The Role of Glial Cells in the Neuro-Vascular Unit in Health and Disease

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuroglia".

Deadline for manuscript submissions: 15 December 2024 | Viewed by 821

Special Issue Editors


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Department of Experimental and Clinical Medicine, Anatomy Section, School of Human Health Sciences, University of Florence, 50121 Florence, Italy
Interests: blood–brain barrier; vitamin D; cadmium toxicity; cannabidiol; neuroprotection
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Department of Experimental and Clinical Medicine (DMSC), Anatomy Section, School of Human Health Sciences, University of Florence, Florence, Italy
Interests: neuropathic pain; blood–brain barrier; cadmium toxicity; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are delighted to announce this Special Issue, titled “The Role of Glial Cells in the Neuro-vascular Unit in Health and Disease”, of Brain Sciences.

Nowadays, the pathologies affecting the central nervous system are deleterious constants mainly due to the longer life expectancy of modern humans.

Glial cells play a pivotal role within the central nervous system, even though for decades they came second to neurons as a research object. The term “glia” includes three main different types of cells: astrocytes, microglia, and oligodendrocytes. While our primary understanding of glial cells encompassed a trophic and support role, over the years, our knowledge of other functions has increased dramatically, both contributing to knowledge on the physiological function of the central nervous system and many processes associated with brain pathologies, including acute or chronic damage. The plasticity of glia is widely known, which could be due to the interactive position of glial cells within the neuro-vascular unit between brain endothelial cells and neurons. This active interconnection is able to trigger detrimental events that can occur within the CNS but also ameliorate and prevent deleterious effects in order to restore the brain homeostasis. For these reasons, our understanding of the role of glial cells is still incomplete and fragmented; indeed, whether CNS damage is triggered by glial activation or brain impairments that induce glial activation is still unclear, thus complicating the pathology.

This Special Issue of Brain Sciences aims to collect the most significant advances in understanding NVU glial cells’ function and interplay within the central nervous system both during normal and pathological conditions. Original research articles and comprehensive reviews are welcome.

Dr. Jacopo Junio Valerio Branca
Prof. Dr. Alessandra Pacini
Guest Editors

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Keywords

  • glial cells
  • astrocytes
  • microglia
  • oligodendrocytes
  • neuro-vascular unit
  • central nervous system

Published Papers (1 paper)

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Research

14 pages, 1069 KiB  
Article
Natural Compounds Oridonin and Shikonin Exhibit Potentially Beneficial Regulatory Effects on Select Functions of Microglia
by Bridget K. Greuel, Dylan E. Da Silva, Victoria N. Robert-Gostlin and Andis Klegeris
Brain Sci. 2024, 14(4), 328; https://doi.org/10.3390/brainsci14040328 - 28 Mar 2024
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Abstract
Accumulating evidence indicates that the adverse neuroimmune activation of microglia, brain immunocytes that support neurons, contributes to a range of neuroinflammatory disorders, including Alzheimer’s disease. Correcting the abnormal functions of microglia is a potential therapeutic strategy for these diseases. Nucleotide-binding domain leucine-rich repeat [...] Read more.
Accumulating evidence indicates that the adverse neuroimmune activation of microglia, brain immunocytes that support neurons, contributes to a range of neuroinflammatory disorders, including Alzheimer’s disease. Correcting the abnormal functions of microglia is a potential therapeutic strategy for these diseases. Nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor (NLRP) 3 inflammasomes are implicated in adverse microglial activation and their inhibitors, such as the natural compounds oridonin and shikonin, reduce microglial immune responses. We hypothesized that some of the beneficial effects of oridonin and shikonin on microglia are independent of their suppression of NLRP3 inflammasomes. Murine and human microglia-like cells were stimulated with bacterial lipopolysaccharide (LPS) only, which did not induce NLRP3 inflammasome activation or the resulting secretion of interleukin (IL)-1β, allowing for the identification of other anti-inflammatory effects. Under these experimental conditions, both oridonin and shikonin reduced nitric oxide (NO) secretion and the cytotoxicity of BV-2 murine microglia towards HT-22 murine neuronal cells, but upregulated BV-2 cell phagocytic activity. Only oridonin inhibited the secretion of tumor necrosis factor (TNF) by stimulated BV-2 microglia, while only shikonin suppressed the respiratory burst response of human HL-60 microglia-like cells. This observed discrepancy indicates that these natural compounds may have different molecular targets in microglia. Overall, our results suggest that oridonin and shikonin should be further investigated as pharmacological agents capable of correcting dysfunctional microglia, supporting their potential use in neuroinflammatory disorders. Full article
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