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Biomedicines
Special Issues
Satellite Glial Cells, Astrocytes, and Microglia: From Structure to Function
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Satellite Glial Cells, Astrocytes, and Microglia: From Structure to Function

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 8084

Special Issue Editors

Dr. Maria Grazia Mola

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnology and Environment, University of Bari Aldo Moro, 70125 Bari, Italy
Interests: cell physiology; neuroscience; astrocytes; biomaterials; water transport; aquaporins; drug screening; Ion channels; inflammation; cancer
Dr. Antonio Cibelli

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnology and Environment, University of Bari Aldo Moro, 70125 Bari, Italy
Interests: neuroscience; astrocytes; blood brain barrier

Special Issue Information

Dear Colleagues,

Glial cells have long been known to exhibit pleiotropic homeostatic activity in the brain during development, adulthood, and recovery from neural injury.

In the embryo, glial cells form a cellular framework that enables development of the nervous system and controls neuronal survival and differentiation.

Glial cells constantly face osmotic challenges resulting from their own metabolic function or that of neighbouring cells, and from cellular behaviours such as cell migration, proliferation, differentiation, signaling, and apoptosis.

They maintain appropriate ion and water levels in the neural environment as they are equipped with a pool of ion and water channels facing fluid-filled spaces, including gap junctions; these enable cells to form an interconnected network where information is exchanged through calcium waves and signaling molecules. Furthermore, glial cells contribute to innate immune surveillance of the brain and are major regulators of neuronal repair.

Glial function dysregulation characterises many neurodegenerative disorders, but complete appreciation of the underlying pathophysiology is lacking.

New insights in glial cell biology, and in the dynamic interactions of neurons and glia, will enrich our understanding of nervous system formation, health, and function. Moreover, emerging developments in neuronal stem cell biology represent an exciting interface between technology and biology.

Thus, the goal of the present Special Issue is to provide a comprehensive overview of the most recent advances in neural differentiation and developmental neurobiology, with a focus on glial cells. We welcome articles containing original research, reviews, and mini-reviews that employ morphological, biophysical, cellular, molecular, pharmacological, or physiological methods to investigate the molecular basis of proliferation, migration, differentiation, circuit formation, and neuron/glia interaction during both normal development and regeneration or disease.

The transplantation of neural stem cells (NSCs) is an emerging treatment for neural degeneration. The use of novel bionanomaterials in guiding the differentiation of neural progenitors could be interesting for regulating the behaviours of NSCs and potentially establishing their use in clinical treatment.

Dr. Maria Grazia Mola
Dr. Antonio Cibelli
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • glial cells
  • neurodevelopment
  • CNS homeostasis
  • water channels
  • ion channels
  • gap junctions
  • biomaterials
  • CNS repair

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Published Papers (2 papers)

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25 pages, 6326 KiB  
Article
The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes
by Vanda Balint, Mina Peric, Sanja Dacic, Danijela Stanisavljevic Ninkovic, Jelena Marjanovic, Jelena Popovic, Milena Stevanovic and Andrijana Lazic
Biomedicines 2024, 12(4), 796; https://doi.org/10.3390/biomedicines12040796 - 3 Apr 2024
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Abstract
Astrocytes are the main homeostatic cells in the central nervous system, with the unique ability to transform from quiescent into a reactive state in response to pathological conditions by reacquiring some precursor properties. This process is known as reactive astrogliosis, a compensatory response [...] Read more.
Astrocytes are the main homeostatic cells in the central nervous system, with the unique ability to transform from quiescent into a reactive state in response to pathological conditions by reacquiring some precursor properties. This process is known as reactive astrogliosis, a compensatory response that mediates tissue damage and recovery. Although it is well known that SOX transcription factors drive the expression of phenotype-specific genetic programs during neurodevelopment, their roles in mature astrocytes have not been studied extensively. We focused on the transcription factors SOX2 and SOX9, shown to be re-expressed in reactive astrocytes, in order to study the reactivation-related functional properties of astrocytes mediated by those proteins. We performed an initial screening of SOX2 and SOX9 expression after sensorimotor cortex ablation injury in rats and conducted gain-of-function studies in vitro using astrocytes derived from the human NT2/D1 cell line. Our results revealed the direct involvement of SOX2 in the reacquisition of proliferation in mature NT2/D1-derived astrocytes, while SOX9 overexpression increased migratory potential and glutamate uptake in these cells. Our results imply that modulation of SOX gene expression may change the functional properties of astrocytes, which holds promise for the discovery of potential therapeutic targets in the development of novel strategies for tissue regeneration and recovery. Full article
(This article belongs to the Special Issue Satellite Glial Cells, Astrocytes, and Microglia: From Structure to Function)
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20 pages, 4304 KiB  
Article
Type VI Secretion System Accessory Protein TagAB-5 Promotes Burkholderia pseudomallei Pathogenicity in Human Microglia
by Sanisa Lohitthai, Amporn Rungruengkitkun, Niramol Jitprasutwit, Thida Kong-Ngoen, Taksaon Duangurai, Sarunporn Tandhavanant, Passanesh Sukphopetch, Narisara Chantratita, Nitaya Indrawattana and Pornpan Pumirat
Biomedicines 2023, 11(11), 2927; https://doi.org/10.3390/biomedicines11112927 - 30 Oct 2023
Cited by 2 | Viewed by 1963
Abstract
Central nervous system (CNS) melioidosis caused by Burkholderia pseudomallei is being increasingly reported. Because of the high mortality associated with CNS melioidosis, understanding the underlying mechanism of B. pseudomallei pathogenesis in the CNS needs to be intensively investigated to develop better therapeutic strategies [...] Read more.
Central nervous system (CNS) melioidosis caused by Burkholderia pseudomallei is being increasingly reported. Because of the high mortality associated with CNS melioidosis, understanding the underlying mechanism of B. pseudomallei pathogenesis in the CNS needs to be intensively investigated to develop better therapeutic strategies against this deadly disease. The type VI secretion system (T6SS) is a multiprotein machine that uses a spring-like mechanism to inject effectors into target cells to benefit the infection process. In this study, the role of the T6SS accessory protein TagAB-5 in B. pseudomallei pathogenicity was examined using the human microglial cell line HCM3, a unique resident immune cell of the CNS acting as a primary mediator of inflammation. We constructed B. pseudomallei tagAB-5 mutant and complementary strains by the markerless allele replacement method. The effects of tagAB-5 deletion on the pathogenicity of B. pseudomallei were studied by bacterial infection assays of HCM3 cells. Compared with the wild type, the tagAB-5 mutant exhibited defective pathogenic abilities in intracellular replication, multinucleated giant cell formation, and induction of cell damage. Additionally, infection by the tagAB-5 mutant elicited a decreased production of interleukin 8 (IL-8) in HCM3, suggesting that efficient pathogenicity of B. pseudomallei is required for IL-8 production in microglia. However, no significant differences in virulence in the Galleria mellonella model were observed between the tagAB-5 mutant and the wild type. Taken together, this study indicated that microglia might be an important intracellular niche for B. pseudomallei, particularly in CNS infection, and TagAB-5 confers B. pseudomallei pathogenicity in these cells. Full article
(This article belongs to the Special Issue Satellite Glial Cells, Astrocytes, and Microglia: From Structure to Function)
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