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Microglial Cells

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 2734

Special Issue Editor


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Guest Editor
Institute of Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany
Interests: Neuroinflammation

Special Issue Information

Dear Colleagues,

Microglia are the resident immune cells of the central nervous system. They derive from the yolk sack, are long-lived cells and, under normal conditions, their population is not replenished by monocytes but is sustained through self-renewal. They are highly motile cells continuously patrolling their environment through their long extensions, but, as active phagocytes, they can acquire an amoeboid morphology, i.e., enlarged cell body and shorter branches. They guide synapse formation and activity, neurogenesis, myelin sheath formation and neuronal and glial functions through phagocytosis, cell-to-cell contact and secretion of cytokines, trophic factors, and other molecules. Human microglia, in particular, present substantial heterogeneity. In human neurodegenerative disease and murine mouse models, microglial cell subpopulations display heterogeneous features, with detrimental as well as protective functions. Delineating the mechanisms that regulate these functions could pave the way for the development of therapeutic strategies for neurodegenerative disease.

Dr. Vasileia Ismini Alexaki
Guest Editor

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Keywords

  • microglia
  • Alzheimer's disease
  • Parkinson's disease
  • multiple sclerosis
  • neuroinflammation
  • neurodegeneration

Published Papers (1 paper)

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Research

14 pages, 2652 KiB  
Article
Functional Expression of Choline Transporters in Microglia and Their Regulation of Microglial M1/M2 Polarization
by Toshio Okada, Eisuke Muto, Tsuyoshi Yamanaka, Hiroyuki Uchino and Masato Inazu
Int. J. Mol. Sci. 2022, 23(16), 8924; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23168924 - 10 Aug 2022
Cited by 3 | Viewed by 2133
Abstract
Background: Microglia are key cells of the immune system in the central nervous system and are suggested to be deeply involved in the development of neurodegenerative diseases. It is well known that microglia have functional plasticity, with an inflammatory M1 phenotype and an [...] Read more.
Background: Microglia are key cells of the immune system in the central nervous system and are suggested to be deeply involved in the development of neurodegenerative diseases. It is well known that microglia have functional plasticity, with an inflammatory M1 phenotype and an anti-inflammatory M2 phenotype. Inhibition of choline transport in macrophages has been reported to suppress the secretion of inflammatory cytokines. However, the role of the choline transport system in regulating microglial M1/M2 polarization has not been fully elucidated to date. In this study, we investigated the mechanism of choline uptake in microglia, and its association with microglial M1/M2 polarization. Methods: The immortalized mouse microglial cell line SIM-A9 was used for [3H]choline uptake and expression analysis of choline transporters. The association between the choline uptake system and the M1/M2 polarization of microglia was also analyzed. Results: Choline transporter-like protein (CTL) 1 and CTL2 were highly expressed in SIM-A9 cells, and CTL1 and CTL2 were localized in the plasma membrane and mitochondria, respectively. Functional analysis of choline uptake demonstrated the existence of Na+-independent, pH-dependent, and intermediate-affinity choline transport systems. Choline uptake was concentration-dependently inhibited by hemicholinium-3 (HC-3), an inhibitor of choline uptake, and increased by lipopolysaccharide (LPS) and interleukin-4 (IL-4). Expression of the mRNA of M1 microglia markers IL-1β and IL-6 was increased by LPS, and their effects were suppressed by choline deprivation and HC-3. In contrast, mRNA expression of the M2 microglial marker arginase-1 (Arg-1) was increased by IL-4, and the effect was enhanced by choline deprivation and HC-3. Conclusions: Our results suggest that inhibition of CTL1-mediated choline uptake in microglia preferentially induces M2 microglia polarization, which is a potential therapeutic approach for inflammatory brain diseases. Full article
(This article belongs to the Special Issue Microglial Cells)
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