RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.
Identifieur interne : 000098 ( PubMed/Corpus ); précédent : 000097; suivant : 000099RAB26-dependent autophagy protects adherens junctional integrity in acute lung injury.
Auteurs : Weijie Dong ; Binfeng He ; Hang Qian ; Qian Liu ; Dong Wang ; Jin Li ; Zhenghua Wei ; Zi Wang ; Zhi Xu ; Guangyu Wu ; Guisheng Qian ; Guansong WangSource :
- Autophagy [ 1554-8635 ] ; 2018.
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
Links to Exploration step
pubmed:29965781Le document en format XML
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<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>
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<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="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="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>
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<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>
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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>
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<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>
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<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>
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