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首页> 外文期刊>BMC Neuroscience >ATF3 upregulation in glia during Wallerian degeneration: differential expression in peripheral nerves and CNS white matter
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ATF3 upregulation in glia during Wallerian degeneration: differential expression in peripheral nerves and CNS white matter

机译：沃勒氏变性期间胶质细胞中的ATF3上调：外周神经和中枢神经系统白质的差异表达

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Background Many changes in gene expression occur in distal stumps of injured nerves but the transcriptional control of these events is poorly understood. We have examined the expression of the transcription factors ATF3 and c-Jun by non-neuronal cells during Wallerian degeneration following injury to sciatic nerves, dorsal roots and optic nerves of rats and mice, using immunohistochemistry and in situ hybridization. Results Following sciatic nerve injury – transection or transection and reanastomosis – ATF3 was strongly upregulated by endoneurial, but not perineurial cells, of the distal stumps of the nerves by 1 day post operation (dpo) and remained strongly expressed in the endoneurium at 30 dpo when axonal regeneration was prevented. Most ATF3+ cells were immunoreactive for the Schwann cell marker, S100. When the nerve was transected and reanastomosed, allowing regeneration of axons, most ATF3 expression had been downregulated by 30 dpo. ATF3 expression was weaker in the proximal stumps of the injured nerves than in the distal stumps and present in fewer cells at all times after injury. ATF3 was upregulated by endoneurial cells in the distal stumps of injured neonatal rat sciatic nerves, but more weakly than in adult animals. ATF3 expression in transected sciatic nerves of mice was similar to that in rats. Following dorsal root injury in adult rats, ATF3 was upregulated in the part of the root between the lesion and the spinal cord (containing Schwann cells), beginning at 1 dpo, but not in the dorsal root entry zone or in the degenerating dorsal column of the spinal cord. Following optic nerve crush in adult rats, ATF3 was found in some cells at the injury site and small numbers of cells within the optic nerve displayed weak immunoreactivity. The pattern of expression of c-Jun in all types of nerve injury was similar to that of ATF3. Conclusion These findings raise the possibility that ATF3/c-Jun heterodimers may play a role in regulating changes in gene expression necessary for preparing the distal segments of injured peripheral nerves for axonal regeneration. The absence of the ATF3 and c-Jun from CNS glia during Wallerian degeneration may limit their ability to support regeneration.
机译：背景技术基因表达的许多变化发生在受损神经的远端残端，但是对这些事件的转录控制了解甚少。我们已经通过免疫组织化学和原位杂交技术检测了大鼠和小鼠坐骨神经，背根和视神经受到损伤后，在Wallerian变性过程中非神经元细胞转录因子ATF3和c-Jun的表达。结果坐骨神经损伤后-横断或横断再吻合-术后1天（dpo），神经远端残端的神经内膜，但不是神经周细胞强烈上调了ATF3，当30 dpo时，其在神经内膜中强烈表达防止了轴突再生。大多数ATF3 +细胞对Schwann细胞标记物S100具有免疫反应性。当神经被横断并重新吻合，允许轴突再生时，大多数ATF3表达已被30 dpo下调。在受伤的神经的近端残端中，ATF3表达较远端的残端弱，并且在受伤后的所有时间中均存在较少的细胞。受损新生鼠坐骨神经末梢残端中的神经内膜细胞可上调ATF3，但比成年动物弱。小鼠坐骨神经横切中的ATF3表达与大鼠相似。成年大鼠背根损伤后，ATF3在病变和脊髓之间的根部（包含雪旺氏细胞）上调，从1 dpo开始，但不在背根进入区或退化的背柱中脊髓。成年大鼠视神经受到挤压后，在损伤部位的一些细胞中发现了ATF3，视神经内的少量细胞显示出弱的免疫反应性。在所有类型的神经损伤中，c-Jun的表达方式与ATF3类似。结论这些发现增加了ATF3 / c-Jun异二聚体可能在调节基因表达变化中发挥作用的可能性，这些基因表达是为受伤的周围神经的远端节段准备轴突再生所必需的。在Wallerian变性期间，CNS胶质细胞缺乏ATF3和c-Jun可能会限制它们支持再生的能力。

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