Acute spinal cord injury could cause activation of autophagy in dorsal root ganglia

Hou, Hongping; Zhang, L; Liu, D; Xiong, Qi; Du, Hongwei; Tang, Peifu

doi:10.1038/sc.2013.52

Cited by 17 publications

(17 citation statements)

References 29 publications

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“…The process of autophagy in Schwann cells is also disrupted after peripheral nerve injury [10]. The activation of autophagy in DRG can be induced by acute spinal cord injury [19]. Here we show that LC3-II was upregulated in DRG after SNL, and a few LC3-II fluorescent puncta in neurons were observed after SNL.…”

Section: Accumulation Of Autophagic Marker In L5 Drg Following Snlmentioning

confidence: 88%

Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury

Guo

Jing

Wang

et al. 2015

Neuroscience Letters

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Section: Accumulation Of Autophagic Marker In L5 Drg Following Snlmentioning

confidence: 88%

Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury

Guo

Jing

Wang

et al. 2015

Neuroscience Letters

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“…57–60 In addition, autophagy is induced after axonal damage in order to halt axonal degeneration. 61 , 62 Therefore, the impaired ability of CMT2B-causing RAB7 mutant proteins to induce autophagy could limit this important neuroprotective mechanism and, in the long term, support the establishment of CMT2B disease.…”

Section: Discussionmentioning

confidence: 99%

Alterations of autophagy in the peripheral neuropathy Charcot-Marie-Tooth type 2B

et al. 2018

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Charcot-Marie-Tooth type 2B (CMT2B) disease is a dominant axonal peripheral neuropathy caused by 5 mutations in the RAB7A gene, a ubiquitously expressed GTPase controlling late endocytic trafficking. In neurons, RAB7A also controls neuronal-specific processes such as NTF (neurotrophin) trafficking and signaling, neurite outgrowth and neuronal migration. Given the involvement of macroautophagy/autophagy in several neurodegenerative diseases and considering that RAB7A is fundamental for autophagosome maturation, we investigated whether CMT2B-causing mutants affect the ability of this gene to regulate autophagy. In HeLa cells, we observed a reduced localization of all CMT2B-causing RAB7A mutants on autophagic compartments. Furthermore, compared to expression of RAB7AWT, expression of these mutants caused a reduced autophagic flux, similar to what happens in cells expressing the dominant negative RAB7AT22N mutant. Consistently, both basal and starvation-induced autophagy were strongly inhibited in skin fibroblasts from a CMT2B patient carrying the RAB7AV162M mutation, suggesting that alteration of the autophagic flux could be responsible for neurodegeneration.

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“…Increased markers of autophagy have also been observed in SCI models ( 27 , 28 , 55 , 60 ). Most reports describe concomitant accumulation of both LC3-II and SQSTM1 after injury, suggesting more uniform inhibition of autophagy flux.…”

Section: Autophagy and Autophagy Flux After Cns Traumamentioning

confidence: 91%

Function and Mechanisms of Autophagy in Brain and Spinal Cord Trauma

Lipinski

Faden

et al. 2015

Antioxidants & Redox Signaling

162

129

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Significance: Traumatic brain injury (TBI) and spinal cord injury (SCI) are major causes of death and long-term disability worldwide. Despite important pathophysiological differences between these disorders, in many respects, mechanisms of injury are similar. During both TBI and SCI, some cells are directly mechanically injured, but more die as a result of injury-induced biochemical changes (secondary injury). Autophagy, a lysosome-dependent cellular degradation pathway with neuroprotective properties, has been implicated both clinically and experimentally in the delayed response to TBI and SCI. However, until recently, its mechanisms and function remained unknown, reflecting in part the difficulty of isolating autophagic processes from ongoing cell death and other cellular events. Recent Advances: Emerging data suggest that depending on the location and severity of traumatic injury, autophagy flux—defined as the progress of cargo through the autophagy system and leading to its degradation—may be either increased or decreased after central nervous system trauma. Critical Issues: While increased autophagy flux may be protective after mild injury, after more severe trauma inhibition of autophagy flux may contribute to neuronal cell death, indicating disruption of autophagy as a part of the secondary injury mechanism. Future Directions: Augmentation and/or restoration of autophagy flux may provide a potential therapeutic target for treatment of TBI and SCI. Development of those treatments will require thorough characterization of changes in autophagy flux, its mechanisms and function over time after injury. Antioxid. Redox Signal. 23, 565–577.

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Acute spinal cord injury could cause activation of autophagy in dorsal root ganglia

Cited by 17 publications

References 29 publications

Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury

Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury

Alterations of autophagy in the peripheral neuropathy Charcot-Marie-Tooth type 2B

Function and Mechanisms of Autophagy in Brain and Spinal Cord Trauma

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