GlutaredoxinV1, Main, Exploration, bibRecord, 000363

Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.

Identifieur interne : 000363 ( Main/Exploration ); précédent : 000362; suivant : 000364

Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.

Source :

Scientific reports [ 2045-2322 ] ; 2017.

RBID : pubmed:29138498

Descripteurs français

KwdFr :
- Animaux (MeSH), Apoptose (MeSH), Athérosclérose (anatomopathologie), Athérosclérose (génétique), Athérosclérose (métabolisme), Cellules cultivées (MeSH), Cellules endothéliales (anatomopathologie), Cellules endothéliales (métabolisme), Glutarédoxines (génétique), Glutarédoxines (physiologie), Humains (MeSH), JNK Mitogen-Activated Protein Kinases (métabolisme), Phosphorylation (MeSH), Protéine O1 à motif en tête de fourche (métabolisme), Protéine-11 analogue à Bcl-2 (métabolisme), Protéines proto-oncogènes c-akt (métabolisme), Régulation positive (MeSH), Souris de lignée C57BL (MeSH), Stress oxydatif (MeSH).
MESH :
- anatomopathologie : Athérosclérose, Cellules endothéliales.
- génétique : Athérosclérose, Glutarédoxines.
- métabolisme : Athérosclérose, Cellules endothéliales, JNK Mitogen-Activated Protein Kinases, Protéine O1 à motif en tête de fourche, Protéine-11 analogue à Bcl-2, Protéines proto-oncogènes c-akt.
- physiologie : Glutarédoxines.
- Animaux, Apoptose, Cellules cultivées, Humains, Phosphorylation, Régulation positive, Souris de lignée C57BL, Stress oxydatif.

English descriptors

KwdEn :
- Animals (MeSH), Apoptosis (MeSH), Atherosclerosis (genetics), Atherosclerosis (metabolism), Atherosclerosis (pathology), Bcl-2-Like Protein 11 (metabolism), Cells, Cultured (MeSH), Endothelial Cells (metabolism), Endothelial Cells (pathology), Forkhead Box Protein O1 (metabolism), Glutaredoxins (genetics), Glutaredoxins (physiology), Humans (MeSH), JNK Mitogen-Activated Protein Kinases (metabolism), Mice, Inbred C57BL (MeSH), Oxidative Stress (MeSH), Phosphorylation (MeSH), Proto-Oncogene Proteins c-akt (metabolism), Up-Regulation (MeSH).
MESH :
- chemical , genetics : Glutaredoxins.
- chemical , metabolism : Bcl-2-Like Protein 11, Forkhead Box Protein O1, JNK Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt.
- genetics : Atherosclerosis.
- metabolism : Atherosclerosis, Endothelial Cells.
- pathology : Atherosclerosis, Endothelial Cells.
- chemical , physiology : Glutaredoxins.
- Animals, Apoptosis, Cells, Cultured, Humans, Mice, Inbred C57BL, Oxidative Stress, Phosphorylation, Up-Regulation.

Abstract

Endothelial cell apoptosis induced by oxidative stress is an early event in the development of atherosclerosis. Several antioxidant enzymes which can cope with oxidative stress are up-regulated by the anti-atherogenic laminar blood flow often seen in straight or unbranched regions of blood vessels. However, the molecular mechanism responsible for flow-induced beneficial effects is incompletely understood. Here we report the role of glutaredoxin 1 (Grx1), an antioxidant enzyme, in flow-mediated protective effect in endothelial cells. Specifically, we found that Grx1 is markedly up-regulated by the steady laminar flow. Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating Akt-FoxO1 signaling and also attenuates H₂O₂-induced Bim activation via inhibiting JNK phosphorylation, subsequently preventing the apoptosis of endothelial cells. Grx1 knockdown abolishes the inhibitory effect of steady laminar flow on Bim. The inhibitory effect of Grx1 on Bim is dependent on Grx1's thioltransferase activity. These findings indicate that Grx1 induction plays a key role in mediating the protective effect of laminar blood flow and suggest that Grx1 may be a potential therapeutic target for atherosclerosis.

DOI: 10.1038/s41598-017-15672-3
PubMed: 29138498
PubMed Central: PMC5686153

Affiliations:

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to stream Main, to step Corpus: 000291
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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.</title>
<author><name sortKey="Li, Yao" sort="Li, Yao" uniqKey="Li Y" first="Yao" last="Li">Yao Li</name>
<affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Ren, Meng" sort="Ren, Meng" uniqKey="Ren M" first="Meng" last="Ren">Meng Ren</name>
<affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Wang, Xiaoqun" sort="Wang, Xiaoqun" uniqKey="Wang X" first="Xiaoqun" last="Wang">Xiaoqun Wang</name>
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<wicri:noRegion>200025</wicri:noRegion>
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<author><name sortKey="Cui, Xingxing" sort="Cui, Xingxing" uniqKey="Cui X" first="Xingxing" last="Cui">Xingxing Cui</name>
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<author><name sortKey="Zhao, Chuanrong" sort="Zhao, Chuanrong" uniqKey="Zhao C" first="Chuanrong" last="Zhao">Chuanrong Zhao</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Zhou, Jing" sort="Zhou, Jing" uniqKey="Zhou J" first="Jing" last="Zhou">Jing Zhou</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing</wicri:regionArea>
<placeName><settlement type="city">Pékin</settlement>
</placeName>
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<author><name sortKey="Guo, Yanan" sort="Guo, Yanan" uniqKey="Guo Y" first="Yanan" last="Guo">Yanan Guo</name>
<affiliation wicri:level="1"><nlm:affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642</wicri:regionArea>
<wicri:noRegion>14642</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Hu, Yi" sort="Hu, Yi" uniqKey="Hu Y" first="Yi" last="Hu">Yi Hu</name>
<affiliation wicri:level="1"><nlm:affiliation>CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. huyi@ihep.ac.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049</wicri:regionArea>
<wicri:noRegion>100049</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yan, Chen" sort="Yan, Chen" uniqKey="Yan C" first="Chen" last="Yan">Chen Yan</name>
<affiliation wicri:level="1"><nlm:affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642</wicri:regionArea>
<wicri:noRegion>14642</wicri:noRegion>
</affiliation>
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<author><name sortKey="Berk, Bradford" sort="Berk, Bradford" uniqKey="Berk B" first="Bradford" last="Berk">Bradford Berk</name>
<affiliation wicri:level="1"><nlm:affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642</wicri:regionArea>
<wicri:noRegion>14642</wicri:noRegion>
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<author><name sortKey="Wang, Jing" sort="Wang, Jing" uniqKey="Wang J" first="Jing" last="Wang">Jing Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. wangjing@ibms.pumc.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005</wicri:regionArea>
<wicri:noRegion>100005</wicri:noRegion>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Apoptosis (MeSH)</term>
<term>Atherosclerosis (genetics)</term>
<term>Atherosclerosis (metabolism)</term>
<term>Atherosclerosis (pathology)</term>
<term>Bcl-2-Like Protein 11 (metabolism)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Endothelial Cells (metabolism)</term>
<term>Endothelial Cells (pathology)</term>
<term>Forkhead Box Protein O1 (metabolism)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (physiology)</term>
<term>Humans (MeSH)</term>
<term>JNK Mitogen-Activated Protein Kinases (metabolism)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Up-Regulation (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Apoptose (MeSH)</term>
<term>Athérosclérose (anatomopathologie)</term>
<term>Athérosclérose (génétique)</term>
<term>Athérosclérose (métabolisme)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Cellules endothéliales (anatomopathologie)</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (physiologie)</term>
<term>Humains (MeSH)</term>
<term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protéine O1 à motif en tête de fourche (métabolisme)</term>
<term>Protéine-11 analogue à Bcl-2 (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Régulation positive (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bcl-2-Like Protein 11</term>
<term>Forkhead Box Protein O1</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Athérosclérose</term>
<term>Cellules endothéliales</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Atherosclerosis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Athérosclérose</term>
<term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Atherosclerosis</term>
<term>Endothelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Athérosclérose</term>
<term>Cellules endothéliales</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
<term>Protéine O1 à motif en tête de fourche</term>
<term>Protéine-11 analogue à Bcl-2</term>
<term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atherosclerosis</term>
<term>Endothelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Cells, Cultured</term>
<term>Humans</term>
<term>Mice, Inbred C57BL</term>
<term>Oxidative Stress</term>
<term>Phosphorylation</term>
<term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Humains</term>
<term>Phosphorylation</term>
<term>Régulation positive</term>
<term>Souris de lignée C57BL</term>
<term>Stress oxydatif</term>
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<front><div type="abstract" xml:lang="en">Endothelial cell apoptosis induced by oxidative stress is an early event in the development of atherosclerosis. Several antioxidant enzymes which can cope with oxidative stress are up-regulated by the anti-atherogenic laminar blood flow often seen in straight or unbranched regions of blood vessels. However, the molecular mechanism responsible for flow-induced beneficial effects is incompletely understood. Here we report the role of glutaredoxin 1 (Grx1), an antioxidant enzyme, in flow-mediated protective effect in endothelial cells. Specifically, we found that Grx1 is markedly up-regulated by the steady laminar flow. Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating Akt-FoxO1 signaling and also attenuates H<sub>2</sub>
O<sub>2</sub>
-induced Bim activation via inhibiting JNK phosphorylation, subsequently preventing the apoptosis of endothelial cells. Grx1 knockdown abolishes the inhibitory effect of steady laminar flow on Bim. The inhibitory effect of Grx1 on Bim is dependent on Grx1's thioltransferase activity. These findings indicate that Grx1 induction plays a key role in mediating the protective effect of laminar blood flow and suggest that Grx1 may be a potential therapeutic target for atherosclerosis.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29138498</PMID>
<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>1</Issue>
<PubDate><Year>2017</Year>
<Month>Nov</Month>
<Day>14</Day>
</PubDate>
</JournalIssue>
<Title>Scientific reports</Title>
<ISOAbbreviation>Sci Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.</ArticleTitle>
<Pagination><MedlinePgn>15539</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-017-15672-3</ELocationID>
<Abstract><AbstractText>Endothelial cell apoptosis induced by oxidative stress is an early event in the development of atherosclerosis. Several antioxidant enzymes which can cope with oxidative stress are up-regulated by the anti-atherogenic laminar blood flow often seen in straight or unbranched regions of blood vessels. However, the molecular mechanism responsible for flow-induced beneficial effects is incompletely understood. Here we report the role of glutaredoxin 1 (Grx1), an antioxidant enzyme, in flow-mediated protective effect in endothelial cells. Specifically, we found that Grx1 is markedly up-regulated by the steady laminar flow. Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating Akt-FoxO1 signaling and also attenuates H<sub>2</sub>
O<sub>2</sub>
-induced Bim activation via inhibiting JNK phosphorylation, subsequently preventing the apoptosis of endothelial cells. Grx1 knockdown abolishes the inhibitory effect of steady laminar flow on Bim. The inhibitory effect of Grx1 on Bim is dependent on Grx1's thioltransferase activity. These findings indicate that Grx1 induction plays a key role in mediating the protective effect of laminar blood flow and suggest that Grx1 may be a potential therapeutic target for atherosclerosis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Yao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Meng</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xiaoqun</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, Ruijin Hospital, Shanghai Jiao-Tong University school of medicine, Shanghai, 200025, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cui</LastName>
<ForeName>Xingxing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Hongmei</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Chuanrong</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Jing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Guo</LastName>
<ForeName>Yanan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. huyi@ihep.ac.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Chen</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berk</LastName>
<ForeName>Bradford</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Aab Cardiovascular Research Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, 14642, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. wangjing@ibms.pumc.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>11</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Sci Rep</MedlineTA>
<NlmUniqueID>101563288</NlmUniqueID>
<ISSNLinking>2045-2322</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000072224">Bcl-2-Like Protein 11</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000606776">Bcl2l11 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C085126">FOXO1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071161">Forkhead Box Protein O1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C494918">AKT1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="D048031">JNK Mitogen-Activated Protein Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050197" MajorTopicYN="N">Atherosclerosis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072224" MajorTopicYN="N">Bcl-2-Like Protein 11</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071161" MajorTopicYN="N">Forkhead Box Protein O1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D048031" MajorTopicYN="N">JNK Mitogen-Activated Protein Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>04</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>10</Month>
<Day>31</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>11</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>11</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>7</Month>
<Day>23</Day>
<Hour>6</Hour>
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<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<settlement><li>Pékin</li>
</settlement>
<orgName><li>Université de Pékin</li>
</orgName>
</list>
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</noRegion>
<name sortKey="Cui, Xingxing" sort="Cui, Xingxing" uniqKey="Cui X" first="Xingxing" last="Cui">Xingxing Cui</name>
<name sortKey="Hu, Yi" sort="Hu, Yi" uniqKey="Hu Y" first="Yi" last="Hu">Yi Hu</name>
<name sortKey="Ren, Meng" sort="Ren, Meng" uniqKey="Ren M" first="Meng" last="Ren">Meng Ren</name>
<name sortKey="Wang, Jing" sort="Wang, Jing" uniqKey="Wang J" first="Jing" last="Wang">Jing Wang</name>
<name sortKey="Wang, Xiaoqun" sort="Wang, Xiaoqun" uniqKey="Wang X" first="Xiaoqun" last="Wang">Xiaoqun Wang</name>
<name sortKey="Zhao, Chuanrong" sort="Zhao, Chuanrong" uniqKey="Zhao C" first="Chuanrong" last="Zhao">Chuanrong Zhao</name>
<name sortKey="Zhao, Hongmei" sort="Zhao, Hongmei" uniqKey="Zhao H" first="Hongmei" last="Zhao">Hongmei Zhao</name>
<name sortKey="Zhou, Jing" sort="Zhou, Jing" uniqKey="Zhou J" first="Jing" last="Zhou">Jing Zhou</name>
</country>
<country name="États-Unis"><noRegion><name sortKey="Guo, Yanan" sort="Guo, Yanan" uniqKey="Guo Y" first="Yanan" last="Guo">Yanan Guo</name>
</noRegion>
<name sortKey="Berk, Bradford" sort="Berk, Bradford" uniqKey="Berk B" first="Bradford" last="Berk">Bradford Berk</name>
<name sortKey="Yan, Chen" sort="Yan, Chen" uniqKey="Yan C" first="Chen" last="Yan">Chen Yan</name>
</country>
</tree>
</affiliations>
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:29138498" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a GlutaredoxinV1

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

Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.

Glutaredoxin 1 mediates the protective effect of steady laminar flow on endothelial cells against oxidative stress-induced apoptosis via inhibiting Bim.

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