GlutaredoxinV1, Main, Exploration, bibRecord, 000960

Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.

Identifieur interne : 000960 ( Main/Exploration ); précédent : 000959; suivant : 000961

Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.

Auteurs : Scott W. Aesif [États-Unis] ; Ine Kuipers ; Jos Van Der Velden ; Jane E. Tully ; Amy S. Guala ; Vikas Anathy ; Juliana I. Sheely ; Niki L. Reynaert ; Emiel F M. Wouters ; Albert Van Der Vliet ; Yvonne M W. Janssen-Heininger

Source :

Free radical biology & medicine [ 1873-4596 ] ; 2011.

RBID : pubmed:21762778

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Cell Line (MeSH), Epithelial Cells (immunology), Epithelial Cells (metabolism), Epithelial Cells (pathology), Gene Expression Regulation (immunology), Glutaredoxins (genetics), Glutaredoxins (immunology), Glutaredoxins (metabolism), I-kappa B Kinase (genetics), Immunization (MeSH), Inflammation Mediators (metabolism), Lipopolysaccharides (immunology), Lipopolysaccharides (metabolism), Lung (pathology), Mice (MeSH), Mice, Transgenic (MeSH), NF-kappa B (genetics), NF-kappa B (metabolism), Promoter Regions, Genetic (genetics), Signal Transduction (genetics), Transcription Factor RelA (metabolism), Transcriptional Activation (genetics), Transgenes (genetics).
MESH :
- chemical , genetics : Glutaredoxins, I-kappa B Kinase, NF-kappa B.
- genetics : Promoter Regions, Genetic, Signal Transduction, Transcriptional Activation, Transgenes.
- immunology : Epithelial Cells, Gene Expression Regulation, Glutaredoxins, Lipopolysaccharides.
- metabolism : Epithelial Cells, Glutaredoxins, Inflammation Mediators, Lipopolysaccharides, NF-kappa B, Transcription Factor RelA.
- pathology : Epithelial Cells, Lung.
- Animals, Cell Line, Immunization, Mice, Mice, Transgenic.

Abstract

The transcription factor nuclear factor κB (NF-κB) is a critical regulator of inflammation and immunity and is negatively regulated via S-glutathionylation. The inhibitory effect of S-glutathionylation is overcome by glutaredoxin-1 (Grx1), which under physiological conditions catalyzes deglutathionylation and enhances NF-κB activation. The mechanisms whereby expression of the Glrx1 gene is regulated remain unknown. Here we examined the role of NF-κB in regulating activation of Glrx1. Transgenic mice that express a doxycycline-inducible constitutively active version of inhibitory κB kinase-β (CA-IKKβ) demonstrate elevated expression of Grx1. Transient transfection of CA-IKKβ also resulted in significant induction of Grx1. A 2-kb region of the Glrx1 promoter that contains two putative NF-κB binding sites was activated by CA-IKKβ, RelA/p50, and lipopolysaccharide (LPS). Chromatin immunoprecipitation experiments confirmed binding of RelA to the promoter of Glrx1 in response to LPS. Stimulation of C10 lung epithelial cells with LPS caused transient increases in Grx1 mRNA expression and time-dependent increases in S-glutathionylation of IKKβ. Overexpression of Grx1 decreased S-glutathionylation of IKKβ, prolonged NF-κB activation, and increased levels of proinflammatory mediators. Collectively, this study demonstrates that the Glrx1 gene is positively regulated by NF-κB and suggests a feed-forward mechanism to promote NF-κB signaling by decreasing S-glutathionylation.

DOI: 10.1016/j.freeradbiomed.2011.06.025
PubMed: 21762778
PubMed Central: PMC3181077

Affiliations:

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

to stream Main, to step Corpus: 000912
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Le document en format XML

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<term>Cell Line (MeSH)</term>
<term>Epithelial Cells (immunology)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Epithelial Cells (pathology)</term>
<term>Gene Expression Regulation (immunology)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (immunology)</term>
<term>Glutaredoxins (metabolism)</term>
<term>I-kappa B Kinase (genetics)</term>
<term>Immunization (MeSH)</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Lipopolysaccharides (immunology)</term>
<term>Lipopolysaccharides (metabolism)</term>
<term>Lung (pathology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>NF-kappa B (genetics)</term>
<term>NF-kappa B (metabolism)</term>
<term>Promoter Regions, Genetic (genetics)</term>
<term>Signal Transduction (genetics)</term>
<term>Transcription Factor RelA (metabolism)</term>
<term>Transcriptional Activation (genetics)</term>
<term>Transgenes (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation de la transcription (génétique)</term>
<term>Animaux (MeSH)</term>
<term>Cellules épithéliales (anatomopathologie)</term>
<term>Cellules épithéliales (immunologie)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (génétique)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur de transcription RelA (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (immunologie)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>I-kappa B Kinase (génétique)</term>
<term>Immunisation (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lipopolysaccharides (immunologie)</term>
<term>Lipopolysaccharides (métabolisme)</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Poumon (anatomopathologie)</term>
<term>Régions promotrices (génétique) (génétique)</term>
<term>Régulation de l'expression des gènes (immunologie)</term>
<term>Souris (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>Transduction du signal (génétique)</term>
<term>Transgènes (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>I-kappa B Kinase</term>
<term>NF-kappa B</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Promoter Regions, Genetic</term>
<term>Signal Transduction</term>
<term>Transcriptional Activation</term>
<term>Transgenes</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Activation de la transcription</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Glutarédoxines</term>
<term>I-kappa B Kinase</term>
<term>Régions promotrices (génétique)</term>
<term>Transduction du signal</term>
<term>Transgènes</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Glutarédoxines</term>
<term>Lipopolysaccharides</term>
<term>Régulation de l'expression des gènes</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Epithelial Cells</term>
<term>Gene Expression Regulation</term>
<term>Glutaredoxins</term>
<term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
<term>Glutaredoxins</term>
<term>Inflammation Mediators</term>
<term>Lipopolysaccharides</term>
<term>NF-kappa B</term>
<term>Transcription Factor RelA</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Facteur de transcription RelA</term>
<term>Glutarédoxines</term>
<term>Lipopolysaccharides</term>
<term>Médiateurs de l'inflammation</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Epithelial Cells</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Immunization</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Immunisation</term>
<term>Lignée cellulaire</term>
<term>Souris</term>
<term>Souris transgéniques</term>
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<front><div type="abstract" xml:lang="en">The transcription factor nuclear factor κB (NF-κB) is a critical regulator of inflammation and immunity and is negatively regulated via S-glutathionylation. The inhibitory effect of S-glutathionylation is overcome by glutaredoxin-1 (Grx1), which under physiological conditions catalyzes deglutathionylation and enhances NF-κB activation. The mechanisms whereby expression of the Glrx1 gene is regulated remain unknown. Here we examined the role of NF-κB in regulating activation of Glrx1. Transgenic mice that express a doxycycline-inducible constitutively active version of inhibitory κB kinase-β (CA-IKKβ) demonstrate elevated expression of Grx1. Transient transfection of CA-IKKβ also resulted in significant induction of Grx1. A 2-kb region of the Glrx1 promoter that contains two putative NF-κB binding sites was activated by CA-IKKβ, RelA/p50, and lipopolysaccharide (LPS). Chromatin immunoprecipitation experiments confirmed binding of RelA to the promoter of Glrx1 in response to LPS. Stimulation of C10 lung epithelial cells with LPS caused transient increases in Grx1 mRNA expression and time-dependent increases in S-glutathionylation of IKKβ. Overexpression of Grx1 decreased S-glutathionylation of IKKβ, prolonged NF-κB activation, and increased levels of proinflammatory mediators. Collectively, this study demonstrates that the Glrx1 gene is positively regulated by NF-κB and suggests a feed-forward mechanism to promote NF-κB signaling by decreasing S-glutathionylation.</div>
</front>
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<DateCompleted><Year>2011</Year>
<Month>12</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
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<Issue>6</Issue>
<PubDate><Year>2011</Year>
<Month>Sep</Month>
<Day>15</Day>
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<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation>
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<ArticleTitle>Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.</ArticleTitle>
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<Abstract><AbstractText>The transcription factor nuclear factor κB (NF-κB) is a critical regulator of inflammation and immunity and is negatively regulated via S-glutathionylation. The inhibitory effect of S-glutathionylation is overcome by glutaredoxin-1 (Grx1), which under physiological conditions catalyzes deglutathionylation and enhances NF-κB activation. The mechanisms whereby expression of the Glrx1 gene is regulated remain unknown. Here we examined the role of NF-κB in regulating activation of Glrx1. Transgenic mice that express a doxycycline-inducible constitutively active version of inhibitory κB kinase-β (CA-IKKβ) demonstrate elevated expression of Grx1. Transient transfection of CA-IKKβ also resulted in significant induction of Grx1. A 2-kb region of the Glrx1 promoter that contains two putative NF-κB binding sites was activated by CA-IKKβ, RelA/p50, and lipopolysaccharide (LPS). Chromatin immunoprecipitation experiments confirmed binding of RelA to the promoter of Glrx1 in response to LPS. Stimulation of C10 lung epithelial cells with LPS caused transient increases in Grx1 mRNA expression and time-dependent increases in S-glutathionylation of IKKβ. Overexpression of Grx1 decreased S-glutathionylation of IKKβ, prolonged NF-κB activation, and increased levels of proinflammatory mediators. Collectively, this study demonstrates that the Glrx1 gene is positively regulated by NF-κB and suggests a feed-forward mechanism to promote NF-κB signaling by decreasing S-glutathionylation.</AbstractText>
<CopyrightInformation>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aesif</LastName>
<ForeName>Scott W</ForeName>
<Initials>SW</Initials>
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<ForeName>Albert</ForeName>
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<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
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<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
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<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D051550" MajorTopicYN="N">I-kappa B Kinase</DescriptorName>
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<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
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<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
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<MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.

Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.

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