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Cells
Special Issues
Unveiling Axon-Glia Communication in Health and Disease
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Unveiling Axon-Glia Communication in Health and Disease

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 (20 January 2025) | Viewed by 1616

Special Issue Editors

Prof. Michela Rigoni

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padua, Via U. Bassi 58b, 35131 Padua, Italy
Interests: neuromuscular junction; neurotoxins, peripheral nerve regeneration; Schwann cells; amyotrophic lateral sclerosis
Dr. Samuele Negro

E-Mail Website
Guest Editor
U.O.C. Clinica Neurologica, Azienda Ospedale-Università Padova, Via Giustiniani 5, 35128 Padua, Italy
Interests: neuromuscular junction; neurotoxins; peripheral nerve regeneration; amyotrophic lateral sclerosis

Special Issue Information

Dear Colleagues,

The increasing number of non-cell autonomous neurodevelopmental and neurodegenerative disorders pushes the scientific community to improve its current knowledge on intimate and finely regulated time and space connection bridging neurons and glial cells. Indeed, neurons are constantly supported in their life-essential tasks by different glial subtypes on a structural, metabolic and functional level, and in the response to injury. Not surprisingly, dysfunction in this close relationship contributes to neurodevelopment defects and neurodegeneration.

The focus of this Special Issue is to collect a series of original research and reviews updating the many ways by which axons and the different glial subtypes communicate throughout development and adulthood, to maintain or restore central and peripheral homeostasis, and how alterations in this bidirectional communication can contribute to aging and pathology. 

We are confident that this collection will add to our comprehension of different aspects of nervous system physiology and pathology and pave the way for novel therapeutic interventions.

We are looking to explore glia-axon communication in:

  • Neurodevelopment;
  • Aging;
  • Neurodegeneration/Neuroregeneration;
  • Enteric nervous system;
  • Cancer;
  • Pain.

Prof. Michela Rigoni
Dr. Samuele Negro
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glia-axon communication
  • oligodendrocytes
  • astrocytes
  • microglia
  • Schwann cells
  • enteric glia
  • neurodevelopment
  • neurodegeneration
  • neuroregeneration
  • cancer
  • pain
  • aging

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Published Papers (2 papers)

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Research

15 pages, 1459 KiB  
Article
Effects of Selective α7 Nicotinic Acetylcholine Receptor Stimulation in Oligodendrocytes: Putative Implication in Neuroinflammation
by Claudia Guerriero, Giulia Puliatti, Tamara Di Marino, Giulia Scanavino, Carlo Matera, Clelia Dallanoce and Ada Maria Tata
Cells 2025, 14(13), 948; https://doi.org/10.3390/cells14130948 - 20 Jun 2025
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Abstract
α7 nAChRs are known to modulate several physiological and pathological functions in glial cells, and their selective activation might have anti-inflammatory effects in the central and peripheral nervous system. OL progenitors (OPCs) respond to cholinergic stimuli via muscarinic receptors that are mainly involved [...] Read more.
α7 nAChRs are known to modulate several physiological and pathological functions in glial cells, and their selective activation might have anti-inflammatory effects in the central and peripheral nervous system. OL progenitors (OPCs) respond to cholinergic stimuli via muscarinic receptors that are mainly involved in the modulation of their proliferation. Conversely, the role of nicotinic receptors, particularly α7 nAChRs, has been poorly investigated. In this study, we evaluated the expression of α7 nAChRs in a model of OPCs (Oli neu) and the potential effects mediated by their selective activation. Methods: Oli neu cells were used as a murine immortalized OPCs model. The effects of α7 nAChRs stimulation on cell proliferation and survival were assessed by the MTT assay. RT-PCR and Western blot analysis were used to analyze the expression of α7 nAChRs and proliferative and differentiative markers (PCNA, MBP). LPS exposure was used to induce the environment in which the antioxidant and anti-inflammatory properties of α7 nAChRs were analyzed, evaluating NFR2 and TNF-α expression, ROS levels through DCFDA staining while Oil Red O staining was used for the analysis of lipid droplet content as a marker of cellular inflammation response. Results: The α7 nAChR is expressed both in OPCs and OLs, and its stimulation by the selective agonist ICH3 increases cell proliferation without modifying the OLs’ differentiation capability. Moreover, ICH3 showed anti-inflammatory and antioxidant effects against LPS exposure. Conclusions: The results herein obtained confirm the role of α7 nAChR in the modulation of neuroinflammatory processes as well as their protective effects on OLs. Full article
(This article belongs to the Special Issue Unveiling Axon-Glia Communication in Health and Disease)
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15 pages, 4838 KiB  
Article
Hydrogen Peroxide Modulates the Timely Activation of Jun and Erk in Schwann Cells at the Injury Site and Is Required for Motor Axon Regeneration
by Samuele Negro, Chiara Baggio, Marika Tonellato, Marco Stazi, Giorgia D’Este, Aram Megighian, Cesare Montecucco and Michela Rigoni
Cells 2025, 14(9), 671; https://doi.org/10.3390/cells14090671 - 3 May 2025
Viewed by 822
Abstract
Peripheral nervous system (PNS) neurons, including motor neurons (MNs), possess a remarkable ability to regenerate and reinnervate target muscles following nerve injury. This process is orchestrated by a combination of intrinsic neuronal properties and extrinsic factors, with Schwann cells (SCs) playing a central [...] Read more.
Peripheral nervous system (PNS) neurons, including motor neurons (MNs), possess a remarkable ability to regenerate and reinnervate target muscles following nerve injury. This process is orchestrated by a combination of intrinsic neuronal properties and extrinsic factors, with Schwann cells (SCs) playing a central role. Upon injury, SCs transition into a repair phenotype that allows axonal regeneration through molecular signaling and structural guidance. However, the identity of the SCs’ reprogramming factors is only partially known. We previously identified hydrogen peroxide (H2O2) as an early and key driver of nerve repair, inducing gene expression rewiring in SCs to support nerve re-growth. In this study, we quantitatively assessed the role of H2O2 in the activation of key pro-regenerative signaling pathways in SCs following sciatic nerve compression, specifically the extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun, which are essential for functional nerve recovery. Notably, we found that H2O2 neutralization does not impact degeneration, but it significantly affects the regenerative response. Collectively, our findings establish H2O2 as a promising regulator of the Schwann cell injury response at the injury site, linking oxidative signaling to the molecular mechanisms governing nerve regeneration. Full article
(This article belongs to the Special Issue Unveiling Axon-Glia Communication in Health and Disease)
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