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The Function of Glial Cells in the Nervous System
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The Function of Glial Cells in the Nervous System

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 2961

Special Issue Editor

Dr. Krista Minéia Wartchow

E-Mail Website
Guest Editor
Brain Health Imaging Institute, Department of Radiology, Weill Cornell Medicine, New York, NY 10044, USA
Interests: astroglial cells; glial–neuronal interaction in synapses; biomarkers; S100B; Alzheimer’s disease; cognition

Special Issue Information

Dear Colleagues,

In nervous system homeostasis, glial cells, or neuroglia, play a collective role. Essentially all aspects of the nervous system's formation and function are orchestrated by the diverse and dynamic functions of glial cells. These include forming synapses, regulating synaptic transmission and plasticity, maintaining redox balance, maintaining ion and water homeostasis, establishing the blood–brain barrier, controlling toxicity in the extracellular space, and establishing myelin sheets. Furthermore, these cells play a crucial role in immune and inflammatory functions in pathological conditions, contributing to both healthy and diseased states with neurological outcomes. In this regard, a major objective of this Special Issue is to collect studies and reviews on glial cells and the glial–neuronal interaction rearrangements that occur during aging or in neurodegenerative diseases, possible glial biomarkers, as well as studies on therapeutic approaches with which to counteract these compromised mechanisms.

Dr. Krista Minéia Wartchow
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • glial cells
  • glial–neuronal interaction
  • glial biomarkers
  • neurodegenerative diseases
  • therapeutic approaches

Published Papers (4 papers)

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Research

20 pages, 1533 KiB  
Article
Sox10 Activity and the Timing of Schwann Cell Differentiation Are Controlled by a Tle4-Dependent Negative Feedback Loop
by Tim Aberle, Anna Walter, Sandra Piefke, Simone Hillgärtner, Hannah M. Wüst, Michael Wegner and Melanie Küspert
Int. J. Mol. Sci. 2024, 25(10), 5234; https://doi.org/10.3390/ijms25105234 (registering DOI) - 11 May 2024
Viewed by 118
Abstract
The HMG-domain containing transcription factor Sox10 plays a crucial role in regulating Schwann cell survival and differentiation and is expressed throughout the entire Schwann cell lineage. While its importance in peripheral myelination is well established, little is known about its role in the [...] Read more.
The HMG-domain containing transcription factor Sox10 plays a crucial role in regulating Schwann cell survival and differentiation and is expressed throughout the entire Schwann cell lineage. While its importance in peripheral myelination is well established, little is known about its role in the early stages of Schwann cell development. In a search for direct target genes of Sox10 in Schwann cell precursors, the transcriptional co-repressor Tle4 was identified. At least two regions upstream of the Tle4 gene appear involved in mediating the Sox10-dependent activation. Once induced, Tle4 works in tandem with the bHLH transcriptional repressor Hes1 and exerts a dual inhibitory effect on Sox10 by preventing the Sox10 protein from transcriptionally activating maturation genes and by suppressing Sox10 expression through known enhancers of the gene. This mechanism establishes a regulatory barrier that prevents premature activation of factors involved in differentiation and myelin formation by Sox10 in immature Schwann cells. The identification of Tle4 as a critical downstream target of Sox10 sheds light on the gene regulatory network in the early phases of Schwann cell development. It unravels an elaborate regulatory circuitry that fine-tunes the timing and extent of Schwann cell differentiation and myelin gene expression. Full article
(This article belongs to the Special Issue The Function of Glial Cells in the Nervous System)
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18 pages, 5890 KiB  
Article
Effect of Regulation of Chemerin/Chemokine-like Receptor 1/Stimulator of Interferon Genes Pathway on Astrocyte Recruitment to Aβ Plaques
by Zhen Liu, Yijun Chen, Yanqing Chen, Jiayi Zheng, Wanning Wu, Linlin Wang, Hanqi Wang and Yang Yu
Int. J. Mol. Sci. 2024, 25(8), 4324; https://doi.org/10.3390/ijms25084324 - 13 Apr 2024
Viewed by 523
Abstract
Recruitment and accumulation of reactive astrocytes around senile plaques are common pathological features of Alzheimer’s disease (AD), with unclear mechanisms. Chemerin, an adipokine implicated in neuroinflammation, acts through its receptor, chemokine-like receptor 1 (CMKLR1), which also functions as a receptor for amyloid β [...] Read more.
Recruitment and accumulation of reactive astrocytes around senile plaques are common pathological features of Alzheimer’s disease (AD), with unclear mechanisms. Chemerin, an adipokine implicated in neuroinflammation, acts through its receptor, chemokine-like receptor 1 (CMKLR1), which also functions as a receptor for amyloid β (Aβ). The impact of the chemerin/CMKLR1 axis on astrocyte migration towards Aβ plaques is unknown. Here we investigated the effect of CMKLR1 on astrocyte migration around Aβ deposition in APP/PS1 mice with Cmklr1 knockout (APP/PS1-Cmklr1−/−). CMKLR1-expressed astrocytes were upregulated in the cortices and hippocampi of 9-month-old APP/PS1 mice. Chemerin mainly co-localized with neurons, and its expression was reduced in the brains of APP/PS1 mice, compared to WT mice. CMKLR1 deficiency decreased astrocyte colocalization with Aβ plaques in APP/PS1-Cmklr1−/− mice, compared to APP/PS1 mice. Activation of the chemerin/CMKLR1 axis promoted the migration of primary cultured astrocytes and U251 cells, and reduced astrocyte clustering induced by Aβ42. Mechanistic studies revealed that chemerin/CMKLR1 activation induced STING phosphorylation. Deletion of STING attenuated the promotion of the chemerin/CMKLR1 axis relative to astrocyte migration and abolished the inhibitory effect of chemerin on Aβ42-induced astrocyte clustering. These findings suggest the involvement of the chemerin/CMKLR1/STING pathway in the regulation of astrocyte migration and recruitment to Aβ plaques/Aβ42. Full article
(This article belongs to the Special Issue The Function of Glial Cells in the Nervous System)
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21 pages, 5532 KiB  
Article
Neuroprotection via Carbon Monoxide Depends on the Circadian Regulation of CD36-Mediated Microglial Erythrophagocytosis in Hemorrhagic Stroke
by Sandra Kaiser, Luise Henrich, Iva Kiessling, Benedikt Loy and Nils Schallner
Int. J. Mol. Sci. 2024, 25(3), 1680; https://doi.org/10.3390/ijms25031680 - 30 Jan 2024
Viewed by 820
Abstract
The molecular basis for circadian dependency in stroke due to subarachnoid hemorrhagic stroke (SAH) remains unclear. We reasoned that microglial erythrophagocytosis, crucial for SAH response, follows a circadian pattern involving carbon monoxide (CO) and CD36 surface expression. The microglial BV-2 cell line and [...] Read more.
The molecular basis for circadian dependency in stroke due to subarachnoid hemorrhagic stroke (SAH) remains unclear. We reasoned that microglial erythrophagocytosis, crucial for SAH response, follows a circadian pattern involving carbon monoxide (CO) and CD36 surface expression. The microglial BV-2 cell line and primary microglia (PMG) under a clocked medium change were exposed to blood ± CO (250 ppm, 1 h) in vitro. Circadian dependency and the involvement of CD36 were analyzed in PMG isolated from control mice and CD36−/− mice and by RNA interference targeting Per-2. In vivo investigations, including phagocytosis, vasospasm, microglia activation and spatial memory, were conducted in an SAH model using control and CD36−/− mice at different zeitgeber times (ZT). In vitro, the surface expression of CD36 and its dependency on CO and phagocytosis occurred with changed circadian gene expression. CD36−/− PMG exhibited altered circadian gene expression, phagocytosis and impaired responsiveness to CO. In vivo, control mice with SAH demonstrated circadian dependency in microglia activation, erythrophagocytosis and CO-mediated protection at ZT2, in contrast to CD36−/− mice. Our study indicates that circadian rhythmicity modulates microglial activation and subsequent CD36-dependent phagocytosis. CO altered circadian-dependent neuroprotection and CD36 induction, determining the functional outcome in a hemorrhagic stroke model. This study emphasizes how circadian rhythmicity influences neuronal damage after neurovascular events. Full article
(This article belongs to the Special Issue The Function of Glial Cells in the Nervous System)
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18 pages, 6364 KiB  
Article
Astroglial S100B Secretion Is Mediated by Ca2+ Mobilization from Endoplasmic Reticulum: A Study Using Forskolin and DMSO as Secretagogues
by Marina C. Leite, Fabiana Galland, Maria Cristina Guerra, Letícia Rodrigues, Jéssica Taday, Priscila T. Monteforte, Hanko Hirata, Carmem Gottfried, Rosario Donato, Soraya Smaili and Carlos-Alberto Gonçalves
Int. J. Mol. Sci. 2023, 24(23), 16576; https://doi.org/10.3390/ijms242316576 - 21 Nov 2023
Cited by 2 | Viewed by 834
Abstract
S100B, a homodimeric Ca2+-binding protein, is produced and secreted by astrocytes, and its extracellular levels have been used as a glial marker in brain damage and neurodegenerative and psychiatric diseases; however, its mechanism of secretion is elusive. We used primary astrocyte [...] Read more.
S100B, a homodimeric Ca2+-binding protein, is produced and secreted by astrocytes, and its extracellular levels have been used as a glial marker in brain damage and neurodegenerative and psychiatric diseases; however, its mechanism of secretion is elusive. We used primary astrocyte cultures and calcium measurements from real-time fluorescence microscopy to investigate the role of intracellular calcium in S100B secretion. In addition, the dimethyl sulfoxide (DMSO) effect on S100B was investigated in vitro and in vivo using Wistar rats. We found that DMSO, a widely used vehicle in biological assays, is a powerful S100B secretagogue, which caused a biphasic response of Ca2+ mobilization. Our data show that astroglial S100B secretion is triggered by the increase in intracellular Ca2+ and indicate that this increase is due to Ca2+ mobilization from the endoplasmic reticulum. Also, blocking plasma membrane Ca2+ channels involved in the Ca2+ replenishment of internal stores decreased S100B secretion. The DMSO-induced S100B secretion was confirmed in vivo and in ex vivo hippocampal slices. Our data support a nonclassic vesicular export of S100B modulated by Ca2+, and the results might contribute to understanding the mechanism underlying the astroglial release of S100B. Full article
(This article belongs to the Special Issue The Function of Glial Cells in the Nervous System)
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