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Cells
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Role of Glial Cells in Neuropathic Pain
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Role of Glial Cells in Neuropathic Pain

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 June 2023) | Viewed by 12398

Special Issue Editor

Prof. Dr. Sung Joong Lee

E-Mail Website
Guest Editor
Department of Neuroscience and Physiology, Seoul National University School of Dentistry, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, Korea
Interests: microglia; astrocyte; satellite glia; neuropathic pain; nerve injury

Special Issue Information

Dear Colleagues,

Neuropathic pain is chronic pain caused by damage or dysfunction of nervous system. It is a debilitating neurological disorder affecting millions of people worldwide, yet the pathogenic mechanism is elusive and thus efficient treatment is absent. Neuroscience over past two decades has revealed glial cells play key role in the development of neuropathic pain. Aberrant activation of microglia and astrocyte after peripheral nerve injury causes central sensitization by affecting pain transmitting neurons or neural circuits in the central nervous system via diverse pathways. More recently, peripheral glia including satellite glia or Schwann cells are also implicated in the development of central and peripheral sensitization. Therefore, glial cells have been emerged as novel cellular targets for the treatment of neuropathic pain. In this Special Issue, we invite investigators to contribute original research or review articles that highlight recent important advances in this exciting field. Potential topics include but are not limited to the following:

  • Role of glia in neuropathic pain
  • Molecular and cellular mechanisms of gliopathic central and peripheral sensitization
  • Mechanisms of glial cell activation in neuropathic pain
  • Sexual dimorphism of gliopathic pain
  • Development of glia-targeting drug or treatment strategy for neuropathic pain

Prof. Dr. Sung Joong Lee
Guest Editor

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

  • astrocyte
  • microglia
  • satellite glia
  • oligodendrocyte/Schwann cells
  • neuropathic pain
  • peripheral/central sensitization

Published Papers (5 papers)

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Research

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27 pages, 4896 KiB  
Article
Differential Effects of Regulatory T Cells in the Meninges and Spinal Cord of Male and Female Mice with Neuropathic Pain
by Nathan T. Fiore, Brooke A. Keating, Yuting Chen, Sarah I. Williams and Gila Moalem-Taylor
Cells 2023, 12(18), 2317; https://doi.org/10.3390/cells12182317 - 20 Sep 2023
Cited by 3 | Viewed by 1368
Abstract
Immune cells play a critical role in promoting neuroinflammation and the development of neuropathic pain. However, some subsets of immune cells are essential for pain resolution. Among them are regulatory T cells (Tregs), a specialised subpopulation of T cells that limit excessive immune [...] Read more.
Immune cells play a critical role in promoting neuroinflammation and the development of neuropathic pain. However, some subsets of immune cells are essential for pain resolution. Among them are regulatory T cells (Tregs), a specialised subpopulation of T cells that limit excessive immune responses and preserve immune homeostasis. In this study, we utilised intrathecal adoptive transfer of activated Tregs in male and female mice after peripheral nerve injury to investigate Treg migration and whether Treg-mediated suppression of pain behaviours is associated with changes in peripheral immune cell populations in lymphoid and meningeal tissues and spinal microglial and astrocyte reactivity and phenotypes. Treatment with Tregs suppressed mechanical pain hypersensitivity and improved changes in exploratory behaviours after chronic constriction injury (CCI) of the sciatic nerve in both male and female mice. The injected Treg cells were detected in the choroid plexus and the pia mater and in peripheral lymphoid organs in both male and female recipient mice. Nonetheless, Treg treatment resulted in differential changes in meningeal and lymph node immune cell profiles in male and female mice. Moreover, in male mice, adoptive transfer of Tregs ameliorated the CCI-induced increase in microglia reactivity and inflammatory phenotypic shift, increasing M2-like phenotypic markers and attenuating astrocyte reactivity and neurotoxic astrocytes. Contrastingly, in CCI female mice, Treg injection increased astrocyte reactivity and neuroprotective astrocytes. These findings show that the adoptive transfer of Tregs modulates meningeal and peripheral immunity, as well as spinal glial populations, and alleviates neuropathic pain, potentially through different mechanisms in males and females. Full article
(This article belongs to the Special Issue Role of Glial Cells in Neuropathic Pain)
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14 pages, 14481 KiB  
Article
Estrogen Mediates the Sexual Dimorphism of GT1b-Induced Central Pain Sensitization
by Jaesung Lee, Seohyun Chung, Minkyu Hwang, Yeongkag Kwon, Seung Hyun Han and Sung Joong Lee
Cells 2023, 12(5), 808; https://doi.org/10.3390/cells12050808 - 06 Mar 2023
Cited by 2 | Viewed by 1687
Abstract
We have previously reported that the intrathecal (i.t.) administration of GT1b, a ganglioside, induces spinal cord microglia activation and central pain sensitization as an endogenous agonist of Toll-like receptor 2 on microglia. In this study, we investigated the sexual dimorphism of GT1b-induced central [...] Read more.
We have previously reported that the intrathecal (i.t.) administration of GT1b, a ganglioside, induces spinal cord microglia activation and central pain sensitization as an endogenous agonist of Toll-like receptor 2 on microglia. In this study, we investigated the sexual dimorphism of GT1b-induced central pain sensitization and the underlying mechanisms. GT1b administration induced central pain sensitization only in male but not in female mice. Spinal tissue transcriptomic comparison between male and female mice after GT1b injection suggested the putative involvement of estrogen (E2)-mediated signaling in the sexual dimorphism of GT1b-induced pain sensitization. Upon ovariectomy-reducing systemic E2, female mice became susceptible to GT1b-induced central pain sensitization, which was completely reversed by systemic E2 supplementation. Meanwhile, orchiectomy of male mice did not affect pain sensitization. As an underlying mechanism, we present evidence that E2 inhibits GT1b-induced inflammasome activation and subsequent IL-1β production. Our findings demonstrate that E2 is responsible for sexual dimorphism in GT1b-induced central pain sensitization. Full article
(This article belongs to the Special Issue Role of Glial Cells in Neuropathic Pain)
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Review

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12 pages, 684 KiB  
Review
Sexual Dimorphism in the Mechanism of Pain Central Sensitization
by Ellane Barcelon, Seohyun Chung, Jaesung Lee and Sung Joong Lee
Cells 2023, 12(16), 2028; https://doi.org/10.3390/cells12162028 - 09 Aug 2023
Cited by 3 | Viewed by 1361
Abstract
It has long been recognized that men and women have different degrees of susceptibility to chronic pain. Greater recognition of the sexual dimorphism in chronic pain has resulted in increasing numbers of both clinical and preclinical studies that have identified factors and mechanisms [...] Read more.
It has long been recognized that men and women have different degrees of susceptibility to chronic pain. Greater recognition of the sexual dimorphism in chronic pain has resulted in increasing numbers of both clinical and preclinical studies that have identified factors and mechanisms underlying sex differences in pain sensitization. Here, we review sexually dimorphic pain phenotypes in various research animal models and factors involved in the sex difference in pain phenotypes. We further discuss putative mechanisms for the sexual dimorphism in pain sensitization, which involves sex hormones, spinal cord microglia, and peripheral immune cells. Elucidating the sexually dimorphic mechanism of pain sensitization may provide important clinical implications and aid the development of sex-specific therapeutic strategies to treat chronic pain. Full article
(This article belongs to the Special Issue Role of Glial Cells in Neuropathic Pain)
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18 pages, 1249 KiB  
Review
EZH2 Methyltransferase Regulates Neuroinflammation and Neuropathic Pain
by Han-Rong Weng, Kyle Taing, Lawrence Chen and Angela Penney
Cells 2023, 12(7), 1058; https://doi.org/10.3390/cells12071058 - 31 Mar 2023
Cited by 2 | Viewed by 2399
Abstract
Recent studies by us and others have shown that enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, in glial cells regulates the genesis of neuropathic pain by modulating the production of proinflammatory cytokines and chemokines. In this review, we summarize recent advances in [...] Read more.
Recent studies by us and others have shown that enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, in glial cells regulates the genesis of neuropathic pain by modulating the production of proinflammatory cytokines and chemokines. In this review, we summarize recent advances in this research area. EZH2 is a subunit of polycomb repressive complex 2 (PRC2), which primarily serves as a histone methyltransferase to catalyze methylation of histone 3 on lysine 27 (H3K27), ultimately resulting in transcriptional repression. Animals with neuropathic pain exhibit increased EZH2 activity and neuroinflammation of the injured nerve, spinal cord, and anterior cingulate cortex. Inhibition of EZH2 with DZNep or GSK-126 ameliorates neuroinflammation and neuropathic pain. EZH2 protein expression increases upon activation of Toll-like receptor 4 and calcitonin gene-related peptide receptors, downregulation of miR-124-3p and miR-378 microRNAs, or upregulation of Lncenc1 and MALAT1 long noncoding RNAs. Genes suppressed by EZH2 include suppressor of cytokine signaling 3 (SOCS3), nuclear factor (erythroid-derived 2)-like-2 factor (NrF2), miR-29b-3p, miR-146a-5p, and brain-specific angiogenesis inhibitor 1 (BAI1). Pro-inflammatory mediators facilitate neuronal activation along pain-signaling pathways by sensitizing nociceptors in the periphery, as well as enhancing excitatory synaptic activities and suppressing inhibitory synaptic activities in the CNS. These studies collectively reveal that EZH2 is implicated in signaling pathways known to be key players in the process of neuroinflammation and genesis of neuropathic pain. Therefore, targeting the EZH2 signaling pathway may open a new avenue to mitigate neuroinflammation and neuropathic pain. Full article
(This article belongs to the Special Issue Role of Glial Cells in Neuropathic Pain)
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21 pages, 2505 KiB  
Review
The Similar and Distinct Roles of Satellite Glial Cells and Spinal Astrocytes in Neuropathic Pain
by Aidan McGinnis and Ru-Rong Ji
Cells 2023, 12(6), 965; https://doi.org/10.3390/cells12060965 - 22 Mar 2023
Cited by 7 | Viewed by 4937
Abstract
Preclinical studies have identified glial cells as pivotal players in the genesis and maintenance of neuropathic pain after nerve injury associated with diabetes, chemotherapy, major surgeries, and virus infections. Satellite glial cells (SGCs) in the dorsal root and trigeminal ganglia of the peripheral [...] Read more.
Preclinical studies have identified glial cells as pivotal players in the genesis and maintenance of neuropathic pain after nerve injury associated with diabetes, chemotherapy, major surgeries, and virus infections. Satellite glial cells (SGCs) in the dorsal root and trigeminal ganglia of the peripheral nervous system (PNS) and astrocytes in the central nervous system (CNS) express similar molecular markers and are protective under physiological conditions. They also serve similar functions in the genesis and maintenance of neuropathic pain, downregulating some of their homeostatic functions and driving pro-inflammatory neuro-glial interactions in the PNS and CNS, i.e., “gliopathy”. However, the role of SGCs in neuropathic pain is not simply as “peripheral astrocytes”. We delineate how these peripheral and central glia participate in neuropathic pain by producing different mediators, engaging different parts of neurons, and becoming active at different stages following nerve injury. Finally, we highlight the recent findings that SGCs are enriched with proteins related to fatty acid metabolism and signaling such as Apo-E, FABP7, and LPAR1. Targeting SGCs and astrocytes may lead to novel therapeutics for the treatment of neuropathic pain. Full article
(This article belongs to the Special Issue Role of Glial Cells in Neuropathic Pain)
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