Molecular and Epigenetic Mechanisms Regulating Neurons and Glial Cells in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 1911

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Guest Editor
Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117594, Singapore
Interests: neurodevelopmental disorders; microglia-mediated neuroinflammation; neuropathology
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Special Issue Information

Dear Colleagues,

Modern neuroscience has revealed the increasing emphasis on neurons and glial cells as well as their crosstalk in the pathology and progression of neurodegenerative disorders. Microglia, oligodendrocytes and astrocytes perform critical roles in healthy functioning and upkeep of neurons in the brain and spinal cord. However, under pathological conditions, biomechanisms governing this cellular milieu begin to dysregulate the microenvironment in pursuit of reinstating homeostasis; this initiates molecular, and epigenetic cascades that more often than not turn detrimental to neuronal function through numerous pathways involving factors such as inflammatory cytokines, proteinopathies and impaired neuron–glia communication leading to events such as excitotoxicity. It has become imperative to approach neurological disorders that may be pathological (i.e., strokes, spinal cord injury) or physiological (i.e., Alzheimer’s dementia, age-associated cognitive deficits) from the perspective of understanding glia and their complex role in the induction and evolution of such disorders.

In this Special Issue of Cells, we look forward to publishing original research articles and reviews on the mechanisms of neurons and glial and their roles in neurological and neurodegenerative conditions. We hope that this approach shall be constructive towards realizing breakthroughs and improved therapeutic strategies for neurological conditions.

Porf. Dr. S. Thameem Dheen
Guest Editor

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Keywords

  • neurodegenerative disorders
  • neurons
  • glial cells
  • neuropathology

Published Papers (1 paper)

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Research

18 pages, 7669 KiB  
Article
Maternal Diabetes Deregulates the Expression of Mecp2 via miR-26b-5p in Mouse Embryonic Neural Stem Cells
by Sukanya Shyamasundar, Seshadri Ramya, Deepika Kandilya, Dinesh Kumar Srinivasan, Boon Huat Bay, Suraiya Anjum Ansari and S Thameem Dheen
Cells 2023, 12(11), 1516; https://doi.org/10.3390/cells12111516 - 30 May 2023
Cited by 2 | Viewed by 1658
Abstract
Maternal diabetes has been associated with a greater risk of neurodevelopmental disorders in offspring. It has been established that hyperglycemia alters the expression of genes and microRNAs (miRNAs) regulating the fate of neural stem cells (NSCs) during brain development. In this study, the [...] Read more.
Maternal diabetes has been associated with a greater risk of neurodevelopmental disorders in offspring. It has been established that hyperglycemia alters the expression of genes and microRNAs (miRNAs) regulating the fate of neural stem cells (NSCs) during brain development. In this study, the expression of methyl-CpG-binding protein-2 (Mecp2), a global chromatin organizer and a crucial regulator of synaptic proteins, was analyzed in NSCs obtained from the forebrain of embryos of diabetic mice. Mecp2 was significantly downregulated in NSCs derived from embryos of diabetic mice when compared to controls. miRNA target prediction revealed that the miR-26 family could regulate the expression of Mecp2, and further validation confirmed that Mecp2 is a target of miR-26b-5p. Knockdown of Mecp2 or overexpression of miR-26b-5p altered the expression of tau protein and other synaptic proteins, suggesting that miR-26b-5p alters neurite outgrowth and synaptogenesis via Mecp2. This study revealed that maternal diabetes upregulates the expression of miR-26b-5p in NSCs, resulting in downregulation of its target, Mecp2, which in turn perturbs neurite outgrowth and expression of synaptic proteins. Overall, hyperglycemia dysregulates synaptogenesis that may manifest as neurodevelopmental disorders in offspring from diabetic pregnancy. Full article
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