Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity

被引:0
|
作者
Ying Wang [1 ]
Wen-Yuan Li [1 ]
Zhi-Gang Li [2 ]
Li-Xin Guan [3 ]
Ling-Xiao Deng [4 ]
机构
[1] Department of Anatomy,Mudanjiang College of Medicine
[2] Department of General Surgery,First Affiliated Hospital of Mudanjiang College of Medicine
[3] Department of Pharmacy,Mudanjiang College of Medicine
[4] Spinal Cord and Brain Injury Research Group,Stark Neurosciences Research Institute,Indiana University School of Medicine
基金
中国国家自然科学基金;
关键词
Nervous system injury; Dendrite plasticity; Transcription factors; Epigenetics;
D O I
暂无
中图分类号
R741 [神经病学];
学科分类号
1002 ;
摘要
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 modifications via histone 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.
引用
收藏
页码:85 / 94
页数:10
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