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The Role of Glial Cells in Health and Disease

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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: closed (30 November 2022) | Viewed by 14212

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Prof. Dr. Jean-Denis Troadec

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Cognitive Neurosciences Laboratory- CNRS 7291, Aix-Marseille University, Marseille, France
Interests: astrocytes; microglia; tanycytes; food intake; obesity; leptin
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Dear Colleagues,

‘Hitherto, gentlemen, in considering the nervous system, I have only spoken of the really nervous parts of it. But if we would study the nervous system in its real relations in the body, it is extremely important to have a knowledge of that substance also which lies between the proper nervous parts, holds them together and gives the whole its form in a greater or less degree’. It was with these visionary words, spoken on April 3, 1858, during a lecture to medical students at the Charité hospital in Berlin, that Rudolf Virchow clearly indicated the path to follow in order to understand the functioning of the nervous system and demonstrated the importance of the definition of neuroglia. Despite this vision and the magnificent histological observations of Santiago Ramón y Cajal and his pupil, Pío del Río Hortega, which allowed astrocytes, microglia, and oligodendrocytes to be identified a few years later, glial cells spent decades in the shadow of neurons. The wheel has turned, and the glial cells are now in the spotlight. The data accumulated over two decades highlight their importance in the nervous system. These cells contribute to the physiological functioning of the nervous system and are also involved in many pathophysiological processes associated with acute or chronic damage to the brain. Despite these undeniable advances, our understanding of the role and place of glial cells in the brain, however, remains incomplete and fragmented. We must continue and intensify our efforts to learn more about these cells.

This Special Issue of the International Journal of Molecular Sciences aims to compile research that significantly advances our understanding of glial cells and their roles in normal and pathological brain processes. Glial plasticity, homeostatic glial functions, neuroglial and glial interactions, glial expression of neurotransmitter receptors, glial signaling, glia cell functions, and even the release of gliotransmitters are all welcomed research topics. We accept original research articles and comprehensive reviews.

Prof. Dr. Jean-Denis Troadec
Guest Editor

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Keywords

astrocytes
microglia
oligodendrocytes
plasticity
physiology
physiopathology
synapse
neuroglial interactions
gliotransmitters

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Published Papers (5 papers)

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Research

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17 pages, 4029 KiB

Open AccessArticle

Neuronal Prosurvival Role of Ceramide Synthase 2 by Olidogendrocyte-to-Neuron Extracellular Vesicle Transfer

by Álvaro Casadomé-Perales, Sara Naya, Elisa Fernández-Martínez, Bea G. Mille, Marta Guerrero-Valero, Héctor Peinado, Francesc X. Guix, Carlos G. Dotti and Ernest Palomer

Int. J. Mol. Sci. 2023, 24(6), 5986; https://doi.org/10.3390/ijms24065986 - 22 Mar 2023

Cited by 2 | Viewed by 2462

Abstract

Ageing is associated with notorious alterations in neurons, i.e., in gene expression, mitochondrial function, membrane degradation or intercellular communication. However, neurons live for the entire lifespan of the individual. One of the reasons why neurons remain functional in elderly people is survival mechanisms prevail over death mechanisms. While many signals are either pro-survival or pro-death, others can play both roles. Extracellular vesicles (EVs) can signal both pro-toxicity and survival. We used young and old animals, primary neuronal and oligodendrocyte cultures and neuroblastoma and oligodendrocytic lines. We analysed our samples using a combination of proteomics and artificial neural networks, biochemistry and immunofluorescence approaches. We found an age-dependent increase in ceramide synthase 2 (CerS2) in cortical EVs, expressed by oligodendrocytes. In addition, we show that CerS2 is present in neurons via the uptake of oligodendrocyte-derived EVs. Finally, we show that age-associated inflammation and metabolic stress favour CerS2 expression and that oligodendrocyte-derived EVs loaded with CerS2 lead to the expression of the antiapoptotic factor Bcl2 in inflammatory conditions. Our study shows that intercellular communication is altered in the ageing brain, which favours neuronal survival through the transfer of oligodendrocyte-derived EVs containing CerS2. Full article

(This article belongs to the Special Issue The Role of Glial Cells in Health and Disease)

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22 pages, 3518 KiB

Open AccessArticle

p27^kip1 Modulates the Morphology and Phagocytic Activity of Microglia

by Jolien Beeken, Sofie Kessels, Jean-Michel Rigo, Yeranddy A. Alpizar, Laurent Nguyen and Bert Brône

Int. J. Mol. Sci. 2022, 23(18), 10432; https://doi.org/10.3390/ijms231810432 - 9 Sep 2022

Viewed by 2495

Abstract

p27^kip1 is a multifunctional protein that promotes cell cycle exit by blocking the activity of cyclin/cyclin-dependent kinase complexes as well as migration and motility via signaling pathways that converge on the actin and microtubule cytoskeleton. Despite the broad characterization of p27^kip1 function in neural cells, little is known about its relevance in microglia. Here, we studied the role of p27^kip1 in microglia using a combination of in vitro and in situ approaches. While the loss of p27^kip1 did not affect microglial density in the cerebral cortex, it altered their morphological complexity in situ. However, despite the presence of p27^kip1 in microglial processes, as shown by immunofluorescence in cultured cells, loss of p27^kip1 did not change microglial process motility and extension after applying laser-induced brain damage in cortical brain slices. Primary microglia lacking p27^kip1 showed increased phagocytic uptake of synaptosomes, while a cell cycle dead variant negatively affected phagocytosis. These findings indicate that p27^kip1 plays specific roles in microglia. Full article

(This article belongs to the Special Issue The Role of Glial Cells in Health and Disease)

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Review

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31 pages, 1374 KiB

Open AccessReview

The Physio-Pathological Role of Group I Metabotropic Glutamate Receptors Expressed by Microglia in Health and Disease with a Focus on Amyotrophic Lateral Sclerosis

by Matilde Balbi, Giambattista Bonanno, Tiziana Bonifacino and Marco Milanese

Int. J. Mol. Sci. 2023, 24(6), 5240; https://doi.org/10.3390/ijms24065240 - 9 Mar 2023

Cited by 2 | Viewed by 3202

Abstract

Microglia cells are the resident immune cells of the central nervous system. They act as the first-line immune guardians of nervous tissue and central drivers of neuroinflammation. Any homeostatic alteration that can compromise neuron and tissue integrity could activate microglia. Once activated, microglia exhibit highly diverse phenotypes and functions related to either beneficial or harmful consequences. Microglia activation is associated with the release of protective or deleterious cytokines, chemokines, and growth factors that can in turn determine defensive or pathological outcomes. This scenario is complicated by the pathology-related specific phenotypes that microglia can assume, thus leading to the so-called disease-associated microglia phenotypes. Microglia express several receptors that regulate the balance between pro- and anti-inflammatory features, sometimes exerting opposite actions on microglial functions according to specific conditions. In this context, group I metabotropic glutamate receptors (mGluRs) are molecular structures that may contribute to the modulation of the reactive phenotype of microglia cells, and this is worthy of exploration. Here, we summarize the role of group I mGluRs in shaping microglia cells’ phenotype in specific physio-pathological conditions, including some neurodegenerative disorders. A significant section of the review is specifically focused on amyotrophic lateral sclerosis (ALS) since it represents an entirely unexplored topic of research in the field. Full article

(This article belongs to the Special Issue The Role of Glial Cells in Health and Disease)

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19 pages, 2049 KiB

Open AccessReview

GABA Release from Astrocytes in Health and Disease

by Werner Kilb and Sergei Kirischuk

Int. J. Mol. Sci. 2022, 23(24), 15859; https://doi.org/10.3390/ijms232415859 - 13 Dec 2022

Cited by 19 | Viewed by 4307

Abstract

Astrocytes are the most abundant glial cells in the central nervous system (CNS) mediating a variety of homeostatic functions, such as spatial K⁺ buffering or neurotransmitter reuptake. In addition, astrocytes are capable of releasing several biologically active substances, including glutamate and GABA. Astrocyte-mediated GABA release has been a matter of debate because the expression level of the main GABA synthesizing enzyme glutamate decarboxylase is quite low in astrocytes, suggesting that low intracellular GABA concentration ([GABA]_i) might be insufficient to support a non-vesicular GABA release. However, recent studies demonstrated that, at least in some regions of the CNS, [GABA]_i in astrocytes might reach several millimoles both under physiological and especially pathophysiological conditions, thereby enabling GABA release from astrocytes via GABA-permeable anion channels and/or via GABA transporters operating in reverse mode. In this review, we summarize experimental data supporting both forms of GABA release from astrocytes in health and disease, paying special attention to possible feedback mechanisms that might govern the fine-tuning of astrocytic GABA release and, in turn, the tonic GABA_A receptor-mediated inhibition in the CNS. Full article

(This article belongs to the Special Issue The Role of Glial Cells in Health and Disease)

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11 pages, 2128 KiB

Open AccessBrief Report

Pulsating Extremely Low-Frequency Electromagnetic Fields Influence Differentiation of Mouse Neural Stem Cells towards Astrocyte-like Phenotypes: In Vitro Pilot Study

by Jasmina Isaković, Filip Slatković, Denis Jagečić, Dražen Juraj Petrović and Dinko Mitrečić

Int. J. Mol. Sci. 2024, 25(7), 4038; https://doi.org/10.3390/ijms25074038 - 4 Apr 2024

Viewed by 1130

Abstract

Even though electromagnetic fields have been reported to assist endogenous neurogenesis, little is known about the exact mechanisms of their action. In this pilot study, we investigated the effects of pulsating extremely low-frequency electromagnetic fields on neural stem cell differentiation towards specific phenotypes, such as neurons and astrocytes. Neural stem cells isolated from the telencephalic wall of B6(Cg)-Tyrc-2J/J mouse embryos (E14.5) were randomly divided into three experimental groups and three controls. Electromagnetic field application setup included a solenoid placed within an incubator. Each of the experimental groups was exposed to 50Hz ELF-EMFs of varied strengths for 1 h. The expression of each marker (NES, GFAP, β-3 tubulin) was then assessed by immunocytochemistry. The application of high-strength ELF-EMF significantly increased and low-strength ELF-EMF decreased the expression of GFAP. A similar pattern was observed for β-3 tubulin, with high-strength ELF-EMFs significantly increasing the immunoreactivity of β-3 tubulin and medium- and low-strength ELF-EMFs decreasing it. Changes in NES expression were observed for medium-strength ELF-EMFs, with a demonstrated significant upregulation. This suggests that, even though ELF-EMFs appear to inhibit or promote the differentiation of neural stem cells into neurons or astrocytes, this effect highly depends on the strength and frequency of the fields as well as the duration of their application. While numerous studies have demonstrated the capacity of EMFs to guide the differentiation of NSCs into neuron-like cells or β-3 tubulin+ neurons, this is the first study to suggest that ELF-EMFs may also steer NSC differentiation towards astrocyte-like phenotypes. Full article

(This article belongs to the Special Issue The Role of Glial Cells in Health and Disease)

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