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Axon injury induced endoplasmic reticulum stress and neurodegeneration

Axon injury induced endoplasmic reticulum stress and neurodegeneration

作     者:Yang Hu 

作者机构:Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation) Temple University School of Medicine 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2016年第11卷第10期

页      面:1557-1559页

核心收录:

学科分类:1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基  金:supported by grants from National Eye Institute(R01EY023295,R01EY024932) BrightF ocus Foundation(G2013046) National Multiple Sclerosis Society(RG 5021A1)to YH 

主  题:endoplasmic reticulum stress axonopathy retinal ganglion cell optic nerve neurodegeneration CHOP XBP-1 

摘      要:Injury to central nervous system axons is a common early characteristic of neurodegenerative diseases. Depending on its location and the type of neuron, axon injury often leads to axon degeneration, retrograde neuronal cell death and progressive permanent loss of vital neuronal functions. Although these sequential events are clearly connected, ample evidence indicates that neuronal soma and axon degenerations are active autonomous processes with distinct molecular mechanisms. By exploiting the anatomical and techni- cal advantages of the retinal ganglion cell (RGC)/optic nerve (ON) system, we demonstrated that inhibition of the PERK-eIF2a-CHOP pathway and activation of the X-box binding protein 1 pathway synergistically protect RGC soma and axon, and preserve visual function, in both acute ON traumatic injury and chronic glaucomatous neuropathy. The autonomous endoplasmic reticulum (ER) stress pathway in neurons has been implicated in several other neurodegenerative diseases. In addition to the emerging role of ER mor- phology in axon maintenance, we propose that ER stress is a common upstream signal for disturbances in axon integrity, and that it leads to a retrograde signal that can subsequently induce neuronal soma death. Therefore manipulation of the ER stress pathway may be a key step toward developing the effective neuro- protectants that are greatly needed in the clinic.

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