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Extracellular Vesicles-Related Cellular Events in Neuronal Biology: Regulated Cell Death,...
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Extracellular Vesicles-Related Cellular Events in Neuronal Biology: Regulated Cell Death, Autophagy, Unfolded Protein Response, and Stress-Related Pathways

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

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 3882

Special Issue Editor

Prof. Dr. Theologos Michaelidis

E-Mail Website
Guest Editor
1. Associate Professor, Department of Biological Applications and Technologies, University of Ioannina, Ioannina, Greece
2. Collaborating Research Scientist/Group Leader, Institute of Biomedical Research, Foundation for Research and Technology, Hellas, Greece
Interests: programmed cell death; neuronal differentiation; signal transduction pathways; early-life stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A better understanding of the mechanisms governing nervous system development and controlling neuronal response to stress, as well as synaptic plasticity and neurogenesis can lead to new therapeutic approaches for the prevention and management of neurodegeneration. Extracellular vesicles (EVs) have recently emerged as versatile elements of cellular communication in the nervous system, transporting a variety of biologically active molecules such as lipids, nucleic acids, and proteins that can regulate tissue homeostasis. They are secreted by virtually all brain cell types, including neurons, oligodendrocytes, astrocytes, and microglia, and play instrumental roles in the homeostasis and function of the nervous system. Accumulating evidence suggests that neuron-derived and glia-derived EVs in adult neurogenic niches represent a novel mechanism of intercellular communication that plays major roles in the maintenance of neuronal function and in normal brain physiology. The EVs are also involved in the unfolded protein response (UPR), an adaptive mechanism that is triggered by endoplasmic reticulum (ER) stress and helps the cell restore homeostasis. A growing body of research demonstrates an important and intricate crosstalk between EVs and autophagy that can influence cell fate decisions, and further, that EVs can be released by dying cells during different programmed cell death mechanisms thereby contributing to the pathology and spreading of neurodegenerative diseases. The purpose of this Special Issue is to present the latest research on the molecular mechanisms that coordinate the functions of extracellular vesicles and exosomes in ER stress, UPR response, autophagy, and regulated cell death, and how the dysregulation of this balance can lead to pathological processes in the nervous system, including neurodegenerative diseases, spinal cord injuries, or mental disorders. Both original research articles and comprehensive reviews are welcomed. Guest Editor

Dr. Theologos M Michaelidis
Guest Editor

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Keywords

  • extracellular vesicles
  • exosomes
  • regulated (or programmed) cell death
  • autophagy
  • homeostasis, stress
  • unfolded protein response (UPR) signaling pathways
  • endoplasmic reticulum (ER) stress
  • protein quality control (PQC)
  • mitochondria
  • neuron
  • neurogenesis
  • neurodegeneration
  • brain

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Published Papers (1 paper)

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Review

34 pages, 3816 KiB  
Review
The Yin and Yang of Microglia-Derived Extracellular Vesicles in CNS Injury and Diseases
by Mousumi Ghosh and Damien D. Pearse
Cells 2024, 13(22), 1834; https://doi.org/10.3390/cells13221834 - 6 Nov 2024
Cited by 2 | Viewed by 3391
Abstract
Microglia, the resident immune cells of the central nervous system (CNS), play a crucial role in maintaining neural homeostasis but can also contribute to disease and injury when this state is disrupted or conversely play a pivotal role in neurorepair. One way that [...] Read more.
Microglia, the resident immune cells of the central nervous system (CNS), play a crucial role in maintaining neural homeostasis but can also contribute to disease and injury when this state is disrupted or conversely play a pivotal role in neurorepair. One way that microglia exert their effects is through the secretion of small vesicles, microglia-derived exosomes (MGEVs). Exosomes facilitate intercellular communication through transported cargoes of proteins, lipids, RNA, and other bioactive molecules that can alter the behavior of the cells that internalize them. Under normal physiological conditions, MGEVs are essential to homeostasis, whereas the dysregulation of their production and/or alterations in their cargoes have been implicated in the pathogenesis of numerous neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), spinal cord injury (SCI), and traumatic brain injury (TBI). In contrast, MGEVs may also offer therapeutic potential by reversing inflammation or being amenable to engineering for the delivery of beneficial biologics or drugs. The effects of MGEVs are determined by the phenotypic state of the parent microglia. Exosomes from anti-inflammatory or pro-regenerative microglia support neurorepair and cell survival by delivering neurotrophic factors, anti-inflammatory mediators, and molecular chaperones. Further, MGEVs can also deliver components like mitochondrial DNA (mtDNA) and proteins to damaged neurons to enhance cellular metabolism and resilience. MGEVs derived from pro-inflammatory microglia can have detrimental effects on neural health. Their cargo often contains pro-inflammatory cytokines, molecules involved in oxidative stress, and neurotoxic proteins, which can exacerbate neuroinflammation, contribute to neuronal damage, and impair synaptic function, hindering neurorepair processes. The role of MGEVs in neurodegeneration and injury—whether beneficial or harmful—largely depends on how they modulate inflammation through the pro- and anti-inflammatory factors in their cargo, including cytokines and microRNAs. In addition, through the propagation of pathological proteins, such as amyloid-beta and alpha-synuclein, MGEVs can also contribute to disease progression in disorders such as AD and PD, or by the transfer of apoptotic or necrotic factors, they can induce neuron toxicity or trigger glial scarring during neurological injury. In this review, we have provided a comprehensive and up-to-date understanding of the molecular mechanisms underlying the multifaceted role of MGEVs in neurological injury and disease. In particular, the role that specific exosome cargoes play in various pathological conditions, either in disease progression or recovery, will be discussed. The therapeutic potential of MGEVs has been highlighted including potential engineering methodologies that have been employed to alter their cargoes or cell-selective targeting. Understanding the factors that influence the balance between beneficial and detrimental exosome signaling in the CNS is crucial for developing new therapeutic strategies for neurodegenerative diseases and neurotrauma. Full article
(This article belongs to the Special Issue Extracellular Vesicles-Related Cellular Events in Neuronal Biology: Regulated Cell Death, Autophagy, Unfolded Protein Response, and Stress-Related Pathways)
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