Ablation of glutaredoxin 1 promotes pulmonary angiogenesis and alveolar formation in hyperoxia-injured lungs by modifying HIF-1α stability and inhibiting the NF-κB pathway.
Identifieur interne : 000094 ( Main/Exploration ); précédent : 000093; suivant : 000095Ablation of glutaredoxin 1 promotes pulmonary angiogenesis and alveolar formation in hyperoxia-injured lungs by modifying HIF-1α stability and inhibiting the NF-κB pathway.
Auteurs : Xuwei Liu [République populaire de Chine] ; Kexin Li [République populaire de Chine] ; Fengmei Zhang [République populaire de Chine] ; Yunfei Zhang [République populaire de Chine] ; Chun Deng [République populaire de Chine] ; Chunbao Guo [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Délétion de gène (MeSH), Facteur de croissance endothéliale vasculaire de type A (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Hyperoxie (anatomopathologie), Hyperoxie (génétique), Néovascularisation physiologique (MeSH), Poumon (anatomopathologie), Poumon (métabolisme), Poumon (vascularisation), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme), Stabilité protéique (MeSH), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Hyperoxie, Poumon.
- génétique : Glutarédoxines, Hyperoxie.
- métabolisme : Facteur de croissance endothéliale vasculaire de type A, Facteur de transcription NF-kappa B, Glutarédoxines, Poumon, Sous-unité alpha du facteur-1 induit par l'hypoxie.
- vascularisation : Poumon.
- Animaux, Délétion de gène, Néovascularisation physiologique, Souris, Souris de lignée C57BL, Souris knockout, Stabilité protéique, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Gene Deletion (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Hyperoxia (genetics), Hyperoxia (pathology), Hypoxia-Inducible Factor 1, alpha Subunit (metabolism), Lung (blood supply), Lung (metabolism), Lung (pathology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), NF-kappa B (metabolism), Neovascularization, Physiologic (MeSH), Protein Stability (MeSH), Signal Transduction (MeSH), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , genetics : Glutaredoxins.
- chemical , metabolism : Glutaredoxins, Hypoxia-Inducible Factor 1, alpha Subunit, NF-kappa B, Vascular Endothelial Growth Factor A.
- blood supply : Lung.
- genetics : Hyperoxia.
- metabolism : Lung.
- pathology : Hyperoxia, Lung.
- Animals, Gene Deletion, Mice, Mice, Inbred C57BL, Mice, Knockout, Neovascularization, Physiologic, Protein Stability, Signal Transduction.
Abstract
Glutaredoxin 1 (Grx1) is an important thiol transferase that catalyses the deglutathionylation of proteins through its active site. Deletion of Grx1 increases levels of glutathione-protein adducts and improves ischaemic revascularization. In this study, we investigated whether the absence of Grx1 ameliorates pathological changes in blood vessels and alveoli in a mouse model exposed to hyperoxic conditions. High oxygen exposure for three consecutive weeks increased the levels of Grx1 in the lungs of hyperoxic mice from control levels, while Grx1 levels in Grx1 knockout (KO) mice were significantly reduced under high oxygen conditions. Exposure to 85% oxygen for 21 days reduced alveolarization in wild-type (WT) mice but increased the numbers of alveoli and the survival rate of Grx1 KO littermates. Importantly, vascular endothelial growth factor receptor 2 (VEGFR2) and vascular endothelial growth factor A (VEGFA) expressions were increased in Grx1 KO mice after hyperoxia treatment, and these effects were probably attributable to increased hypoxia-inducible factor (HIF)-1α expression. On the other hand, in response to nuclear factor (NF)-κB inhibition by Grx1 ablation, chemokine and caspase-3 levels were reduced, although the Bcl-2:Bax ratio was increased. Here, we provide evidence that Grx1 plays an important role in regulating pathological damage under hyperoxic conditions by promoting HIF-1α stability and inhibiting the NF-κB pathway in vivo. Our study highlights the functional importance of the Grx1/protein S-glutathionylation (PSSG) redox module in the regulation of ischaemic revascularization, indicating potential clinical and therapeutic applications.
DOI: 10.1016/j.bbrc.2020.02.129
PubMed: 32113683
Affiliations:
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Electronic address: dengcgcb@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Yongchuan Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China. Electronic address: guochunbao@cqmu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics</wicri:regionArea><wicri:noRegion>PR China; Chongqing Key Laboratory of Pediatrics</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32113683</idno><idno type="pmid">32113683</idno><idno type="doi">10.1016/j.bbrc.2020.02.129</idno><idno type="wicri:Area/Main/Corpus">000078</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000078</idno><idno type="wicri:Area/Main/Curation">000078</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000078</idno><idno type="wicri:Area/Main/Exploration">000078</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ablation of glutaredoxin 1 promotes pulmonary angiogenesis and alveolar formation in hyperoxia-injured lungs by modifying HIF-1α stability and inhibiting the NF-κB pathway.</title><author><name sortKey="Liu, Xuwei" sort="Liu, Xuwei" uniqKey="Liu X" first="Xuwei" last="Liu">Xuwei Liu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neonatology, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neonatology, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics</wicri:regionArea><wicri:noRegion>PR China; Chongqing Key Laboratory of Pediatrics</wicri:noRegion></affiliation></author><author><name sortKey="Li, Kexin" sort="Li, Kexin" uniqKey="Li K" first="Kexin" last="Li">Kexin Li</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory Animal Center, Chongqing Medical University, Chongqing, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory Animal Center, Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Fengmei" sort="Zhang, Fengmei" uniqKey="Zhang F" first="Fengmei" last="Zhang">Fengmei Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory Animal Center, Chongqing Medical University, Chongqing, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Laboratory Animal Center, Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Yunfei" sort="Zhang, Yunfei" uniqKey="Zhang Y" first="Yunfei" last="Zhang">Yunfei Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics</wicri:regionArea><wicri:noRegion>PR China; Chongqing Key Laboratory of Pediatrics</wicri:noRegion></affiliation></author><author><name sortKey="Deng, Chun" sort="Deng, Chun" uniqKey="Deng C" first="Chun" last="Deng">Chun Deng</name><affiliation wicri:level="1"><nlm:affiliation>Yongchuan Hospital of Chongqing Medical University, Chongqing, PR China. Electronic address: dengcgcb@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Yongchuan Hospital of Chongqing Medical University, Chongqing</wicri:regionArea><wicri:noRegion>Chongqing</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China. Electronic address: guochunbao@cqmu.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics</wicri:regionArea><wicri:noRegion>PR China; Chongqing Key Laboratory of Pediatrics</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Gene Deletion (MeSH)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Hyperoxia (genetics)</term><term>Hyperoxia (pathology)</term><term>Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)</term><term>Lung (blood supply)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>NF-kappa B (metabolism)</term><term>Neovascularization, Physiologic (MeSH)</term><term>Protein Stability (MeSH)</term><term>Signal Transduction (MeSH)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Délétion de gène (MeSH)</term><term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Hyperoxie (anatomopathologie)</term><term>Hyperoxie (génétique)</term><term>Néovascularisation physiologique (MeSH)</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Poumon (vascularisation)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term><term>Sous-unité alpha du facteur-1 induit par l'hypoxie (métabolisme)</term><term>Stabilité protéique (MeSH)</term><term>Transduction du signal (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>Glutaredoxins</term><term>Hypoxia-Inducible Factor 1, alpha Subunit</term><term>NF-kappa B</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hyperoxie</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hyperoxia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term><term>Hyperoxie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Facteur de transcription NF-kappa B</term><term>Glutarédoxines</term><term>Poumon</term><term>Sous-unité alpha du facteur-1 induit par l'hypoxie</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hyperoxia</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Deletion</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Neovascularization, Physiologic</term><term>Protein Stability</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Délétion de gène</term><term>Néovascularisation physiologique</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Stabilité protéique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutaredoxin 1 (Grx1) is an important thiol transferase that catalyses the deglutathionylation of proteins through its active site. Deletion of Grx1 increases levels of glutathione-protein adducts and improves ischaemic revascularization. In this study, we investigated whether the absence of Grx1 ameliorates pathological changes in blood vessels and alveoli in a mouse model exposed to hyperoxic conditions. High oxygen exposure for three consecutive weeks increased the levels of Grx1 in the lungs of hyperoxic mice from control levels, while Grx1 levels in Grx1 knockout (KO) mice were significantly reduced under high oxygen conditions. Exposure to 85% oxygen for 21 days reduced alveolarization in wild-type (WT) mice but increased the numbers of alveoli and the survival rate of Grx1 KO littermates. Importantly, vascular endothelial growth factor receptor 2 (VEGFR2) and vascular endothelial growth factor A (VEGFA) expressions were increased in Grx1 KO mice after hyperoxia treatment, and these effects were probably attributable to increased hypoxia-inducible factor (HIF)-1α expression. On the other hand, in response to nuclear factor (NF)-κB inhibition by Grx1 ablation, chemokine and caspase-3 levels were reduced, although the Bcl-2:Bax ratio was increased. Here, we provide evidence that Grx1 plays an important role in regulating pathological damage under hyperoxic conditions by promoting HIF-1α stability and inhibiting the NF-κB pathway in vivo. Our study highlights the functional importance of the Grx1/protein S-glutathionylation (PSSG) redox module in the regulation of ischaemic revascularization, indicating potential clinical and therapeutic applications.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32113683</PMID><DateCompleted><Year>2020</Year><Month>11</Month><Day>11</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>525</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>04</Month><Day>30</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Ablation of glutaredoxin 1 promotes pulmonary angiogenesis and alveolar formation in hyperoxia-injured lungs by modifying HIF-1α stability and inhibiting the NF-κB pathway.</ArticleTitle><Pagination><MedlinePgn>528-535</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(20)30410-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2020.02.129</ELocationID><Abstract><AbstractText>Glutaredoxin 1 (Grx1) is an important thiol transferase that catalyses the deglutathionylation of proteins through its active site. Deletion of Grx1 increases levels of glutathione-protein adducts and improves ischaemic revascularization. In this study, we investigated whether the absence of Grx1 ameliorates pathological changes in blood vessels and alveoli in a mouse model exposed to hyperoxic conditions. High oxygen exposure for three consecutive weeks increased the levels of Grx1 in the lungs of hyperoxic mice from control levels, while Grx1 levels in Grx1 knockout (KO) mice were significantly reduced under high oxygen conditions. Exposure to 85% oxygen for 21 days reduced alveolarization in wild-type (WT) mice but increased the numbers of alveoli and the survival rate of Grx1 KO littermates. Importantly, vascular endothelial growth factor receptor 2 (VEGFR2) and vascular endothelial growth factor A (VEGFA) expressions were increased in Grx1 KO mice after hyperoxia treatment, and these effects were probably attributable to increased hypoxia-inducible factor (HIF)-1α expression. On the other hand, in response to nuclear factor (NF)-κB inhibition by Grx1 ablation, chemokine and caspase-3 levels were reduced, although the Bcl-2:Bax ratio was increased. Here, we provide evidence that Grx1 plays an important role in regulating pathological damage under hyperoxic conditions by promoting HIF-1α stability and inhibiting the NF-κB pathway in vivo. Our study highlights the functional importance of the Grx1/protein S-glutathionylation (PSSG) redox module in the regulation of ischaemic revascularization, indicating potential clinical and therapeutic applications.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xuwei</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Neonatology, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Kexin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center, Chongqing Medical University, Chongqing, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Fengmei</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Laboratory Animal Center, Chongqing Medical University, Chongqing, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yunfei</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Chun</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Yongchuan Hospital of Chongqing Medical University, Chongqing, PR China. Electronic address: dengcgcb@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Chunbao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Hepatology and Liver Transplantation Center, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Chongqing Key Laboratory of Pediatrics, PR China. Electronic address: guochunbao@cqmu.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>02</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051795">Hypoxia-Inducible Factor 1, alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018496" MajorTopicYN="N">Hyperoxia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051795" MajorTopicYN="N">Hypoxia-Inducible Factor 1, alpha Subunit</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018919" MajorTopicYN="N">Neovascularization, Physiologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055550" MajorTopicYN="N">Protein Stability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Bronchopulmonary dysplasia</Keyword><Keyword MajorTopicYN="Y">Glutaredoxin</Keyword><Keyword MajorTopicYN="Y">Hypoxia-inducible factor-1α</Keyword><Keyword MajorTopicYN="Y">Nuclear factor-κB</Keyword><Keyword MajorTopicYN="Y">Protein S-Glutathionylation</Keyword><Keyword MajorTopicYN="Y">Vascular endothelial growth factor</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declared that they have no conflicts of interest to this work. We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>02</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>02</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>3</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>3</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32113683</ArticleId><ArticleId IdType="pii">S0006-291X(20)30410-1</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2020.02.129</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Liu, Xuwei" sort="Liu, Xuwei" uniqKey="Liu X" first="Xuwei" last="Liu">Xuwei Liu</name></noRegion><name sortKey="Deng, Chun" sort="Deng, Chun" uniqKey="Deng C" first="Chun" last="Deng">Chun Deng</name><name sortKey="Guo, Chunbao" sort="Guo, Chunbao" uniqKey="Guo C" first="Chunbao" last="Guo">Chunbao Guo</name><name sortKey="Li, Kexin" sort="Li, Kexin" uniqKey="Li K" first="Kexin" last="Li">Kexin Li</name><name sortKey="Zhang, Fengmei" sort="Zhang, Fengmei" uniqKey="Zhang F" first="Fengmei" last="Zhang">Fengmei Zhang</name><name sortKey="Zhang, Yunfei" sort="Zhang, Yunfei" uniqKey="Zhang Y" first="Yunfei" last="Zhang">Yunfei Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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