RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.
Identifieur interne : 000C19 ( Main/Exploration ); précédent : 000C18; suivant : 000C20RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.
Auteurs : Weijie Dong [République populaire de Chine] ; Binfeng He [République populaire de Chine] ; Hang Qian [République populaire de Chine] ; Qian Liu [République populaire de Chine] ; Dong Wang [République populaire de Chine] ; Jin Li [République populaire de Chine] ; Zhenghua Wei [République populaire de Chine] ; Zi Wang [République populaire de Chine] ; Zhi Xu [République populaire de Chine] ; Guangyu Wu [États-Unis] ; Guisheng Qian [République populaire de Chine] ; Guansong Wang [République populaire de Chine]Source :
- Autophagy [ 1554-8635 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Antigènes CD (métabolisme), Autophagie, Cadhérines (métabolisme), Cellules endothéliales (), Cellules endothéliales (métabolisme), Délétion de gène, Endocytose (), Endotoxines (toxicité), Guanosine triphosphate (métabolisme), Humains, Jonctions adhérentes (métabolisme), Liaison aux protéines, Lignée cellulaire, Lipopolysaccharides, Lésion pulmonaire aigüe (anatomopathologie), Lésion pulmonaire aigüe (métabolisme), Modèles biologiques, Phosphorylation (), Poumon (anatomopathologie), Poumon (métabolisme), Protéines G rab (métabolisme), Protéines associées à l'autophagie, Protéines de transport (métabolisme), Protéolyse (), Régulation négative (), Souris de lignée C57BL, Transduction du signal, src-Family kinases (métabolisme).
- MESH :
- anatomopathologie : Lésion pulmonaire aigüe, Poumon.
- métabolisme : Antigènes CD, Cadhérines, Cellules endothéliales, Guanosine triphosphate, Jonctions adhérentes, Lésion pulmonaire aigüe, Poumon, Protéines G rab, Protéines de transport, src-Family kinases.
- toxicité : Endotoxines.
- Animaux, Autophagie, Cellules endothéliales, Délétion de gène, Endocytose, Humains, Liaison aux protéines, Lignée cellulaire, Lipopolysaccharides, Modèles biologiques, Phosphorylation, Protéines associées à l'autophagie, Protéolyse, Régulation négative, Souris de lignée C57BL, Transduction du signal.
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:
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Le document en format XML
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China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Qian, Hang" sort="Qian, Hang" uniqKey="Qian H" first="Hang" last="Qian">Hang Qian</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wang, Dong" sort="Wang, Dong" uniqKey="Wang D" first="Dong" last="Wang">Dong Wang</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Li, Jin" sort="Li, Jin" uniqKey="Li J" first="Jin" last="Li">Jin Li</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wei, Zhenghua" sort="Wei, Zhenghua" uniqKey="Wei Z" first="Zhenghua" last="Wei">Zhenghua Wei</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wang, Zi" sort="Wang, Zi" uniqKey="Wang Z" first="Zi" last="Wang">Zi Wang</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Xu, Zhi" sort="Xu, Zhi" uniqKey="Xu Z" first="Zhi" last="Xu">Zhi Xu</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wu, Guangyu" sort="Wu, Guangyu" uniqKey="Wu G" first="Guangyu" last="Wu">Guangyu Wu</name><affiliation wicri:level="1"><nlm:affiliation>b Department of Pharmacology and Toxicology , Georgia Regents University , Augusta , Georgia , USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>b Department of Pharmacology and Toxicology , Georgia Regents University , Augusta , Georgia </wicri:regionArea><wicri:noRegion>Georgia </wicri:noRegion></affiliation></author><author><name sortKey="Qian, Guisheng" sort="Qian, Guisheng" uniqKey="Qian G" first="Guisheng" last="Qian">Guisheng Qian</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de 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sort="Dong, Weijie" uniqKey="Dong W" first="Weijie" last="Dong">Weijie Dong</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="He, Binfeng" sort="He, Binfeng" uniqKey="He B" first="Binfeng" last="He">Binfeng He</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Qian, Hang" sort="Qian, Hang" uniqKey="Qian H" first="Hang" last="Qian">Hang Qian</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Liu, Qian" sort="Liu, Qian" uniqKey="Liu Q" first="Qian" last="Liu">Qian Liu</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wang, Dong" sort="Wang, Dong" uniqKey="Wang D" first="Dong" last="Wang">Dong Wang</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Li, Jin" sort="Li, Jin" uniqKey="Li J" first="Jin" last="Li">Jin Li</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wei, Zhenghua" sort="Wei, Zhenghua" uniqKey="Wei Z" first="Zhenghua" last="Wei">Zhenghua Wei</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wang, Zi" sort="Wang, Zi" uniqKey="Wang Z" first="Zi" last="Wang">Zi Wang</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Xu, Zhi" sort="Xu, Zhi" uniqKey="Xu Z" first="Zhi" last="Xu">Zhi Xu</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wu, Guangyu" sort="Wu, Guangyu" uniqKey="Wu G" first="Guangyu" last="Wu">Guangyu Wu</name><affiliation wicri:level="1"><nlm:affiliation>b Department of Pharmacology and Toxicology , Georgia Regents University , Augusta , Georgia , USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>b Department of Pharmacology and Toxicology , Georgia Regents University , Augusta , Georgia </wicri:regionArea><wicri:noRegion>Georgia </wicri:noRegion></affiliation></author><author><name sortKey="Qian, Guisheng" sort="Qian, Guisheng" uniqKey="Qian G" first="Guisheng" last="Qian">Guisheng Qian</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author><author><name sortKey="Wang, Guansong" sort="Wang, Guansong" uniqKey="Wang G" first="Guansong" last="Wang">Guansong Wang</name><affiliation wicri:level="1"><nlm:affiliation>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing </wicri:regionArea><wicri:noRegion>Chongqing </wicri:noRegion></affiliation></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><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></textClass></profileDesc></teiHeader><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><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>Pour manipuler ce document sous Unix (Dilib)
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