Klinik für Anästhesiologie, Universitätsmedizin Mainz, 55131 Mainz, Germany.
Cell Tissue Res. 2012 Jul;349(1):39-48. doi: 10.1007/s00441-012-1345-4. Epub 2012 Feb 28.
The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during the last few decades has identified axon sprouting as an anatomical correlate for the regenerative capability of the CNS to establish new connections. The immunoglobulin superfamily member L1CAM has been shown to promote the capability of neurons for regenerative axon sprouting and to improve behavioral outcomes after CNS injury. Here, we discuss the cell-autonomous role of L1CAM for axon sprouting in experimental rodent injury models and highlight the molecular interactions of L1CAM with ankyrins, ezrin-radixin-moesin proteins and the Sema3A/Neuropilin ligand-receptor complex in the context of axonal branching.
中枢神经系统（CNS）传统上被认为是一种在受伤时无法再生的器官。事实上，受损的中枢神经系统在再生过程中面临着许多障碍，包括轴突再生的整体非许可环境。然而，在过去几十年的研究中，已经确定轴突发芽是中枢神经系统建立新连接的再生能力的解剖学相关物。免疫球蛋白超家族成员 L1CAM 已被证明可促进神经元再生性轴突发芽的能力，并改善中枢神经系统损伤后的行为结果。在这里，我们讨论了 L1CAM 在实验性啮齿动物损伤模型中对轴突发芽的细胞自主作用，并强调了 L1CAM 与锚蛋白、埃兹蛋白-根蛋白-肌球蛋白和 Sema3A/神经纤毛蛋白配体-受体复合物在轴突分支中的分子相互作用。
