Advances in Axon Degeneration and Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 7765

Special Issue Editors


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Guest Editor
1. Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Baldiri Reixac 15-21, E-08028 Barcelona, Spain
2. Department of Cell Biology, Physiology and Immunology, Universitat de Barcelona, 08028 Barcelona, Spain
3. Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Barcelona, Spain
4. Institute of Neuroscience, University of Barcelona, 08007 Barcelona, Spain
Interests: in vitro models of neurodegeneration and regeneration; lab-on-chip technologies; inhibitory molecules after lesion; olphactory enshething cells

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Guest Editor
Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, Baldiri Reixac 15-21, E-08028 Barcelona, Spain
Interests: axonal injuries; neuroinflamation; intrinsic mechanisms of neural regeneration; neurorehabilitation; metabolism in axonal injuries

Special Issue Information

Dear Colleagues,

Traumatic neuronal injuries, including peripheral nerve injuries (PNI), traumatic brain injury (TBI), or spinal cord injury (SCI), cause long-term functional deficits that represent a big hurdle in the quality of life of patients who suffer them. Loss of function is caused by the disconnection of axons. Injured axons undergo a degenerative process and are unable to reattach to restore function. Consequently, axon degeneration and the lack of functional axonal regeneration are the pivotal pathological events of acute traumatic neuronal injuries. Axon degeneration is an active cellular program and yet molecularly distinct from cell death. In recent years, much effort has been devoted toward understanding the nature of axon degeneration and promoting axon regeneration; however, the fundamental mechanisms of self-destruction of damaged axons and the intrinsic inability to regenerate still remain unclear, causing a worrying lack of effective treatments for chronic axonal injuries. In this Special Issue, we aim to include breakthrough findings, ranking from new strategies (in vitro or in vivo) to clinical approaches to understand fundamental and challenging issues behind axonal regeneration failure. We will focus on how these mechanistic insights hold promises for accelerating and identifying potential therapeutic targets for chronic axonal injuries. Both original research articles and reviews are welcome.

Dr. José Antonio Del Río
Dr. Arnau Hervera
Guest Editors

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Keywords

  • Advances in mechanisms of axonal degeneration: Cellular signalling, paracrine communication.
  • Advances in axonal regeneration: Neurorehabilitation, Neuroinflammation, Intrisic mechanisms, Metabolic regulation.
  • Novel in vitro and in vivo models of axonal degeneration and regeneration

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Published Papers (2 papers)

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Research

23 pages, 9681 KiB  
Article
Cyclic Stretch of Either PNS or CNS Located Nerves Can Stimulate Neurite Outgrowth
by Vasileios Kampanis, Bahardokht Tolou-Dabbaghian, Luming Zhou, Wolfgang Roth and Radhika Puttagunta
Cells 2021, 10(1), 32; https://doi.org/10.3390/cells10010032 - 28 Dec 2020
Cited by 7 | Viewed by 3209
Abstract
The central nervous system (CNS) does not recover from traumatic axonal injury, but the peripheral nervous system (PNS) does. We hypothesize that this fundamental difference in regenerative capacity may be based upon the absence of stimulatory mechanical forces in the CNS due to [...] Read more.
The central nervous system (CNS) does not recover from traumatic axonal injury, but the peripheral nervous system (PNS) does. We hypothesize that this fundamental difference in regenerative capacity may be based upon the absence of stimulatory mechanical forces in the CNS due to the protective rigidity of the vertebral column and skull. We developed a bioreactor to apply low-strain cyclic axonal stretch to adult rat dorsal root ganglia (DRG) connected to either the peripheral or central nerves in an explant model for inducing axonal growth. In response, larger diameter DRG neurons, mechanoreceptors and proprioceptors showed enhanced neurite outgrowth as well as increased Activating Transcription Factor 3 (ATF3). Full article
(This article belongs to the Special Issue Advances in Axon Degeneration and Regeneration)
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22 pages, 6334 KiB  
Article
Ascorbic Acid Promotes Functional Restoration after Spinal Cord Injury Partly by Epigenetic Modulation
by Jin Young Hong, Ganchimeg Davaa, Hyunjin Yoo, Kwonho Hong and Jung Keun Hyun
Cells 2020, 9(5), 1310; https://doi.org/10.3390/cells9051310 - 25 May 2020
Cited by 13 | Viewed by 4009
Abstract
Axonal regeneration after spinal cord injury (SCI) is difficult to achieve, and no fundamental treatment can be applied in clinical settings. DNA methylation has been suggested to play a role in regeneration capacity and neuronal growth after SCI by controlling the expression of [...] Read more.
Axonal regeneration after spinal cord injury (SCI) is difficult to achieve, and no fundamental treatment can be applied in clinical settings. DNA methylation has been suggested to play a role in regeneration capacity and neuronal growth after SCI by controlling the expression of regeneration-associated genes (RAGs). The aim of this study was to examine changes in neuronal DNA methylation status after SCI and to determine whether modulation of DNA methylation with ascorbic acid can enhance neuronal regeneration or functional restoration after SCI. Changes in epigenetic marks (5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC)); the expression of Ten-eleven translocation (Tet) family genes; and the expression of genes related to inflammation, regeneration, and degeneration in the brain motor cortex were determined following SCI. The 5hmC level within the brain was increased after SCI, especially in the acute and subacute stages, and the mRNA levels of Tet gene family members (Tet1, Tet2, and Tet3) were also increased. Administration of ascorbic acid (100 mg/kg) to SCI rats enhanced 5hmC levels; increased the expression of the Tet1, Tet2, and Tet3 genes within the brain motor cortex; promoted axonal sprouting within the lesion cavity of the spinal cord; and enhanced recovery of locomotor function until 12 weeks. In conclusion, we found that epigenetic status in the brain motor cortex is changed after SCI and that epigenetic modulation using ascorbic acid may contribute to functional recovery after SCI. Full article
(This article belongs to the Special Issue Advances in Axon Degeneration and Regeneration)
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