Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.
Identifieur interne : 000182 ( Main/Exploration ); précédent : 000181; suivant : 000183Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.
Auteurs : Olga Gorelenkova Miller [États-Unis] ; John J. Mieyal [États-Unis]Source :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Dosage génique (MeSH), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Maladie de Parkinson (génétique), Maladie de Parkinson (métabolisme), Microglie (métabolisme), Mésencéphale (métabolisme), Neurones dopaminergiques (métabolisme), Protein deglycase DJ-1 (métabolisme), Régulation négative (MeSH), Âge de début (MeSH).
- MESH :
- génétique : Glutarédoxines, Maladie de Parkinson.
- métabolisme : Glutarédoxines, Maladie de Parkinson, Microglie, Mésencéphale, Neurones dopaminergiques, Protein deglycase DJ-1.
- Animaux, Dosage génique, Humains, Régulation négative, Âge de début.
English descriptors
- KwdEn :
- Age of Onset (MeSH), Animals (MeSH), Dopaminergic Neurons (metabolism), Down-Regulation (MeSH), Gene Dosage (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Humans (MeSH), Mesencephalon (metabolism), Microglia (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Protein Deglycase DJ-1 (metabolism).
- MESH :
- chemical , genetics : Glutaredoxins.
- genetics : Parkinson Disease.
- metabolism : Dopaminergic Neurons, Glutaredoxins, Mesencephalon, Microglia, Parkinson Disease, Protein Deglycase DJ-1.
- Age of Onset, Animals, Down-Regulation, Gene Dosage, Humans.
Abstract
SIGNIFICANCE
Glutaredoxin (Grx)1, an evolutionarily conserved and ubiquitous enzyme, regulates redox signal transduction and protein redox homeostasis by catalyzing reversible S-glutathionylation. Grx1 plays different roles in different cell types. In Parkinson's disease (PD), Grx1 regulates apoptosis signaling in dopaminergic neurons, so that loss of Grx1 leads to increased cell death; in microglial cells, Grx1 regulates proinflammatory signaling, so that upregulation of Grx1 promotes cytokine production. Here we examine the regulatory roles of Grx1 in PD with a view toward therapeutic innovation. Recent Advances: In postmortem midbrain PD samples, Grx1 was decreased relative to controls, specifically within dopaminergic neurons. In Caenorhabditis elegans models of PD, loss of the Grx1 homologue led to exacerbation of the neurodegenerative phenotype. This effect was partially relieved by overexpression of neuroprotective DJ-1, consistent with regulation of DJ-1 content by Grx1. Increased GLRX copy number in PD patients was associated with earlier PD onset; and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-α in mouse and human brain samples. In vitro studies showed Grx1 to be upregulated on proinflammatory activation of microglia. Direct overexpression of Grx1 increased microglial activation; silencing Grx1 diminished activation. Grx1 upregulation in microglia corresponded to increased neuronal cell death in coculture. Overall, these studies identify competing roles of Grx1 in PD etiology.
CRITICAL ISSUES
The dilemma regarding Grx1 as a PD therapeutic target is whether to stimulate its upregulation for neuroprotection or inhibit its proinflammatory activity.
FUTURE DIRECTIONS
Further investigation is needed to understand the preponderant role of Grx1 regarding dopaminergic neuronal survival.
DOI: 10.1089/ars.2017.7411
PubMed: 29183158
PubMed Central: PMC6391617
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Mieyal</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Ohio</region></placeName><wicri:cityArea>Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland</wicri:cityArea></affiliation></author></analytic><series><title level="j">Antioxidants & redox signaling</title><idno type="eISSN">1557-7716</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age of Onset (MeSH)</term><term>Animals (MeSH)</term><term>Dopaminergic Neurons (metabolism)</term><term>Down-Regulation (MeSH)</term><term>Gene Dosage (MeSH)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Humans (MeSH)</term><term>Mesencephalon (metabolism)</term><term>Microglia (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Protein Deglycase DJ-1 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Dosage génique (MeSH)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Humains (MeSH)</term><term>Maladie de Parkinson (génétique)</term><term>Maladie de Parkinson (métabolisme)</term><term>Microglie (métabolisme)</term><term>Mésencéphale (métabolisme)</term><term>Neurones dopaminergiques (métabolisme)</term><term>Protein deglycase DJ-1 (métabolisme)</term><term>Régulation négative (MeSH)</term><term>Âge de début (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term><term>Maladie de Parkinson</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term><term>Glutaredoxins</term><term>Mesencephalon</term><term>Microglia</term><term>Parkinson Disease</term><term>Protein Deglycase DJ-1</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutarédoxines</term><term>Maladie de Parkinson</term><term>Microglie</term><term>Mésencéphale</term><term>Neurones dopaminergiques</term><term>Protein deglycase DJ-1</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age of Onset</term><term>Animals</term><term>Down-Regulation</term><term>Gene Dosage</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Dosage génique</term><term>Humains</term><term>Régulation négative</term><term>Âge de début</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b></p><p>Glutaredoxin (Grx)1, an evolutionarily conserved and ubiquitous enzyme, regulates redox signal transduction and protein redox homeostasis by catalyzing reversible S-glutathionylation. Grx1 plays different roles in different cell types. In Parkinson's disease (PD), Grx1 regulates apoptosis signaling in dopaminergic neurons, so that loss of Grx1 leads to increased cell death; in microglial cells, Grx1 regulates proinflammatory signaling, so that upregulation of Grx1 promotes cytokine production. Here we examine the regulatory roles of Grx1 in PD with a view toward therapeutic innovation. Recent Advances: In postmortem midbrain PD samples, Grx1 was decreased relative to controls, specifically within dopaminergic neurons. In Caenorhabditis elegans models of PD, loss of the Grx1 homologue led to exacerbation of the neurodegenerative phenotype. This effect was partially relieved by overexpression of neuroprotective DJ-1, consistent with regulation of DJ-1 content by Grx1. Increased GLRX copy number in PD patients was associated with earlier PD onset; and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-α in mouse and human brain samples. In vitro studies showed Grx1 to be upregulated on proinflammatory activation of microglia. Direct overexpression of Grx1 increased microglial activation; silencing Grx1 diminished activation. Grx1 upregulation in microglia corresponded to increased neuronal cell death in coculture. Overall, these studies identify competing roles of Grx1 in PD etiology.</p></div><div type="abstract" xml:lang="en"><p><b>CRITICAL ISSUES</b></p><p>The dilemma regarding Grx1 as a PD therapeutic target is whether to stimulate its upregulation for neuroprotection or inhibit its proinflammatory activity.</p></div><div type="abstract" xml:lang="en"><p><b>FUTURE DIRECTIONS</b></p><p>Further investigation is needed to understand the preponderant role of Grx1 regarding dopaminergic neuronal survival.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29183158</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>24</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>10</Issue><PubDate><Year>2019</Year><Month>04</Month><Day>01</Day></PubDate></JournalIssue><Title>Antioxidants & redox signaling</Title><ISOAbbreviation>Antioxid Redox Signal</ISOAbbreviation></Journal><ArticleTitle>Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.</ArticleTitle><Pagination><MedlinePgn>1352-1368</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1089/ars.2017.7411</ELocationID><Abstract><AbstractText Label="SIGNIFICANCE">Glutaredoxin (Grx)1, an evolutionarily conserved and ubiquitous enzyme, regulates redox signal transduction and protein redox homeostasis by catalyzing reversible S-glutathionylation. Grx1 plays different roles in different cell types. In Parkinson's disease (PD), Grx1 regulates apoptosis signaling in dopaminergic neurons, so that loss of Grx1 leads to increased cell death; in microglial cells, Grx1 regulates proinflammatory signaling, so that upregulation of Grx1 promotes cytokine production. Here we examine the regulatory roles of Grx1 in PD with a view toward therapeutic innovation. Recent Advances: In postmortem midbrain PD samples, Grx1 was decreased relative to controls, specifically within dopaminergic neurons. In Caenorhabditis elegans models of PD, loss of the Grx1 homologue led to exacerbation of the neurodegenerative phenotype. This effect was partially relieved by overexpression of neuroprotective DJ-1, consistent with regulation of DJ-1 content by Grx1. Increased GLRX copy number in PD patients was associated with earlier PD onset; and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-α in mouse and human brain samples. In vitro studies showed Grx1 to be upregulated on proinflammatory activation of microglia. Direct overexpression of Grx1 increased microglial activation; silencing Grx1 diminished activation. Grx1 upregulation in microglia corresponded to increased neuronal cell death in coculture. Overall, these studies identify competing roles of Grx1 in PD etiology.</AbstractText><AbstractText Label="CRITICAL ISSUES">The dilemma regarding Grx1 as a PD therapeutic target is whether to stimulate its upregulation for neuroprotection or inhibit its proinflammatory activity.</AbstractText><AbstractText Label="FUTURE DIRECTIONS">Further investigation is needed to understand the preponderant role of Grx1 regarding dopaminergic neuronal survival.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gorelenkova Miller</LastName><ForeName>Olga</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mieyal</LastName><ForeName>John J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>I01 BX000290</GrantID><Acronym>BX</Acronym><Agency>BLRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS085503</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antioxid Redox 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