Special Issue "Astrocyte Antioxidant Systems"

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 May 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Gethin J. McBean

UCD School of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin 4, Ireland
Website | E-Mail
Interests: mechanisms of action of antioxidants in the brain; Particularly, the importance of sulfur-containing amino acids in thiol redox balance and antioxidant defence in astrocytes and microglial cells

Special Issue Information

Dear Colleagues,

Astrocytes play an essential role in protecting the brain from oxidative stress, particularly in the context of providing antioxidant support for neurons. Several species of antioxidant, including thiol-based antioxidants and phase II antioxidant enzymes, which include heme oxygenase-1, NAD(P)H: quinone oxidoreductase, manganese superoxide dismutase and catalase are expressed in astrocytes. In the past 10–15 years, details have emerged of how astrocytes are responsible for the de novo synthesis of antioxidants, and for mediating the transfer of the components of major antioxidant molecules, such as glutathione, to neurons. Much remains to be discovered of how antioxidant production in astrocytes is regulated and how these cells respond to oxidative stress to boost their antioxidant capacity and neuroprotective function.
This Special Issue will publish original research papers and reviews on aspects of astrocyte antioxidants that relate to the following topics: the function and regulation of antioxidants in astrocytes; understanding the pathways of thiol redox homeostasis and of provision of precursors for antioxidant synthesis; the relationship between astrocyte antioxidants and neuroprotection; agents that promote the antioxidant capacity of astrocytes; and the potential of antioxidant systems in astrocytes as a therapeutic target.  

Prof. Dr. Gethin McBean
Guest Editor

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 papers will be 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. Antioxidants 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 550 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

  • Glutathione
  • Thioredoxin
  • Glutaredoxin
  • Peroxideroxin
  • Transcription factor Nrf2
  • Cysteine/cystine
  • Transulfuration
  • Hemeoxygenase
  • NAD(P)H:quinone oxidoreductase
  • Superoxide dismutase

Published Papers (5 papers)

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Editorial

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Open AccessEditorial Astrocyte Antioxidant Systems
Antioxidants 2018, 7(9), 112; https://doi.org/10.3390/antiox7090112
Received: 17 August 2018 / Accepted: 23 August 2018 / Published: 27 August 2018
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(This article belongs to the Special Issue Astrocyte Antioxidant Systems)

Research

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Open AccessArticle Interleukin-1β Protects Neurons against Oxidant-Induced Injury via the Promotion of Astrocyte Glutathione Production
Antioxidants 2018, 7(8), 100; https://doi.org/10.3390/antiox7080100
Received: 8 June 2018 / Revised: 4 July 2018 / Accepted: 21 July 2018 / Published: 25 July 2018
Cited by 1 | PDF Full-text (2737 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervous System (CNS), is enhanced in many neurological diseases/disorders. Although IL-1β contributes to and/or sustains pathophysiological processes in the CNS, we recently demonstrated that IL-1β can protect cortical astrocytes from oxidant injury
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Interleukin-1β (IL-1β), a key cytokine that drives neuroinflammation in the Central Nervous System (CNS), is enhanced in many neurological diseases/disorders. Although IL-1β contributes to and/or sustains pathophysiological processes in the CNS, we recently demonstrated that IL-1β can protect cortical astrocytes from oxidant injury in a glutathione (GSH)-dependent manner. To test whether IL-1β could similarly protect neurons against oxidant stress, near pure neuronal cultures or mixed cortical cell cultures containing neurons and astrocytes were exposed to the organic peroxide, tert-butyl hydroperoxide (t-BOOH), following treatment with IL-1β or its vehicle. Neurons and astrocytes in mixed cultures, but not pure neurons, were significantly protected from the toxicity of t-BOOH following treatment with IL-1β in association with enhanced GSH production/release. IL-1β failed to increase the GSH levels or to provide protection against t-BOOH toxicity in chimeric mixed cultures consisting of IL-1R1+/+ neurons plated on top of IL-1R1−/− astrocytes. The attenuation of GSH release via block of multidrug resistance-associated protein 1 (MRP1) transport also abrogated the protective effect of IL-1β. These protective effects were not strictly an in vitro phenomenon as we found an increased striatal vulnerability to 3-nitropropionic acid-mediated oxidative stress in IL-1R1 null mice. Overall, our data indicate that IL-1β protects neurons against oxidant injury and that this likely occurs in a non-cell-autonomous manner that relies on an increase in astrocyte GSH production and release. Full article
(This article belongs to the Special Issue Astrocyte Antioxidant Systems)
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Open AccessArticle Early and Late Induction of KRAS and HRAS Proto-Oncogenes by Reactive Oxygen Species in Primary Astrocytes
Antioxidants 2017, 6(3), 48; https://doi.org/10.3390/antiox6030048
Received: 1 June 2017 / Revised: 17 June 2017 / Accepted: 19 June 2017 / Published: 29 June 2017
Cited by 1 | PDF Full-text (3593 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Astrocytes, one of the predominant types of glial cells, function as both supportive and metabolic cells for the brain. Among mammalian tissues, the highest levels of p21Ras protein are detected in the brain. Here, we investigated the expression of KRAS and HRAS
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Astrocytes, one of the predominant types of glial cells, function as both supportive and metabolic cells for the brain. Among mammalian tissues, the highest levels of p21Ras protein are detected in the brain. Here, we investigated the expression of KRAS and HRAS proto-oncogenes in primary astrocytes following acute oxidative stimulation. Reactive oxygen species (ROS) changed the expression of proto-oncogenes at both transcriptional and translational levels. De novo protein synthesis analysis measured approximate values of proteins half-life, ranging from 1–4 h, of the different H- and K- isoforms by western blot analysis. Quantitative gene expression analysis of KRAS and HRAS revealed an unexpected short-term induction of KRAS mRNA in primary astrocytes in response to acute stimulation. Indeed, cultured astrocytes responded to proteasomal inhibition by preventing the reduction of c-K-Ras. A fraction of K-Ras protein accumulated in the presence of ROS and cycloheximide, while a substantial proportion was continuously synthesized. These data indicate that ROS regulate in a complementary fashion p21Ras isoforms in primary astrocytes: K-Ras is rapidly and transiently induced by post-translational and post-transcriptional mechanisms, while H-Ras is stably induced by mRNA accumulation. We suggest that K-Ras and H-Ras are ROS sensors that adapt cells to metabolic needs and oxidative stress. Full article
(This article belongs to the Special Issue Astrocyte Antioxidant Systems)
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Review

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Open AccessReview Are Astrocytes the Predominant Cell Type for Activation of Nrf2 in Aging and Neurodegeneration?
Antioxidants 2017, 6(3), 65; https://doi.org/10.3390/antiox6030065
Received: 13 June 2017 / Revised: 11 August 2017 / Accepted: 16 August 2017 / Published: 18 August 2017
Cited by 6 | PDF Full-text (702 KB) | HTML Full-text | XML Full-text
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates hundreds of antioxidant genes, and is activated in response to oxidative stress. Given that many neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease and multiple sclerosis
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Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates hundreds of antioxidant genes, and is activated in response to oxidative stress. Given that many neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease and multiple sclerosis are characterised by oxidative stress, Nrf2 is commonly activated in these diseases. Evidence demonstrates that Nrf2 activity is repressed in neurons in vitro, and only cultured astrocytes respond strongly to Nrf2 inducers, leading to the interpretation that Nrf2 signalling is largely restricted to astrocytes. However, Nrf2 activity can be observed in neurons in post-mortem brain tissue and animal models of disease. Thus this interpretation may be false, and a detailed analysis of the cell type expression of Nrf2 in neurodegenerative diseases is required. This review describes the evidence for Nrf2 activation in each cell type in prominent neurodegenerative diseases and normal aging in human brain and animal models of neurodegeneration, the response to pharmacological and genetic modulation of Nrf2, and clinical trials involving Nrf2-modifying drugs. Full article
(This article belongs to the Special Issue Astrocyte Antioxidant Systems)
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Open AccessReview Cysteine, Glutathione, and Thiol Redox Balance in Astrocytes
Antioxidants 2017, 6(3), 62; https://doi.org/10.3390/antiox6030062
Received: 13 July 2017 / Revised: 31 July 2017 / Accepted: 1 August 2017 / Published: 3 August 2017
Cited by 9 | PDF Full-text (917 KB) | HTML Full-text | XML Full-text
Abstract
This review discusses the current understanding of cysteine and glutathione redox balance in astrocytes. Particular emphasis is placed on the impact of oxidative stress and astrocyte activation on pathways that provide cysteine as a precursor for glutathione. The effect of the disruption of
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This review discusses the current understanding of cysteine and glutathione redox balance in astrocytes. Particular emphasis is placed on the impact of oxidative stress and astrocyte activation on pathways that provide cysteine as a precursor for glutathione. The effect of the disruption of thiol-containing amino acid metabolism on the antioxidant capacity of astrocytes is also discussed. Full article
(This article belongs to the Special Issue Astrocyte Antioxidant Systems)
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