ChloroquineV1, PubMed, Checkpoint, bibRecord, 000092

RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.

Identifieur interne : 000092 ( PubMed/Checkpoint ); précédent : 000091; suivant : 000093

RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.

Source :

Autophagy [ 1554-8635 ] ; 2018.

RBID : pubmed:29965781

Descripteurs français

English descriptors

KwdEn :
- Acute Lung Injury (metabolism), Acute Lung Injury (pathology), Adherens Junctions (metabolism), Animals, Antigens, CD (metabolism), Autophagy, Autophagy-Related Proteins, Cadherins (metabolism), Carrier Proteins (metabolism), Cell Line, Down-Regulation (drug effects), Endocytosis (drug effects), Endothelial Cells (drug effects), Endothelial Cells (metabolism), Endotoxins (toxicity), Gene Deletion, Guanosine Triphosphate (metabolism), Humans, Lipopolysaccharides, Lung (metabolism), Lung (pathology), Mice, Inbred C57BL, Models, Biological, Phosphorylation (drug effects), Protein Binding, Proteolysis (drug effects), Signal Transduction, rab GTP-Binding Proteins (metabolism), src-Family Kinases (metabolism).
MESH :
- chemical , metabolism : Antigens, CD, Cadherins, Carrier Proteins, Guanosine Triphosphate, rab GTP-Binding Proteins, src-Family Kinases.
- drug effects : Down-Regulation, Endocytosis, Endothelial Cells, Phosphorylation, Proteolysis.
- metabolism : Acute Lung Injury, Adherens Junctions, Endothelial Cells, Lung.
- pathology : Acute Lung Injury, Lung.
- chemical , toxicity : Endotoxins.
- Animals, Autophagy, Autophagy-Related Proteins, Cell Line, Gene Deletion, Humans, Lipopolysaccharides, Mice, Inbred C57BL, Models, Biological, Protein Binding, Signal Transduction.

Abstract

Microvascular barrier dysfunction is the central pathophysiological feature of acute lung injury (ALI). RAB26 is a newly identified small GTPase involved in the regulation of endothelial cell (EC) permeability. However, the mechanism behind this protection has not been clearly elucidated. Here we found that RAB26 promoted the integrity of adherens junctions (AJs) in a macroautophagy/autophagy-dependent manner in ALI. RAB26 is frequently downregulated in mouse lungs after LPS treatment. Mice lacking Rab26 exhibited phosphorylated SRC expression and increased CDH5/VE-cadherin phosphorylation, leading to AJ destruction. rab26-null mice showed further aggravation of the effects of endotoxin insult on lung vascular permeability and water content. Depletion of RAB26 resulted in upregulation of phosphorylated SRC, enhancement of CDH5 phosphorylation, and aggravation of CDH5 internalization, thereby weakening AJ integrity and endothelial barrier function in human pulmonary microvascular endothelial cells (HPMECs). RAB26 overexpression caused active interaction between SRC and the autophagy marker LC3-II and promoted degradation of phosphorylated SRC. Furthermore, RAB26 was involved in a direct and activation-dependent manner in autophagy induction through interaction with ATG16L1 in its GTP-bound form. These findings demonstrate that RAB26 exerts a protective effect on endothelial cell (EC) permeability, which is in part dependent on autophagic targeting of active SRC, and the resultant CDH5 dephosphorylation maintains AJ stabilization. Thus, RAB26-mediated autophagic targeting of phosphorylated SRC can maintain barrier integrity when flux through the RAB26-SRC pathway is protected. These findings suggest that activation of RAB26-SRC signaling provides a new therapeutic opportunity to prevent vascular leakage in ALI.

DOI: 10.1080/15548627.2018.1476811
PubMed: 29965781

Affiliations:

République populaire de Chine, États-Unis

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Le document en format XML

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<series><title level="j">Autophagy</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (metabolism)</term>
<term>Acute Lung Injury (pathology)</term>
<term>Adherens Junctions (metabolism)</term>
<term>Animals</term>
<term>Antigens, CD (metabolism)</term>
<term>Autophagy</term>
<term>Autophagy-Related Proteins</term>
<term>Cadherins (metabolism)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Cell Line</term>
<term>Down-Regulation (drug effects)</term>
<term>Endocytosis (drug effects)</term>
<term>Endothelial Cells (drug effects)</term>
<term>Endothelial Cells (metabolism)</term>
<term>Endotoxins (toxicity)</term>
<term>Gene Deletion</term>
<term>Guanosine Triphosphate (metabolism)</term>
<term>Humans</term>
<term>Lipopolysaccharides</term>
<term>Lung (metabolism)</term>
<term>Lung (pathology)</term>
<term>Mice, Inbred C57BL</term>
<term>Models, Biological</term>
<term>Phosphorylation (drug effects)</term>
<term>Protein Binding</term>
<term>Proteolysis (drug effects)</term>
<term>Signal Transduction</term>
<term>rab GTP-Binding Proteins (metabolism)</term>
<term>src-Family Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Antigènes CD (métabolisme)</term>
<term>Autophagie</term>
<term>Cadhérines (métabolisme)</term>
<term>Cellules endothéliales ()</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Délétion de gène</term>
<term>Endocytose ()</term>
<term>Endotoxines (toxicité)</term>
<term>Guanosine triphosphate (métabolisme)</term>
<term>Humains</term>
<term>Jonctions adhérentes (métabolisme)</term>
<term>Liaison aux protéines</term>
<term>Lignée cellulaire</term>
<term>Lipopolysaccharides</term>
<term>Lésion pulmonaire aigüe (anatomopathologie)</term>
<term>Lésion pulmonaire aigüe (métabolisme)</term>
<term>Modèles biologiques</term>
<term>Phosphorylation ()</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (métabolisme)</term>
<term>Protéines G rab (métabolisme)</term>
<term>Protéines associées à l'autophagie</term>
<term>Protéines de transport (métabolisme)</term>
<term>Protéolyse ()</term>
<term>Régulation négative ()</term>
<term>Souris de lignée C57BL</term>
<term>Transduction du signal</term>
<term>src-Family kinases (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD</term>
<term>Cadherins</term>
<term>Carrier Proteins</term>
<term>Guanosine Triphosphate</term>
<term>rab GTP-Binding Proteins</term>
<term>src-Family Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lésion pulmonaire aigüe</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Down-Regulation</term>
<term>Endocytosis</term>
<term>Endothelial Cells</term>
<term>Phosphorylation</term>
<term>Proteolysis</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Lung Injury</term>
<term>Adherens Junctions</term>
<term>Endothelial Cells</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD</term>
<term>Cadhérines</term>
<term>Cellules endothéliales</term>
<term>Guanosine triphosphate</term>
<term>Jonctions adhérentes</term>
<term>Lésion pulmonaire aigüe</term>
<term>Poumon</term>
<term>Protéines G rab</term>
<term>Protéines de transport</term>
<term>src-Family kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acute Lung Injury</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Endotoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Endotoxines</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Autophagy</term>
<term>Autophagy-Related Proteins</term>
<term>Cell Line</term>
<term>Gene Deletion</term>
<term>Humans</term>
<term>Lipopolysaccharides</term>
<term>Mice, Inbred C57BL</term>
<term>Models, Biological</term>
<term>Protein Binding</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Autophagie</term>
<term>Cellules endothéliales</term>
<term>Délétion de gène</term>
<term>Endocytose</term>
<term>Humains</term>
<term>Liaison aux protéines</term>
<term>Lignée cellulaire</term>
<term>Lipopolysaccharides</term>
<term>Modèles biologiques</term>
<term>Phosphorylation</term>
<term>Protéines associées à l'autophagie</term>
<term>Protéolyse</term>
<term>Régulation négative</term>
<term>Souris de lignée C57BL</term>
<term>Transduction du signal</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Microvascular barrier dysfunction is the central pathophysiological feature of acute lung injury (ALI). RAB26 is a newly identified small GTPase involved in the regulation of endothelial cell (EC) permeability. However, the mechanism behind this protection has not been clearly elucidated. Here we found that RAB26 promoted the integrity of adherens junctions (AJs) in a macroautophagy/autophagy-dependent manner in ALI. RAB26 is frequently downregulated in mouse lungs after LPS treatment. Mice lacking Rab26 exhibited phosphorylated SRC expression and increased CDH5/VE-cadherin phosphorylation, leading to AJ destruction. rab26-null mice showed further aggravation of the effects of endotoxin insult on lung vascular permeability and water content. Depletion of RAB26 resulted in upregulation of phosphorylated SRC, enhancement of CDH5 phosphorylation, and aggravation of CDH5 internalization, thereby weakening AJ integrity and endothelial barrier function in human pulmonary microvascular endothelial cells (HPMECs). RAB26 overexpression caused active interaction between SRC and the autophagy marker LC3-II and promoted degradation of phosphorylated SRC. Furthermore, RAB26 was involved in a direct and activation-dependent manner in autophagy induction through interaction with ATG16L1 in its GTP-bound form. These findings demonstrate that RAB26 exerts a protective effect on endothelial cell (EC) permeability, which is in part dependent on autophagic targeting of active SRC, and the resultant CDH5 dephosphorylation maintains AJ stabilization. Thus, RAB26-mediated autophagic targeting of phosphorylated SRC can maintain barrier integrity when flux through the RAB26-SRC pathway is protected. These findings suggest that activation of RAB26-SRC signaling provides a new therapeutic opportunity to prevent vascular leakage in ALI.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29965781</PMID>
<DateCompleted><Year>2019</Year>
<Month>10</Month>
<Day>03</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<Issue>10</Issue>
<PubDate><Year>2018</Year>
</PubDate>
</JournalIssue>
<Title>Autophagy</Title>
<ISOAbbreviation>Autophagy</ISOAbbreviation>
</Journal>
<ArticleTitle>RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.</ArticleTitle>
<Pagination><MedlinePgn>1677-1692</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2018.1476811</ELocationID>
<Abstract><AbstractText>Microvascular barrier dysfunction is the central pathophysiological feature of acute lung injury (ALI). RAB26 is a newly identified small GTPase involved in the regulation of endothelial cell (EC) permeability. However, the mechanism behind this protection has not been clearly elucidated. Here we found that RAB26 promoted the integrity of adherens junctions (AJs) in a macroautophagy/autophagy-dependent manner in ALI. RAB26 is frequently downregulated in mouse lungs after LPS treatment. Mice lacking Rab26 exhibited phosphorylated SRC expression and increased CDH5/VE-cadherin phosphorylation, leading to AJ destruction. rab26-null mice showed further aggravation of the effects of endotoxin insult on lung vascular permeability and water content. Depletion of RAB26 resulted in upregulation of phosphorylated SRC, enhancement of CDH5 phosphorylation, and aggravation of CDH5 internalization, thereby weakening AJ integrity and endothelial barrier function in human pulmonary microvascular endothelial cells (HPMECs). RAB26 overexpression caused active interaction between SRC and the autophagy marker LC3-II and promoted degradation of phosphorylated SRC. Furthermore, RAB26 was involved in a direct and activation-dependent manner in autophagy induction through interaction with ATG16L1 in its GTP-bound form. These findings demonstrate that RAB26 exerts a protective effect on endothelial cell (EC) permeability, which is in part dependent on autophagic targeting of active SRC, and the resultant CDH5 dephosphorylation maintains AJ stabilization. Thus, RAB26-mediated autophagic targeting of phosphorylated SRC can maintain barrier integrity when flux through the RAB26-SRC pathway is protected. These findings suggest that activation of RAB26-SRC signaling provides a new therapeutic opportunity to prevent vascular leakage in ALI.</AbstractText>
<AbstractText Label="ABBREVIATIONS">AJs: adherens junctions; ALI: acute lung injury; ARDS: acute respiratory distress syndrome; ATG5: autophagy related 5; ATG12: autophagy related 12; ATG 16L1: autophagy related 16 like; 1 BALF: bronchoalveolar lavage fluidCQ: chloroquine; Ctrl: control; EC: endothelial cell; GFP: green fluorescent protein; HA-tagged; RAB26<sup>WT</sup>
: HA-tagged wild-type; RAB26  HA-tagged; RAB26<sup>QL</sup>
: HA-tagged; RAB26<sup>Q123L</sup>
HA-tagged; RAB26<sup>NI</sup>
: HA-tagged; RAB26<sup>N177I</sup>
HPMECs: human pulmonary microvascular endothelial cells; H&E: hematoxylin & eosin; IgG: immunoglobulin; GIF: immunofluorescence; IP: immunoprecipitationi;. p.: intraperitoneal; LPS: lipopolysaccharide; PBS: phosphate-buffered salinesi; RNA: small interfering;RNASQSTM1/p62, sequestosome; 1TBS: Tris-buffered saline; VEGF: vascular endothelial growth factor; WB: western blot; WT: wild-type.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dong</LastName>
<ForeName>Weijie</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Binfeng</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qian</LastName>
<ForeName>Hang</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Qian</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Dong</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Zhenghua</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Zi</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Zhi</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Guangyu</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>b Department of Pharmacology and Toxicology , Georgia Regents University , Augusta , Georgia , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qian</LastName>
<ForeName>Guisheng</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Guansong</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</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>2018</Year>
<Month>07</Month>
<Day>26</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Autophagy</MedlineTA>
<NlmUniqueID>101265188</NlmUniqueID>
<ISSNLinking>1554-8627</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D015703">Antigens, CD</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C532820">Atg16l1 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071183">Autophagy-Related Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D015820">Cadherins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004731">Endotoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000626081">Rab26 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C094954">cadherin 5</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>86-01-1</RegistryNumber>
<NameOfSubstance UI="D006160">Guanosine Triphosphate</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.2</RegistryNumber>
<NameOfSubstance UI="D019061">src-Family Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber>
<NameOfSubstance UI="D020691">rab GTP-Binding Proteins</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D055371" MajorTopicYN="N">Acute Lung Injury</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D022005" MajorTopicYN="N">Adherens Junctions</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015703" MajorTopicYN="N">Antigens, CD</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071183" MajorTopicYN="N">Autophagy-Related Proteins</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015820" MajorTopicYN="N">Cadherins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004705" MajorTopicYN="N">Endocytosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004731" MajorTopicYN="N">Endotoxins</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006160" MajorTopicYN="N">Guanosine Triphosphate</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059748" MajorTopicYN="N">Proteolysis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020691" MajorTopicYN="N">rab GTP-Binding Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019061" MajorTopicYN="N">src-Family Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ATG16L1</Keyword>
<Keyword MajorTopicYN="Y">Acute lung injury (ALI)</Keyword>
<Keyword MajorTopicYN="Y">CDH5</Keyword>
<Keyword MajorTopicYN="Y">RAB26 GTPase</Keyword>
<Keyword MajorTopicYN="Y">SRC</Keyword>
<Keyword MajorTopicYN="Y">adherens junctions (AJs)</Keyword>
<Keyword MajorTopicYN="Y">autophagy</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>7</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>10</Month>
<Day>8</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>7</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">29965781</ArticleId>
<ArticleId IdType="doi">10.1080/15548627.2018.1476811</ArticleId>
<ArticleId IdType="pmc">PMC6135632</ArticleId>
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<Reference><Citation>Lancet Respir Med. 2017 Jun;5(6):524-534</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28664851</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Dong, Weijie" sort="Dong, Weijie" uniqKey="Dong W" first="Weijie" last="Dong">Weijie Dong</name>
</noRegion>
<name sortKey="He, Binfeng" sort="He, Binfeng" uniqKey="He B" first="Binfeng" last="He">Binfeng He</name>
<name sortKey="Li, Jin" sort="Li, Jin" uniqKey="Li J" first="Jin" last="Li">Jin Li</name>
<name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name>
<name sortKey="Qian, Guisheng" sort="Qian, Guisheng" uniqKey="Qian G" first="Guisheng" last="Qian">Guisheng Qian</name>
<name sortKey="Qian, Hang" sort="Qian, Hang" uniqKey="Qian H" first="Hang" last="Qian">Hang Qian</name>
<name sortKey="Wang, Dong" sort="Wang, Dong" uniqKey="Wang D" first="Dong" last="Wang">Dong Wang</name>
<name sortKey="Wang, Guansong" sort="Wang, Guansong" uniqKey="Wang G" first="Guansong" last="Wang">Guansong Wang</name>
<name sortKey="Wang, Zi" sort="Wang, Zi" uniqKey="Wang Z" first="Zi" last="Wang">Zi Wang</name>
<name sortKey="Wei, Zhenghua" sort="Wei, Zhenghua" uniqKey="Wei Z" first="Zhenghua" last="Wei">Zhenghua Wei</name>
<name sortKey="Xu, Zhi" sort="Xu, Zhi" uniqKey="Xu Z" first="Zhi" last="Xu">Zhi Xu</name>
</country>
<country name="États-Unis"><noRegion><name sortKey="Wu, Guangyu" sort="Wu, Guangyu" uniqKey="Wu G" first="Guangyu" last="Wu">Guangyu Wu</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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   |texte=   RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.
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RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.

RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.

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