GlutaredoxinV1, Main, Exploration, bibRecord, 000827

Reactive oxygen species-induced actin glutathionylation controls actin dynamics in neutrophils.

Identifieur interne : 000827 ( Main/Exploration ); précédent : 000826; suivant : 000828

Reactive oxygen species-induced actin glutathionylation controls actin dynamics in neutrophils.

Auteurs : Jiro Sakai [États-Unis] ; Jingyu Li ; Kulandayan K. Subramanian ; Subhanjan Mondal ; Besnik Bajrami ; Hidenori Hattori ; Yonghui Jia ; Bryan C. Dickinson ; Jia Zhong ; Keqiang Ye ; Christopher J. Chang ; Ye-Shih Ho ; Jun Zhou ; Hongbo R. Luo

Source :

Immunity [ 1097-4180 ] ; 2012.

RBID : pubmed:23159440

Descripteurs français

KwdFr :
- Actines (métabolisme), Animaux (MeSH), Cellules cultivées (MeSH), Chimiotaxie (immunologie), Espèces réactives de l'oxygène (métabolisme), Glutarédoxines (génétique), Glutarédoxines (immunologie), Granulocytes neutrophiles (immunologie), Granulocytes neutrophiles (métabolisme), Humains (MeSH), Infections bactériennes (génétique), Infections bactériennes (immunologie), Liaison aux protéines (MeSH), NADPH oxidase (métabolisme), Pseudopodes (métabolisme), Souris (MeSH), Souris knockout (MeSH).
MESH :
- génétique : Glutarédoxines, Infections bactériennes.
- immunologie : Chimiotaxie, Glutarédoxines, Granulocytes neutrophiles, Infections bactériennes.
- métabolisme : Actines, Espèces réactives de l'oxygène, Granulocytes neutrophiles, NADPH oxidase, Pseudopodes.
- Animaux, Cellules cultivées, Humains, Liaison aux protéines, Souris, Souris knockout.

English descriptors

KwdEn :
- Actins (metabolism), Animals (MeSH), Bacterial Infections (genetics), Bacterial Infections (immunology), Cells, Cultured (MeSH), Chemotaxis (immunology), Glutaredoxins (genetics), Glutaredoxins (immunology), Humans (MeSH), Mice (MeSH), Mice, Knockout (MeSH), NADPH Oxidases (metabolism), Neutrophils (immunology), Neutrophils (metabolism), Protein Binding (MeSH), Pseudopodia (metabolism), Reactive Oxygen Species (metabolism).
MESH :
- chemical , genetics : Glutaredoxins.
- chemical , immunology : Glutaredoxins.
- chemical , metabolism : Actins, NADPH Oxidases, Reactive Oxygen Species.
- genetics : Bacterial Infections.
- immunology : Bacterial Infections, Chemotaxis, Neutrophils.
- metabolism : Neutrophils, Pseudopodia.
- Animals, Cells, Cultured, Humans, Mice, Mice, Knockout, Protein Binding.

Abstract

The regulation of actin dynamics is pivotal for cellular processes such as cell adhesion, migration, and phagocytosis and thus is crucial for neutrophils to fulfill their roles in innate immunity. Many factors have been implicated in signal-induced actin polymerization, but the essential nature of the potential negative modulators are still poorly understood. Here we report that NADPH oxidase-dependent physiologically generated reactive oxygen species (ROS) negatively regulate actin polymerization in stimulated neutrophils via driving reversible actin glutathionylation. Disruption of glutaredoxin 1 (Grx1), an enzyme that catalyzes actin deglutathionylation, increased actin glutathionylation, attenuated actin polymerization, and consequently impaired neutrophil polarization, chemotaxis, adhesion, and phagocytosis. Consistently, Grx1-deficient murine neutrophils showed impaired in vivo recruitment to sites of inflammation and reduced bactericidal capability. Together, these results present a physiological role for glutaredoxin and ROS- induced reversible actin glutathionylation in regulation of actin dynamics in neutrophils.

DOI: 10.1016/j.immuni.2012.08.017
PubMed: 23159440
PubMed Central: PMC3525814

Affiliations:

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

to stream Main, to step Corpus: 000790
to stream Main, to step Curation: 000790

Le document en format XML

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<term>Glutarédoxines (génétique)</term>
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<term>Infections bactériennes (immunologie)</term>
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<front><div type="abstract" xml:lang="en">The regulation of actin dynamics is pivotal for cellular processes such as cell adhesion, migration, and phagocytosis and thus is crucial for neutrophils to fulfill their roles in innate immunity. Many factors have been implicated in signal-induced actin polymerization, but the essential nature of the potential negative modulators are still poorly understood. Here we report that NADPH oxidase-dependent physiologically generated reactive oxygen species (ROS) negatively regulate actin polymerization in stimulated neutrophils via driving reversible actin glutathionylation. Disruption of glutaredoxin 1 (Grx1), an enzyme that catalyzes actin deglutathionylation, increased actin glutathionylation, attenuated actin polymerization, and consequently impaired neutrophil polarization, chemotaxis, adhesion, and phagocytosis. Consistently, Grx1-deficient murine neutrophils showed impaired in vivo recruitment to sites of inflammation and reduced bactericidal capability. Together, these results present a physiological role for glutaredoxin and ROS- induced reversible actin glutathionylation in regulation of actin dynamics in neutrophils.</div>
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<Abstract><AbstractText>The regulation of actin dynamics is pivotal for cellular processes such as cell adhesion, migration, and phagocytosis and thus is crucial for neutrophils to fulfill their roles in innate immunity. Many factors have been implicated in signal-induced actin polymerization, but the essential nature of the potential negative modulators are still poorly understood. Here we report that NADPH oxidase-dependent physiologically generated reactive oxygen species (ROS) negatively regulate actin polymerization in stimulated neutrophils via driving reversible actin glutathionylation. Disruption of glutaredoxin 1 (Grx1), an enzyme that catalyzes actin deglutathionylation, increased actin glutathionylation, attenuated actin polymerization, and consequently impaired neutrophil polarization, chemotaxis, adhesion, and phagocytosis. Consistently, Grx1-deficient murine neutrophils showed impaired in vivo recruitment to sites of inflammation and reduced bactericidal capability. Together, these results present a physiological role for glutaredoxin and ROS- induced reversible actin glutathionylation in regulation of actin dynamics in neutrophils.</AbstractText>
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Reactive oxygen species-induced actin glutathionylation controls actin dynamics in neutrophils.

Reactive oxygen species-induced actin glutathionylation controls actin dynamics in neutrophils.

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