GlutaredoxinV1, Main, Exploration, bibRecord, 000400

Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.

Identifieur interne : 000400 ( Main/Exploration ); précédent : 000399; suivant : 000401

Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.

Auteurs : Olga Gorelenkova Miller [États-Unis] ; Jessica Belle Behring [États-Unis] ; Sandra L. Siedlak [États-Unis] ; Sirui Jiang [États-Unis] ; Reiko Matsui [États-Unis] ; Markus M. Bachschmid [États-Unis] ; Xiongwei Zhu [États-Unis] ; John J. Mieyal [États-Unis]

Source :

Antioxidants & redox signaling [ 1557-7716 ] ; 2016.

RBID : pubmed:27224303

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Cell Death (MeSH), Cytokines (metabolism), Disease Models, Animal (MeSH), Dopamine (metabolism), Dopaminergic Neurons (metabolism), Dopaminergic Neurons (pathology), Gene Dosage (MeSH), Gene Expression (MeSH), Gene Expression Regulation (MeSH), Gene Silencing (MeSH), Genetic Predisposition to Disease (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Humans (MeSH), Inflammation Mediators (metabolism), Lipopolysaccharides (immunology), Mice (MeSH), Mice, Knockout (MeSH), Microglia (immunology), Microglia (metabolism), Models, Biological (MeSH), NF-kappa B (metabolism), Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (immunology), Neurodegenerative Diseases (metabolism), Neurodegenerative Diseases (pathology), Neurons (metabolism), Neurons (pathology), Nuclear Receptor Subfamily 4, Group A, Member 2 (metabolism), Parkinson Disease (genetics), Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Rats (MeSH), Transcription Factor AP-1 (metabolism), Tyrosine 3-Monooxygenase (metabolism).
MESH :
- chemical , genetics : Glutaredoxins.
- chemical , immunology : Lipopolysaccharides.
- chemical , metabolism : Cytokines, Dopamine, Glutaredoxins, Inflammation Mediators, NF-kappa B, Nuclear Receptor Subfamily 4, Group A, Member 2, Transcription Factor AP-1, Tyrosine 3-Monooxygenase.
- genetics : Neurodegenerative Diseases, Parkinson Disease.
- immunology : Microglia, Neurodegenerative Diseases, Parkinson Disease.
- metabolism : Dopaminergic Neurons, Microglia, Neurodegenerative Diseases, Neurons, Parkinson Disease.
- pathology : Dopaminergic Neurons, Neurodegenerative Diseases, Neurons, Parkinson Disease.
- Animals, Cell Death, Disease Models, Animal, Gene Dosage, Gene Expression, Gene Expression Regulation, Gene Silencing, Genetic Predisposition to Disease, Humans, Mice, Mice, Knockout, Models, Biological, Rats.

Abstract

AIMS

Neuroinflammation and redox dysfunction are recognized factors in Parkinson's disease (PD) pathogenesis, and diabetes is implicated as a potentially predisposing condition. Remarkably, upregulation of glutaredoxin-1 (Grx1) is implicated in regulation of inflammatory responses in various disease contexts, including diabetes. In this study, we investigated the potential impact of Grx1 upregulation in the central nervous system on dopaminergic (DA) viability.

RESULTS

Increased GLRX copy number in PD patients was associated with earlier PD onset, and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-alpha (TNF-α) in mouse and human brain samples, prompting mechanistic in vitro studies. Grx1 content/activity in microglia was upregulated by lipopolysaccharide (LPS), or TNF-α, treatment. Adenoviral overexpression of Grx1, matching the extent of induction by LPS, increased microglial activation; Grx1 silencing diminished activation. Selective inhibitors/probes of nuclear factor κB (NF-κB) activation revealed glrx1 induction to be mediated by the Nurr1/NF-κB axis. Upregulation of Grx1 in microglia corresponded to increased death of neuronal cells in coculture. With a mouse diabetes model of diet-induced insulin resistance, we found upregulation of Grx1 in brain was associated with DA loss (decreased tyrosine hydroxylase [TH]; diminished TH-positive striatal axonal terminals); these effects were not seen with Grx1-knockout mice.

INNOVATION

Our results indicate that Grx1 upregulation promotes neuroinflammation and consequent neuronal cell death in vitro, and synergizes with proinflammatory insults to promote DA loss in vivo. Our findings also suggest a genetic link between elevated Grx1 and PD development.

CONCLUSION

In vitro and in vivo data suggest Grx1 upregulation promotes neurotoxic neuroinflammation, potentially contributing to PD. Antioxid. Redox Signal. 25, 967-982.

DOI: 10.1089/ars.2015.6598
PubMed: 27224303
PubMed Central: PMC5175443

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000434
to stream Main, to step Curation: 000434

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Cell Death (MeSH)</term>
<term>Cytokines (metabolism)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Dopamine (metabolism)</term>
<term>Dopaminergic Neurons (metabolism)</term>
<term>Dopaminergic Neurons (pathology)</term>
<term>Gene Dosage (MeSH)</term>
<term>Gene Expression (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Gene Silencing (MeSH)</term>
<term>Genetic Predisposition to Disease (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Lipopolysaccharides (immunology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Microglia (immunology)</term>
<term>Microglia (metabolism)</term>
<term>Models, Biological (MeSH)</term>
<term>NF-kappa B (metabolism)</term>
<term>Neurodegenerative Diseases (genetics)</term>
<term>Neurodegenerative Diseases (immunology)</term>
<term>Neurodegenerative Diseases (metabolism)</term>
<term>Neurodegenerative Diseases (pathology)</term>
<term>Neurons (metabolism)</term>
<term>Neurons (pathology)</term>
<term>Nuclear Receptor Subfamily 4, Group A, Member 2 (metabolism)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (immunology)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson Disease (pathology)</term>
<term>Rats (MeSH)</term>
<term>Transcription Factor AP-1 (metabolism)</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cytokines (métabolisme)</term>
<term>Dopamine (métabolisme)</term>
<term>Dosage génique (MeSH)</term>
<term>Expression des gènes (MeSH)</term>
<term>Extinction de l'expression des gènes (MeSH)</term>
<term>Facteur de transcription AP-1 (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Lipopolysaccharides (immunologie)</term>
<term>Maladie de Parkinson (anatomopathologie)</term>
<term>Maladie de Parkinson (génétique)</term>
<term>Maladie de Parkinson (immunologie)</term>
<term>Maladie de Parkinson (métabolisme)</term>
<term>Maladies neurodégénératives (anatomopathologie)</term>
<term>Maladies neurodégénératives (génétique)</term>
<term>Maladies neurodégénératives (immunologie)</term>
<term>Maladies neurodégénératives (métabolisme)</term>
<term>Membre-2 du groupe A de la sous-famille-4 de récepteurs nucléaires (métabolisme)</term>
<term>Microglie (immunologie)</term>
<term>Microglie (métabolisme)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Modèles biologiques (MeSH)</term>
<term>Mort cellulaire (MeSH)</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Neurones (anatomopathologie)</term>
<term>Neurones (métabolisme)</term>
<term>Neurones dopaminergiques (anatomopathologie)</term>
<term>Neurones dopaminergiques (métabolisme)</term>
<term>Prédisposition génétique à une maladie (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Tyrosine 3-monooxygenase (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>Dopamine</term>
<term>Glutaredoxins</term>
<term>Inflammation Mediators</term>
<term>NF-kappa B</term>
<term>Nuclear Receptor Subfamily 4, Group A, Member 2</term>
<term>Transcription Factor AP-1</term>
<term>Tyrosine 3-Monooxygenase</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Maladies neurodégénératives</term>
<term>Neurones</term>
<term>Neurones dopaminergiques</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Neurodegenerative Diseases</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term>
<term>Maladie de Parkinson</term>
<term>Maladies neurodégénératives</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lipopolysaccharides</term>
<term>Maladie de Parkinson</term>
<term>Maladies neurodégénératives</term>
<term>Microglie</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Microglia</term>
<term>Neurodegenerative Diseases</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term>
<term>Microglia</term>
<term>Neurodegenerative Diseases</term>
<term>Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term>
<term>Dopamine</term>
<term>Facteur de transcription AP-1</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Glutarédoxines</term>
<term>Maladie de Parkinson</term>
<term>Maladies neurodégénératives</term>
<term>Membre-2 du groupe A de la sous-famille-4 de récepteurs nucléaires</term>
<term>Microglie</term>
<term>Médiateurs de l'inflammation</term>
<term>Neurones</term>
<term>Neurones dopaminergiques</term>
<term>Tyrosine 3-monooxygenase</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dopaminergic Neurons</term>
<term>Neurodegenerative Diseases</term>
<term>Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Death</term>
<term>Disease Models, Animal</term>
<term>Gene Dosage</term>
<term>Gene Expression</term>
<term>Gene Expression Regulation</term>
<term>Gene Silencing</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Models, Biological</term>
<term>Rats</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Dosage génique</term>
<term>Expression des gènes</term>
<term>Extinction de l'expression des gènes</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Modèles biologiques</term>
<term>Mort cellulaire</term>
<term>Prédisposition génétique à une maladie</term>
<term>Rats</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
<term>Souris knockout</term>
</keywords>
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<front><div type="abstract" xml:lang="en"><p><b>AIMS</b>
</p>
<p>Neuroinflammation and redox dysfunction are recognized factors in Parkinson's disease (PD) pathogenesis, and diabetes is implicated as a potentially predisposing condition. Remarkably, upregulation of glutaredoxin-1 (Grx1) is implicated in regulation of inflammatory responses in various disease contexts, including diabetes. In this study, we investigated the potential impact of Grx1 upregulation in the central nervous system on dopaminergic (DA) viability.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>Increased GLRX copy number in PD patients was associated with earlier PD onset, and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-alpha (TNF-α) in mouse and human brain samples, prompting mechanistic in vitro studies. Grx1 content/activity in microglia was upregulated by lipopolysaccharide (LPS), or TNF-α, treatment. Adenoviral overexpression of Grx1, matching the extent of induction by LPS, increased microglial activation; Grx1 silencing diminished activation. Selective inhibitors/probes of nuclear factor κB (NF-κB) activation revealed glrx1 induction to be mediated by the Nurr1/NF-κB axis. Upregulation of Grx1 in microglia corresponded to increased death of neuronal cells in coculture. With a mouse diabetes model of diet-induced insulin resistance, we found upregulation of Grx1 in brain was associated with DA loss (decreased tyrosine hydroxylase [TH]; diminished TH-positive striatal axonal terminals); these effects were not seen with Grx1-knockout mice.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>INNOVATION</b>
</p>
<p>Our results indicate that Grx1 upregulation promotes neuroinflammation and consequent neuronal cell death in vitro, and synergizes with proinflammatory insults to promote DA loss in vivo. Our findings also suggest a genetic link between elevated Grx1 and PD development.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSION</b>
</p>
<p>In vitro and in vivo data suggest Grx1 upregulation promotes neurotoxic neuroinflammation, potentially contributing to PD. Antioxid. Redox Signal. 25, 967-982.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27224303</PMID>
<DateCompleted><Year>2017</Year>
<Month>08</Month>
<Day>07</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>05</Month>
<Day>08</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>25</Volume>
<Issue>18</Issue>
<PubDate><Year>2016</Year>
<Month>12</Month>
<Day>20</Day>
</PubDate>
</JournalIssue>
<Title>Antioxidants & redox signaling</Title>
<ISOAbbreviation>Antioxid Redox Signal</ISOAbbreviation>
</Journal>
<ArticleTitle>Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.</ArticleTitle>
<Pagination><MedlinePgn>967-982</MedlinePgn>
</Pagination>
<Abstract><AbstractText Label="AIMS">Neuroinflammation and redox dysfunction are recognized factors in Parkinson's disease (PD) pathogenesis, and diabetes is implicated as a potentially predisposing condition. Remarkably, upregulation of glutaredoxin-1 (Grx1) is implicated in regulation of inflammatory responses in various disease contexts, including diabetes. In this study, we investigated the potential impact of Grx1 upregulation in the central nervous system on dopaminergic (DA) viability.</AbstractText>
<AbstractText Label="RESULTS">Increased GLRX copy number in PD patients was associated with earlier PD onset, and Grx1 levels correlated with levels of proinflammatory tumor necrosis factor-alpha (TNF-α) in mouse and human brain samples, prompting mechanistic in vitro studies. Grx1 content/activity in microglia was upregulated by lipopolysaccharide (LPS), or TNF-α, treatment. Adenoviral overexpression of Grx1, matching the extent of induction by LPS, increased microglial activation; Grx1 silencing diminished activation. Selective inhibitors/probes of nuclear factor κB (NF-κB) activation revealed glrx1 induction to be mediated by the Nurr1/NF-κB axis. Upregulation of Grx1 in microglia corresponded to increased death of neuronal cells in coculture. With a mouse diabetes model of diet-induced insulin resistance, we found upregulation of Grx1 in brain was associated with DA loss (decreased tyrosine hydroxylase [TH]; diminished TH-positive striatal axonal terminals); these effects were not seen with Grx1-knockout mice.</AbstractText>
<AbstractText Label="INNOVATION">Our results indicate that Grx1 upregulation promotes neuroinflammation and consequent neuronal cell death in vitro, and synergizes with proinflammatory insults to promote DA loss in vivo. Our findings also suggest a genetic link between elevated Grx1 and PD development.</AbstractText>
<AbstractText Label="CONCLUSION">In vitro and in vivo data suggest Grx1 upregulation promotes neurotoxic neuroinflammation, potentially contributing to PD. Antioxid. Redox Signal. 25, 967-982.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gorelenkova Miller</LastName>
<ForeName>Olga</ForeName>
<Initials>O</Initials>
<AffiliationInfo><Affiliation>1 Department of Pharmacology, School of Medicine, Case Western Reserve University , Cleveland, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Behring</LastName>
<ForeName>Jessica Belle</ForeName>
<Initials>JB</Initials>
<AffiliationInfo><Affiliation>2 Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine , Boston, Massachusetts.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Siedlak</LastName>
<ForeName>Sandra L</ForeName>
<Initials>SL</Initials>
<AffiliationInfo><Affiliation>3 Department of Pathology, School of Medicine, Case Western Reserve University , Cleveland, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Sirui</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>3 Department of Pathology, School of Medicine, Case Western Reserve University , Cleveland, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Matsui</LastName>
<ForeName>Reiko</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>2 Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine , Boston, Massachusetts.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bachschmid</LastName>
<ForeName>Markus M</ForeName>
<Initials>MM</Initials>
<AffiliationInfo><Affiliation>2 Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine , Boston, Massachusetts.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Xiongwei</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>3 Department of Pathology, 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>1 Department of Pharmacology, School of Medicine, Case Western Reserve University , Cleveland, Ohio.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>4 Louis Stokes Cleveland Veterans Administration Medical Research Center , Cleveland, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R21 NS085503</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 NS077888</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL133013</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 HL007501</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 DK103750</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 GM007250</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>06</Month>
<Day>27</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Antioxid Redox Signal</MedlineTA>
<NlmUniqueID>100888899</NlmUniqueID>
<ISSNLinking>1523-0864</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016207">Cytokines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D057126">Nuclear Receptor Subfamily 4, Group A, Member 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018808">Transcription Factor AP-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber>
<NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber>
<NameOfSubstance UI="D004298">Dopamine</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018628" MajorTopicYN="N">Gene Dosage</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020868" MajorTopicYN="N">Gene Silencing</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017628" MajorTopicYN="N">Microglia</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057126" MajorTopicYN="N">Nuclear Receptor Subfamily 4, Group A, Member 2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018808" MajorTopicYN="N">Transcription Factor AP-1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Parkinson's disease</Keyword>
<Keyword MajorTopicYN="Y">diabetes</Keyword>
<Keyword MajorTopicYN="Y">microglia</Keyword>
<Keyword MajorTopicYN="Y">neuroinflammation glutaredoxin</Keyword>
</KeywordList>
<CoiStatement>Author Disclosure Statement No competing financial interests exist.</CoiStatement>
</MedlineCitation>
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<li>Ohio</li>
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<tree><country name="États-Unis"><region name="Ohio"><name sortKey="Gorelenkova Miller, Olga" sort="Gorelenkova Miller, Olga" uniqKey="Gorelenkova Miller O" first="Olga" last="Gorelenkova Miller">Olga Gorelenkova Miller</name>
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<name sortKey="Bachschmid, Markus M" sort="Bachschmid, Markus M" uniqKey="Bachschmid M" first="Markus M" last="Bachschmid">Markus M. Bachschmid</name>
<name sortKey="Behring, Jessica Belle" sort="Behring, Jessica Belle" uniqKey="Behring J" first="Jessica Belle" last="Behring">Jessica Belle Behring</name>
<name sortKey="Jiang, Sirui" sort="Jiang, Sirui" uniqKey="Jiang S" first="Sirui" last="Jiang">Sirui Jiang</name>
<name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name>
<name sortKey="Mieyal, John J" sort="Mieyal, John J" uniqKey="Mieyal J" first="John J" last="Mieyal">John J. Mieyal</name>
<name sortKey="Mieyal, John J" sort="Mieyal, John J" uniqKey="Mieyal J" first="John J" last="Mieyal">John J. Mieyal</name>
<name sortKey="Siedlak, Sandra L" sort="Siedlak, Sandra L" uniqKey="Siedlak S" first="Sandra L" last="Siedlak">Sandra L. Siedlak</name>
<name sortKey="Zhu, Xiongwei" sort="Zhu, Xiongwei" uniqKey="Zhu X" first="Xiongwei" last="Zhu">Xiongwei Zhu</name>
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   |wiki=    Bois
   |area=    GlutaredoxinV1
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   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:27224303
   |texte=   Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.
}}

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Serveur d'exploration sur la glutarédoxine

Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.

Upregulation of Glutaredoxin-1 Activates Microglia and Promotes Neurodegeneration: Implications for Parkinson's Disease.

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