and regulator for the Nogo-66 receptor/p75 signaling complex. LINGO-1 is restricted to express in CNS, neuronal LINGO-1 is shown to be involved in the signal transduction from three myelin proteins, and Lingo-1 in oligodendrocyte negatively regulates the differentiation and myelination of oligodendrocyte. To investigate the potential activity of LINGO-1 in neuronal apoptosis, LINGO-1-Fc fusion protein including the extracellular LRR and IgC2 domain, was used as functional antagonist to study its protective effect on low-potassium induced apoptosis of cerebellar granule neurons （CGNs）. In judgement of the apoptotic nuclei stained by Hoechst, LINGO-1-Fc pretreatment for 2 h significantly prevents apoptosis of CGNs. Although GST-LINGO-1 protein, including the LRR domain, binds to the CGN cultures in the same way with LINGO-1-Fc, it doesn＇t prevent the apoptosis of CGNs. These results indicate that LINGO-1-Fc fusion protein prevents low-potassium induced apoptosis of cerebellar granule neurons in certain conditions and this activity is probably IgC2 domain dependent.