Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity.

Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity.
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损伤介导的神经元树突可塑性的转录和表观遗传调控。

DOI:
10.1007/s12264-016-0071-4
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发表时间:
2017
期刊:
Neurosci Bull
影响因子:
--
通讯作者:
Deng Ling-Xiao
Deng Ling-Xiao
中科院分区:
其他
文献类型:
--
作者:
Wang Ying;Li Wen-Yuan;Li Zhi-Gang;Guan Li-Xin;Deng Ling-Xiao

文献摘要

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神经系统损伤会导致神经结构的局部损伤和原发性损伤引起的神经元死亡,以及神经元间通讯所需的精致树枝状区域的延迟萎缩和可塑性受损。兴奋性毒性和其他继发性生化事件有助于损伤后神经元的形态学变化。有证据表明,各种转录因子参与树突状细胞对损伤的反应和潜在的治疗。转录因子在神经元形态可塑性、树突生长和形成的细胞内调节中起着关键作用。越来越多的证据支持表观遗传修饰的关键作用,通过组蛋白去乙酰化酶,组蛋白乙酰转移酶,DNA甲基转移酶,修改基因表达在神经元损伤和修复过程。通过表观遗传修饰的基因调控在神经创伤研究中引起了极大的兴趣,并且关于损伤如何触发调节这种反应的细胞内事件的早期图片开始出现。本文综述了损伤介导的影响转录调控通过表观遗传修饰,细胞内过程中参与的形态学后果的这种变化,和潜在的方法来治疗操纵神经元表观遗传学调节基因表达,以促进生长和信号通过树突状树枝化损伤后。
Injury to the nervous system induces localized damage in neural structures and neuronal death through the primary insult, as well as delayed atrophy and impaired plasticity of the delicate dendritic fields necessary for interneuronal communication. Excitotoxicity and other secondary biochemical events contribute to morphological changes in neurons following injury. Evidence suggests that various transcription factors are involved in the dendritic response to injury and potential therapies. Transcription factors play critical roles in the intracellular regulation of neuronal morphological plasticity and dendritic growth and patterning. Mounting evidence supports a crucial role for epigenetic modificationsviahistone deacetylases, histone acetyltransferases, and DNA methyltransferases that modify gene expression in neuronal injury and repair processes. Gene regulation through epigenetic modification is of great interest in neurotrauma research, and an early picture is beginning to emerge concerning how injury triggers intracellular events that modulate such responses. This review provides an overview of injury-mediated influences on transcriptional regulation through epigenetic modification, the intracellular processes involved in the morphological consequences of such changes, and potential approaches to the therapeutic manipulation of neuronal epigenetics for regulating gene expression to facilitate growth and signaling through dendritic arborization following injury.