GlutaredoxinV1, Main, Exploration, bibRecord, 000A56

Attenuated cardiovascular hypertrophy and oxidant generation in response to angiotensin II infusion in glutaredoxin-1 knockout mice.

Identifieur interne : 000A56 ( Main/Exploration ); précédent : 000A55; suivant : 000A57

Attenuated cardiovascular hypertrophy and oxidant generation in response to angiotensin II infusion in glutaredoxin-1 knockout mice.

Auteurs : Markus M. Bachschmid [États-Unis] ; Shanqin Xu ; Karlene A. Maitland-Toolan ; Ye-Shih Ho ; Richard A. Cohen ; Reiko Matsui

Source :

Free radical biology & medicine [ 1873-4596 ] ; 2010.

RBID : pubmed:20638471

Descripteurs français

KwdFr :
- Angiotensine-II (administration et posologie), Animaux (MeSH), Aorte (anatomopathologie), Cytosquelette d'actine (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Hypertrophie (anatomopathologie), Hypertrophie (génétique), Hypertrophie (métabolisme), Hypertrophie (prévention et contrôle), Lignée cellulaire (MeSH), Maladies cardiovasculaires (anatomopathologie), Maladies cardiovasculaires (génétique), Maladies cardiovasculaires (métabolisme), Maladies cardiovasculaires (prévention et contrôle), Myocarde (anatomopathologie), Nitric oxide synthase type II (biosynthèse), Nitric oxide synthase type II (génétique), Oxydants (métabolisme), Petit ARN interférent (génétique), Pompes à perfusion (MeSH), Protéine oncogène v-akt (génétique), Protéine oncogène v-akt (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Tyrosine (analogues et dérivés), Tyrosine (métabolisme).
MESH :
- administration et posologie : Angiotensine-II.
- analogues et dérivés : Tyrosine.
- anatomopathologie : Aorte, Hypertrophie, Maladies cardiovasculaires, Myocarde.
- biosynthèse : Nitric oxide synthase type II.
- génétique : Glutarédoxines, Hypertrophie, Maladies cardiovasculaires, Nitric oxide synthase type II, Petit ARN interférent, Protéine oncogène v-akt.
- métabolisme : Cytosquelette d'actine, Glutarédoxines, Hypertrophie, Maladies cardiovasculaires, Oxydants, Protéine oncogène v-akt, Tyrosine.
- prévention et contrôle : Hypertrophie, Maladies cardiovasculaires.
- Animaux, Lignée cellulaire, Pompes à perfusion, Souris, Souris de lignée C57BL, Souris knockout.

English descriptors

KwdEn :
- Actin Cytoskeleton (metabolism), Angiotensin II (administration & dosage), Animals (MeSH), Aorta (pathology), Cardiovascular Diseases (genetics), Cardiovascular Diseases (metabolism), Cardiovascular Diseases (pathology), Cardiovascular Diseases (prevention & control), Cell Line (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Hypertrophy (genetics), Hypertrophy (metabolism), Hypertrophy (pathology), Hypertrophy (prevention & control), Infusion Pumps (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Myocardium (pathology), Nitric Oxide Synthase Type II (biosynthesis), Nitric Oxide Synthase Type II (genetics), Oncogene Protein v-akt (genetics), Oncogene Protein v-akt (metabolism), Oxidants (metabolism), RNA, Small Interfering (genetics), Tyrosine (analogs & derivatives), Tyrosine (metabolism).
MESH :
- chemical , administration & dosage : Angiotensin II.
- chemical , analogs & derivatives : Tyrosine.
- chemical , biosynthesis : Nitric Oxide Synthase Type II.
- genetics : Cardiovascular Diseases, Glutaredoxins, Hypertrophy, Nitric Oxide Synthase Type II, Oncogene Protein v-akt, RNA, Small Interfering.
- metabolism : Actin Cytoskeleton, Cardiovascular Diseases, Glutaredoxins, Hypertrophy, Oncogene Protein v-akt, Oxidants, Tyrosine.
- pathology : Aorta, Cardiovascular Diseases, Hypertrophy, Myocardium.
- prevention & control : Cardiovascular Diseases, Hypertrophy.
- Animals, Cell Line, Infusion Pumps, Mice, Mice, Inbred C57BL, Mice, Knockout.

Abstract

Glutaredoxin-1 (Glrx) is a thioltransferase that regulates protein S-glutathiolation. To elucidate the role of endogenous Glrx in cardiovascular disease, Glrx knockout (KO) mice were infused with angiotensin II (Ang II) for 6days. After Ang II infusion, body weight and blood pressure were similar between WT and Glrx KO mice. However, compared to WT mice, Glrx KO mice demonstrated (1) less cardiac and aortic medial hypertrophy, (2) less oxidant generation in aorta as assessed by dihydroethidium staining and nitrotyrosine, (3) decreased phosphorylation of Akt in the heart, and (4) less expression of inducible NOS in aorta and heart. In cultured embryonic fibroblasts from Glrx KO mice, S-glutathiolation of actin was enhanced and actin depolymerization was impaired after hydrogen peroxide stimulation compared with WT cells. Furthermore, oxidant generation in phorbol ester-stimulated fibroblasts and RAW 264.7 macrophage-like cells was lower with Glrx siRNA knockdown. These data indicate that Ang II-induced oxidant production and hypertrophic responses were attenuated in Glrx KO mice, which may result from impaired NADPH oxidase activation.

DOI: 10.1016/j.freeradbiomed.2010.07.005
PubMed: 20638471
PubMed Central: PMC2930025

Affiliations:

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

to stream Main, to step Corpus: 000988
to stream Main, to step Curation: 000988

Le document en format XML

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<term>Angiotensin II (administration & dosage)</term>
<term>Animals (MeSH)</term>
<term>Aorta (pathology)</term>
<term>Cardiovascular Diseases (genetics)</term>
<term>Cardiovascular Diseases (metabolism)</term>
<term>Cardiovascular Diseases (pathology)</term>
<term>Cardiovascular Diseases (prevention & control)</term>
<term>Cell Line (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Hypertrophy (genetics)</term>
<term>Hypertrophy (metabolism)</term>
<term>Hypertrophy (pathology)</term>
<term>Hypertrophy (prevention & control)</term>
<term>Infusion Pumps (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Myocardium (pathology)</term>
<term>Nitric Oxide Synthase Type II (biosynthesis)</term>
<term>Nitric Oxide Synthase Type II (genetics)</term>
<term>Oncogene Protein v-akt (genetics)</term>
<term>Oncogene Protein v-akt (metabolism)</term>
<term>Oxidants (metabolism)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Tyrosine (analogs & derivatives)</term>
<term>Tyrosine (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Angiotensine-II (administration et posologie)</term>
<term>Animaux (MeSH)</term>
<term>Aorte (anatomopathologie)</term>
<term>Cytosquelette d'actine (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Hypertrophie (anatomopathologie)</term>
<term>Hypertrophie (génétique)</term>
<term>Hypertrophie (métabolisme)</term>
<term>Hypertrophie (prévention et contrôle)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Maladies cardiovasculaires (anatomopathologie)</term>
<term>Maladies cardiovasculaires (génétique)</term>
<term>Maladies cardiovasculaires (métabolisme)</term>
<term>Maladies cardiovasculaires (prévention et contrôle)</term>
<term>Myocarde (anatomopathologie)</term>
<term>Nitric oxide synthase type II (biosynthèse)</term>
<term>Nitric oxide synthase type II (génétique)</term>
<term>Oxydants (métabolisme)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Pompes à  perfusion (MeSH)</term>
<term>Protéine oncogène v-akt (génétique)</term>
<term>Protéine oncogène v-akt (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Tyrosine (analogues et dérivés)</term>
<term>Tyrosine (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Angiotensin II</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tyrosine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Nitric Oxide Synthase Type II</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Angiotensine-II</term>
</keywords>
<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Tyrosine</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Aorte</term>
<term>Hypertrophie</term>
<term>Maladies cardiovasculaires</term>
<term>Myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Nitric oxide synthase type II</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiovascular Diseases</term>
<term>Glutaredoxins</term>
<term>Hypertrophy</term>
<term>Nitric Oxide Synthase Type II</term>
<term>Oncogene Protein v-akt</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term>
<term>Hypertrophie</term>
<term>Maladies cardiovasculaires</term>
<term>Nitric oxide synthase type II</term>
<term>Petit ARN interférent</term>
<term>Protéine oncogène v-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Actin Cytoskeleton</term>
<term>Cardiovascular Diseases</term>
<term>Glutaredoxins</term>
<term>Hypertrophy</term>
<term>Oncogene Protein v-akt</term>
<term>Oxidants</term>
<term>Tyrosine</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytosquelette d'actine</term>
<term>Glutarédoxines</term>
<term>Hypertrophie</term>
<term>Maladies cardiovasculaires</term>
<term>Oxydants</term>
<term>Protéine oncogène v-akt</term>
<term>Tyrosine</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aorta</term>
<term>Cardiovascular Diseases</term>
<term>Hypertrophy</term>
<term>Myocardium</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Cardiovascular Diseases</term>
<term>Hypertrophy</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Hypertrophie</term>
<term>Maladies cardiovasculaires</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Infusion Pumps</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Lignée cellulaire</term>
<term>Pompes à  perfusion</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">Glutaredoxin-1 (Glrx) is a thioltransferase that regulates protein S-glutathiolation. To elucidate the role of endogenous Glrx in cardiovascular disease, Glrx knockout (KO) mice were infused with angiotensin II (Ang II) for 6days. After Ang II infusion, body weight and blood pressure were similar between WT and Glrx KO mice. However, compared to WT mice, Glrx KO mice demonstrated (1) less cardiac and aortic medial hypertrophy, (2) less oxidant generation in aorta as assessed by dihydroethidium staining and nitrotyrosine, (3) decreased phosphorylation of Akt in the heart, and (4) less expression of inducible NOS in aorta and heart. In cultured embryonic fibroblasts from Glrx KO mice, S-glutathiolation of actin was enhanced and actin depolymerization was impaired after hydrogen peroxide stimulation compared with WT cells. Furthermore, oxidant generation in phorbol ester-stimulated fibroblasts and RAW 264.7 macrophage-like cells was lower with Glrx siRNA knockdown. These data indicate that Ang II-induced oxidant production and hypertrophic responses were attenuated in Glrx KO mice, which may result from impaired NADPH oxidase activation.</div>
</front>
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<DateCompleted><Year>2011</Year>
<Month>04</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<Issue>7</Issue>
<PubDate><Year>2010</Year>
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<Day>15</Day>
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<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation>
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<ArticleTitle>Attenuated cardiovascular hypertrophy and oxidant generation in response to angiotensin II infusion in glutaredoxin-1 knockout mice.</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2010.07.005</ELocationID>
<Abstract><AbstractText>Glutaredoxin-1 (Glrx) is a thioltransferase that regulates protein S-glutathiolation. To elucidate the role of endogenous Glrx in cardiovascular disease, Glrx knockout (KO) mice were infused with angiotensin II (Ang II) for 6days. After Ang II infusion, body weight and blood pressure were similar between WT and Glrx KO mice. However, compared to WT mice, Glrx KO mice demonstrated (1) less cardiac and aortic medial hypertrophy, (2) less oxidant generation in aorta as assessed by dihydroethidium staining and nitrotyrosine, (3) decreased phosphorylation of Akt in the heart, and (4) less expression of inducible NOS in aorta and heart. In cultured embryonic fibroblasts from Glrx KO mice, S-glutathiolation of actin was enhanced and actin depolymerization was impaired after hydrogen peroxide stimulation compared with WT cells. Furthermore, oxidant generation in phorbol ester-stimulated fibroblasts and RAW 264.7 macrophage-like cells was lower with Glrx siRNA knockdown. These data indicate that Ang II-induced oxidant production and hypertrophic responses were attenuated in Glrx KO mice, which may result from impaired NADPH oxidase activation.</AbstractText>
<CopyrightInformation>Copyright 2010 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bachschmid</LastName>
<ForeName>Markus M</ForeName>
<Initials>MM</Initials>
<AffiliationInfo><Affiliation>Vascular Biology Unit, Department of Medicine, Boston University, Boston, MA 02118, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Shanqin</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Maitland-Toolan</LastName>
<ForeName>Karlene A</ForeName>
<Initials>KA</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ho</LastName>
<ForeName>Ye-Shih</ForeName>
<Initials>YS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Cohen</LastName>
<ForeName>Richard A</ForeName>
<Initials>RA</Initials>
</Author>
<Author ValidYN="Y"><LastName>Matsui</LastName>
<ForeName>Reiko</ForeName>
<Initials>R</Initials>
</Author>
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<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P01 HL081587</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>R01 AG027080</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL104017</GrantID>
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<Grant><GrantID>R03 AG19078-01</GrantID>
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<Month>07</Month>
<Day>16</Day>
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<MedlineTA>Free Radic Biol Med</MedlineTA>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016877">Oxidants</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
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<Chemical><RegistryNumber>3604-79-3</RegistryNumber>
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<Chemical><RegistryNumber>42HK56048U</RegistryNumber>
<NameOfSubstance UI="D014443">Tyrosine</NameOfSubstance>
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<Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051058">Oncogene Protein v-akt</NameOfSubstance>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName>
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<MeshHeading><DescriptorName UI="D001011" MajorTopicYN="N">Aorta</DescriptorName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<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="D006984" MajorTopicYN="N">Hypertrophy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
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Attenuated cardiovascular hypertrophy and oxidant generation in response to angiotensin II infusion in glutaredoxin-1 knockout mice.

Attenuated cardiovascular hypertrophy and oxidant generation in response to angiotensin II infusion in glutaredoxin-1 knockout mice.

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