GlutaredoxinV1, Main, Exploration, bibRecord, 000166

Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.

Identifieur interne : 000166 ( Main/Exploration ); précédent : 000165; suivant : 000167

Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.

Auteurs : Yuanyuan You ; Junli Chen ; Feimei Zhu ; Qian Xu ; Lu Han [République populaire de Chine] ; Xiang Gao [République populaire de Chine] ; Xiaoyu Zhang [République populaire de Chine] ; Hongbo R. Luo [États-Unis] ; Junming Miao ; Xiaodong Sun [République populaire de Chine] ; Hongyu Ren ; Yu Du ; Lijuan Guo ; Xiaoying Wang ; Yi Wang ; Shanze Chen ; Ning Huang [Oman] ; Jingyu Li [République populaire de Chine]

Source :

The Journal of biological chemistry [ 1083-351X ] ; 2019.

RBID : pubmed:30598505

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Bone Marrow (metabolism), Bone Marrow (pathology), Disease Models, Animal (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), HL-60 Cells (MeSH), Humans (MeSH), Inflammation (genetics), Inflammation (metabolism), Inflammation (pathology), Integrin alpha4 (genetics), Integrin alpha4 (metabolism), Mice, Knockout (MeSH), Neutrophils (metabolism), Neutrophils (pathology), Up-Regulation (MeSH), Vascular Cell Adhesion Molecule-1 (genetics), Vascular Cell Adhesion Molecule-1 (metabolism).
MESH :
- chemical , genetics : Glutaredoxins, Integrin alpha4, Vascular Cell Adhesion Molecule-1.
- genetics : Inflammation.
- metabolism : Bone Marrow, Glutaredoxins, Inflammation, Integrin alpha4, Neutrophils, Vascular Cell Adhesion Molecule-1.
- pathology : Bone Marrow, Inflammation, Neutrophils.
- Animals, Disease Models, Animal, HL-60 Cells, Humans, Mice, Knockout, Up-Regulation.

Abstract

α4 integrin plays a crucial role in retention and release of neutrophils from bone marrow. Although α4 integrin is known to be a potential target of reactive oxygen species (ROS)-induced cysteine glutathionylation, the physiological significance and underlying regulatory mechanism of this event remain elusive. Here, using in vitro and in vivo biochemical and cell biology approaches, we show that physiological ROS-induced glutathionylation of α4 integrin in neutrophils increases the binding of neutrophil-associated α4 integrin to vascular cell adhesion molecule 1 (VCAM-1) on human endothelial cells. This enhanced binding was reversed by extracellular glutaredoxin 1 (Grx1), a thiol disulfide oxidoreductase promoting protein deglutathionylation. Furthermore, in a murine inflammation model, Grx1 disruption dramatically elevated α4 glutathionylation and subsequently enhanced neutrophil egress from the bone marrow. Corroborating this observation, intravenous injection of recombinant Grx1 into mice inhibited α4 glutathionylation and thereby suppressed inflammation-induced neutrophil mobilization from the bone marrow. Taken together, our results establish ROS-elicited glutathionylation and its modulation by Grx1 as pivotal regulatory mechanisms controlling α4 integrin affinity and neutrophil mobilization from the bone marrow under physiological conditions.

DOI: 10.1074/jbc.RA118.006096
PubMed: 30598505
PubMed Central: PMC6393595

Affiliations:

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

to stream Main, to step Corpus: 000178
to stream Main, to step Curation: 000178

Le document en format XML

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<author><name sortKey="Miao, Junming" sort="Miao, Junming" uniqKey="Miao J" first="Junming" last="Miao">Junming Miao</name>
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</affiliation>
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<author><name sortKey="Sun, Xiaodong" sort="Sun, Xiaodong" uniqKey="Sun X" first="Xiaodong" last="Sun">Xiaodong Sun</name>
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<author><name sortKey="Ren, Hongyu" sort="Ren, Hongyu" uniqKey="Ren H" first="Hongyu" last="Ren">Hongyu Ren</name>
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<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
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<author><name sortKey="Guo, Lijuan" sort="Guo, Lijuan" uniqKey="Guo L" first="Lijuan" last="Guo">Lijuan Guo</name>
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<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
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<author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name>
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<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name>
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<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Departments of Pathophysiology and ninghuang2018@163.com.</nlm:affiliation>
<country wicri:rule="url">Oman</country>
</affiliation>
</author>
<author><name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Departments of Pathophysiology and jingyuli@scu.edu.cn.</nlm:affiliation>
<country wicri:rule="url">République populaire de Chine</country>
</affiliation>
</author>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.</title>
<author><name sortKey="You, Yuanyuan" sort="You, Yuanyuan" uniqKey="You Y" first="Yuanyuan" last="You">Yuanyuan You</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Zhu, Feimei" sort="Zhu, Feimei" uniqKey="Zhu F" first="Feimei" last="Zhu">Feimei Zhu</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Xu, Qian" sort="Xu, Qian" uniqKey="Xu Q" first="Qian" last="Xu">Qian Xu</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Han, Lu" sort="Han, Lu" uniqKey="Han L" first="Lu" last="Han">Lu Han</name>
<affiliation wicri:level="1"><nlm:affiliation>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041</wicri:regionArea>
<wicri:noRegion>Chengdu 610041</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Gao, Xiang" sort="Gao, Xiang" uniqKey="Gao X" first="Xiang" last="Gao">Xiang Gao</name>
<affiliation wicri:level="1"><nlm:affiliation>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041</wicri:regionArea>
<wicri:noRegion>Chengdu 610041</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhang, Xiaoyu" sort="Zhang, Xiaoyu" uniqKey="Zhang X" first="Xiaoyu" last="Zhang">Xiaoyu Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>the State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>the State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020</wicri:regionArea>
<placeName><settlement type="city">Tianjin</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Luo, Hongbo R" sort="Luo, Hongbo R" uniqKey="Luo H" first="Hongbo R" last="Luo">Hongbo R. Luo</name>
<affiliation wicri:level="2"><nlm:affiliation>the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Massachusetts</region>
</placeName>
<wicri:cityArea>the Department of Pathology, Harvard Medical School, Boston</wicri:cityArea>
</affiliation>
<affiliation><nlm:affiliation>the Department of Lab Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, and.</nlm:affiliation>
<wicri:noCountry code="subField">and</wicri:noCountry>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>the Dana-Farber/Harvard Cancer Center, Boston, Massachusetts 02115.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Massachusetts</region>
</placeName>
<wicri:cityArea>the Dana-Farber/Harvard Cancer Center, Boston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Miao, Junming" sort="Miao, Junming" uniqKey="Miao J" first="Junming" last="Miao">Junming Miao</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Sun, Xiaodong" sort="Sun, Xiaodong" uniqKey="Sun X" first="Xiaodong" last="Sun">Xiaodong Sun</name>
<affiliation wicri:level="1"><nlm:affiliation>Pharmacology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Pharmacology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041</wicri:regionArea>
<wicri:noRegion>Chengdu 610041</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Ren, Hongyu" sort="Ren, Hongyu" uniqKey="Ren H" first="Hongyu" last="Ren">Hongyu Ren</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Du, Yu" sort="Du, Yu" uniqKey="Du Y" first="Yu" last="Du">Yu Du</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Guo, Lijuan" sort="Guo, Lijuan" uniqKey="Guo L" first="Lijuan" last="Guo">Lijuan Guo</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name>
<affiliation><nlm:affiliation>From the Departments of Pathophysiology and.</nlm:affiliation>
<wicri:noCountry code="no comma">From the Departments of Pathophysiology and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Departments of Pathophysiology and ninghuang2018@163.com.</nlm:affiliation>
<country wicri:rule="url">Oman</country>
</affiliation>
</author>
<author><name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Departments of Pathophysiology and jingyuli@scu.edu.cn.</nlm:affiliation>
<country wicri:rule="url">République populaire de Chine</country>
</affiliation>
</author>
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<series><title level="j">The Journal of biological chemistry</title>
<idno type="eISSN">1083-351X</idno>
<imprint><date when="2019" type="published">2019</date>
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<term>Bone Marrow (metabolism)</term>
<term>Bone Marrow (pathology)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>HL-60 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Inflammation (genetics)</term>
<term>Inflammation (metabolism)</term>
<term>Inflammation (pathology)</term>
<term>Integrin alpha4 (genetics)</term>
<term>Integrin alpha4 (metabolism)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Neutrophils (metabolism)</term>
<term>Neutrophils (pathology)</term>
<term>Up-Regulation (MeSH)</term>
<term>Vascular Cell Adhesion Molecule-1 (genetics)</term>
<term>Vascular Cell Adhesion Molecule-1 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cellules HL-60 (MeSH)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Granulocytes neutrophiles (anatomopathologie)</term>
<term>Granulocytes neutrophiles (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Inflammation (anatomopathologie)</term>
<term>Inflammation (génétique)</term>
<term>Inflammation (métabolisme)</term>
<term>Intégrine alpha4 (génétique)</term>
<term>Intégrine alpha4 (métabolisme)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Moelle osseuse (anatomopathologie)</term>
<term>Moelle osseuse (métabolisme)</term>
<term>Molécule-1 d'adhérence des cellules vasculaires (génétique)</term>
<term>Molécule-1 d'adhérence des cellules vasculaires (métabolisme)</term>
<term>Régulation positive (MeSH)</term>
<term>Souris knockout (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>Integrin alpha4</term>
<term>Vascular Cell Adhesion Molecule-1</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Granulocytes neutrophiles</term>
<term>Inflammation</term>
<term>Moelle osseuse</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Inflammation</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term>
<term>Inflammation</term>
<term>Intégrine alpha4</term>
<term>Molécule-1 d'adhérence des cellules vasculaires</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bone Marrow</term>
<term>Glutaredoxins</term>
<term>Inflammation</term>
<term>Integrin alpha4</term>
<term>Neutrophils</term>
<term>Vascular Cell Adhesion Molecule-1</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutarédoxines</term>
<term>Granulocytes neutrophiles</term>
<term>Inflammation</term>
<term>Intégrine alpha4</term>
<term>Moelle osseuse</term>
<term>Molécule-1 d'adhérence des cellules vasculaires</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Bone Marrow</term>
<term>Inflammation</term>
<term>Neutrophils</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>HL-60 Cells</term>
<term>Humans</term>
<term>Mice, Knockout</term>
<term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules HL-60</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Régulation positive</term>
<term>Souris knockout</term>
</keywords>
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<front><div type="abstract" xml:lang="en">α4 integrin plays a crucial role in retention and release of neutrophils from bone marrow. Although α4 integrin is known to be a potential target of reactive oxygen species (ROS)-induced cysteine glutathionylation, the physiological significance and underlying regulatory mechanism of this event remain elusive. Here, using <i>in vitro</i>
 and <i>in vivo</i>
 biochemical and cell biology approaches, we show that physiological ROS-induced glutathionylation of α4 integrin in neutrophils increases the binding of neutrophil-associated α4 integrin to vascular cell adhesion molecule 1 (VCAM-1) on human endothelial cells. This enhanced binding was reversed by extracellular glutaredoxin 1 (Grx1), a thiol disulfide oxidoreductase promoting protein deglutathionylation. Furthermore, in a murine inflammation model, Grx1 disruption dramatically elevated α4 glutathionylation and subsequently enhanced neutrophil egress from the bone marrow. Corroborating this observation, intravenous injection of recombinant Grx1 into mice inhibited α4 glutathionylation and thereby suppressed inflammation-induced neutrophil mobilization from the bone marrow. Taken together, our results establish ROS-elicited glutathionylation and its modulation by Grx1 as pivotal regulatory mechanisms controlling α4 integrin affinity and neutrophil mobilization from the bone marrow under physiological conditions.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30598505</PMID>
<DateCompleted><Year>2019</Year>
<Month>04</Month>
<Day>29</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>294</Volume>
<Issue>8</Issue>
<PubDate><Year>2019</Year>
<Month>02</Month>
<Day>22</Day>
</PubDate>
</JournalIssue>
<Title>The Journal of biological chemistry</Title>
<ISOAbbreviation>J Biol Chem</ISOAbbreviation>
</Journal>
<ArticleTitle>Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.</ArticleTitle>
<Pagination><MedlinePgn>2616-2627</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.RA118.006096</ELocationID>
<Abstract><AbstractText>α4 integrin plays a crucial role in retention and release of neutrophils from bone marrow. Although α4 integrin is known to be a potential target of reactive oxygen species (ROS)-induced cysteine glutathionylation, the physiological significance and underlying regulatory mechanism of this event remain elusive. Here, using <i>in vitro</i>
 and <i>in vivo</i>
 biochemical and cell biology approaches, we show that physiological ROS-induced glutathionylation of α4 integrin in neutrophils increases the binding of neutrophil-associated α4 integrin to vascular cell adhesion molecule 1 (VCAM-1) on human endothelial cells. This enhanced binding was reversed by extracellular glutaredoxin 1 (Grx1), a thiol disulfide oxidoreductase promoting protein deglutathionylation. Furthermore, in a murine inflammation model, Grx1 disruption dramatically elevated α4 glutathionylation and subsequently enhanced neutrophil egress from the bone marrow. Corroborating this observation, intravenous injection of recombinant Grx1 into mice inhibited α4 glutathionylation and thereby suppressed inflammation-induced neutrophil mobilization from the bone marrow. Taken together, our results establish ROS-elicited glutathionylation and its modulation by Grx1 as pivotal regulatory mechanisms controlling α4 integrin affinity and neutrophil mobilization from the bone marrow under physiological conditions.</AbstractText>
<CopyrightInformation>© 2019 You et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>You</LastName>
<ForeName>Yuanyuan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Junli</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Feimei</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Qian</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Han</LastName>
<ForeName>Lu</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Xiang</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>the State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Xiaoyu</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>the State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Luo</LastName>
<ForeName>Hongbo R</ForeName>
<Initials>HR</Initials>
<AffiliationInfo><Affiliation>the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>the Department of Lab Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, and.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>the Dana-Farber/Harvard Cancer Center, Boston, Massachusetts 02115.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Miao</LastName>
<ForeName>Junming</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Xiaodong</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Pharmacology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Hongyu</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Du</LastName>
<ForeName>Yu</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Guo</LastName>
<ForeName>Lijuan</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xiaoying</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Shanze</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Ning</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and ninghuang2018@163.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jingyu</ForeName>
<Initials>J</Initials>
<Identifier Source="ORCID">0000-0003-0997-9115</Identifier>
<AffiliationInfo><Affiliation>From the Departments of Pathophysiology and jingyuli@scu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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<AccessionNumberList><AccessionNumber>4IRZ</AccessionNumber>
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<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>12</Month>
<Day>31</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Biol Chem</MedlineTA>
<NlmUniqueID>2985121R</NlmUniqueID>
<ISSNLinking>0021-9258</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019010">Vascular Cell Adhesion Molecule-1</NameOfSubstance>
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<Chemical><RegistryNumber>143198-26-9</RegistryNumber>
<NameOfSubstance UI="D039441">Integrin alpha4</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001853" MajorTopicYN="N">Bone Marrow</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018922" MajorTopicYN="N">HL-60 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D039441" MajorTopicYN="N">Integrin alpha4</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009504" MajorTopicYN="N">Neutrophils</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015854" MajorTopicYN="Y">Up-Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019010" MajorTopicYN="N">Vascular Cell Adhesion Molecule-1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">glutathionylation</Keyword>
<Keyword MajorTopicYN="Y">reactive oxygen species (ROS)</Keyword>
<Keyword MajorTopicYN="Y">integrin</Keyword>
<Keyword MajorTopicYN="Y">neutrophil</Keyword>
<Keyword MajorTopicYN="Y">inflammation</Keyword>
<Keyword MajorTopicYN="Y">α4 integrin</Keyword>
<Keyword MajorTopicYN="Y">glutaredoxin</Keyword>
<Keyword MajorTopicYN="Y">immune response</Keyword>
<Keyword MajorTopicYN="Y">neutrophil mobilization</Keyword>
<Keyword MajorTopicYN="Y">vascular cell adhesion molecular 1 (VCAM-1)</Keyword>
</KeywordList>
<CoiStatement>The authors declare that they have no conflicts of interest with the contents of this article.</CoiStatement>
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<name sortKey="Du, Yu" sort="Du, Yu" uniqKey="Du Y" first="Yu" last="Du">Yu Du</name>
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<name sortKey="Gao, Xiang" sort="Gao, Xiang" uniqKey="Gao X" first="Xiang" last="Gao">Xiang Gao</name>
<name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name>
<name sortKey="Sun, Xiaodong" sort="Sun, Xiaodong" uniqKey="Sun X" first="Xiaodong" last="Sun">Xiaodong Sun</name>
<name sortKey="Zhang, Xiaoyu" sort="Zhang, Xiaoyu" uniqKey="Zhang X" first="Xiaoyu" last="Zhang">Xiaoyu Zhang</name>
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<country name="États-Unis"><region name="Massachusetts"><name sortKey="Luo, Hongbo R" sort="Luo, Hongbo R" uniqKey="Luo H" first="Hongbo R" last="Luo">Hongbo R. Luo</name>
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<name sortKey="Luo, Hongbo R" sort="Luo, Hongbo R" uniqKey="Luo H" first="Hongbo R" last="Luo">Hongbo R. Luo</name>
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   |wiki=    Bois
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   |type=    RBID
   |clé=     pubmed:30598505
   |texte=   Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.
}}

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	Serveur d'exploration sur la glutarédoxine
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Serveur d'exploration sur la glutarédoxine

Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.

Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.

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