Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK.
Neuron. 2012 Aug 23;75(4):633-47. doi: 10.1016/j.neuron.2012.06.021.
The radical response of peripheral nerves to injury (Wallerian degeneration) is the cornerstone of nerve repair. We show that activation of the transcription factor c-Jun in Schwann cells is a global regulator of Wallerian degeneration. c-Jun governs major aspects of the injury response, determines the expression of trophic factors, adhesion molecules, the formation of regeneration tracks and myelin clearance and controls the distinctive regenerative potential of peripheral nerves. A key function of c-Jun is the activation of a repair program in Schwann cells and the creation of a cell specialized to support regeneration. We show that absence of c-Jun results in the formation of a dysfunctional repair cell, striking failure of functional recovery, and neuronal death. We conclude that a single glial transcription factor is essential for restoration of damaged nerves, acting to control the transdifferentiation of myelin and Remak Schwann cells to dedicated repair cells in damaged tissue.
周围神经对损伤(Wallerian 变性)的激进反应是神经修复的基石。我们表明,施万细胞中转录因子 c-Jun 的激活是 Wallerian 变性的全局调节剂。c-Jun 控制着损伤反应的主要方面,决定了营养因子、粘附分子的表达、再生轨迹的形成和髓鞘清除,并控制着周围神经独特的再生潜力。c-Jun 的一个关键功能是激活施万细胞中的修复程序,并创建专门支持再生的细胞。我们表明,c-Jun 的缺失会导致形成功能失调的修复细胞,导致功能恢复明显失败和神经元死亡。我们得出结论,单一的神经胶质转录因子对于受损神经的恢复是必不可少的,它可以控制髓鞘和 Remak 施万细胞向受损组织中专门的修复细胞的转分化。