Poly(I:C) Induces Human Lung Endothelial Barrier Dysfunction by Disrupting Tight Junction Expression of Claudin-5.
Identifieur interne : 000351 ( Ncbi/Curation ); précédent : 000350; suivant : 000352Poly(I:C) Induces Human Lung Endothelial Barrier Dysfunction by Disrupting Tight Junction Expression of Claudin-5.
Auteurs : Li-Yun Huang [États-Unis] ; Christine Stuart [États-Unis] ; Kazuyo Takeda [États-Unis] ; Felice D'Agnillo [États-Unis] ; Basil Golding [États-Unis]Source :
- PloS one [ 1932-6203 ] ; 2016.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Cellules endothéliales (cytologie), Cellules endothéliales (métabolisme), Chimiokines (métabolisme), Claudine-5 (génétique), Facteur de transcription NF-kappa B (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Humains, Jonctions serrées (), Jonctions serrées (métabolisme), Perméabilité (), Poly I-C (métabolisme), Poly I-C (pharmacologie), Poumon (cytologie), Protéines adaptatrices du transport vésiculaire (métabolisme), Récepteur de type Toll-3 (métabolisme), Régulation négative (), Transduction du signal ().
- MESH :
- cytologie : Cellules endothéliales, Poumon.
- génétique : ARN messager, Claudine-5.
- métabolisme : ARN messager, Cellules endothéliales, Chimiokines, Facteur de transcription NF-kappa B, Facteur-3 de régulation d'interféron, Jonctions serrées, Poly I-C, Protéines adaptatrices du transport vésiculaire, Récepteur de type Toll-3.
- pharmacologie : Poly I-C.
- Humains, Jonctions serrées, Perméabilité, Régulation négative, Transduction du signal.
English descriptors
- KwdEn :
- Adaptor Proteins, Vesicular Transport (metabolism), Chemokines (metabolism), Claudin-5 (genetics), Down-Regulation (drug effects), Endothelial Cells (cytology), Endothelial Cells (metabolism), Humans, Interferon Regulatory Factor-3 (metabolism), Lung (cytology), NF-kappa B (metabolism), Permeability (drug effects), Poly I-C (metabolism), Poly I-C (pharmacology), RNA, Messenger (genetics), RNA, Messenger (metabolism), Signal Transduction (drug effects), Tight Junctions (drug effects), Tight Junctions (metabolism), Toll-Like Receptor 3 (metabolism).
- MESH :
- chemical , genetics : Claudin-5, RNA, Messenger.
- chemical , metabolism : Adaptor Proteins, Vesicular Transport, Chemokines, Interferon Regulatory Factor-3, NF-kappa B, Poly I-C, RNA, Messenger, Toll-Like Receptor 3.
- cytology : Endothelial Cells, Lung.
- drug effects : Down-Regulation, Permeability, Signal Transduction, Tight Junctions.
- metabolism : Endothelial Cells, Tight Junctions.
- chemical , pharmacology : Poly I-C.
- Humans.
Abstract
Viral infections are often accompanied by pulmonary microvascular leakage and vascular endothelial dysfunction via mechanisms that are not completely defined. Here, we investigated the effect of the Toll-like receptor 3 (TLR3) ligand polyinosinic-polycytidylic acid [Poly(I:C)], a synthetic analog of viral double-stranded RNA (dsRNA) commonly used to simulate viral infections, on the barrier function and tight junction integrity of primary human lung microvascular endothelial cells. Poly(I:C) stimulated IL-6, IL-8, TNFα, and IFNβ production in conjunction with the activation of NF-κB and IRF3 confirming the Poly(I:C)-responsiveness of these cells. Poly(I:C) increased endothelial monolayer permeability with a corresponding dose- and time-dependent decrease in the expression of claudin-5, a transmembrane tight junction protein and reduction of CLDN5 mRNA levels. Immunofluorescence experiments revealed disappearance of membrane-associated claudin-5 and co-localization of cytoplasmic claudin-5 with lysosomal-associated membrane protein 1. Chloroquine and Bay11-7082, inhibitors of TLR3 and NF-κB signaling, respectively, protected against the loss of claudin-5. Together, these findings provide new insight on how dsRNA-activated signaling pathways may disrupt vascular endothelial function and contribute to vascular leakage pathologies.
DOI: 10.1371/journal.pone.0160875
PubMed: 27504984
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<term>Claudin-5 (genetics)</term>
<term>Down-Regulation (drug effects)</term>
<term>Endothelial Cells (cytology)</term>
<term>Endothelial Cells (metabolism)</term>
<term>Humans</term>
<term>Interferon Regulatory Factor-3 (metabolism)</term>
<term>Lung (cytology)</term>
<term>NF-kappa B (metabolism)</term>
<term>Permeability (drug effects)</term>
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<term>RNA, Messenger (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
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<term>Tight Junctions (metabolism)</term>
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<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur-3 de régulation d'interféron (métabolisme)</term>
<term>Humains</term>
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<term>Jonctions serrées (métabolisme)</term>
<term>Perméabilité ()</term>
<term>Poly I-C (métabolisme)</term>
<term>Poly I-C (pharmacologie)</term>
<term>Poumon (cytologie)</term>
<term>Protéines adaptatrices du transport vésiculaire (métabolisme)</term>
<term>Récepteur de type Toll-3 (métabolisme)</term>
<term>Régulation négative ()</term>
<term>Transduction du signal ()</term>
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<term>RNA, Messenger</term>
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<term>Interferon Regulatory Factor-3</term>
<term>NF-kappa B</term>
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<term>RNA, Messenger</term>
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<term>Poumon</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term>
<term>Lung</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Down-Regulation</term>
<term>Permeability</term>
<term>Signal Transduction</term>
<term>Tight Junctions</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
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<term>Chimiokines</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Facteur-3 de régulation d'interféron</term>
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<term>Récepteur de type Toll-3</term>
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<term>Perméabilité</term>
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<front><div type="abstract" xml:lang="en">Viral infections are often accompanied by pulmonary microvascular leakage and vascular endothelial dysfunction via mechanisms that are not completely defined. Here, we investigated the effect of the Toll-like receptor 3 (TLR3) ligand polyinosinic-polycytidylic acid [Poly(I:C)], a synthetic analog of viral double-stranded RNA (dsRNA) commonly used to simulate viral infections, on the barrier function and tight junction integrity of primary human lung microvascular endothelial cells. Poly(I:C) stimulated IL-6, IL-8, TNFα, and IFNβ production in conjunction with the activation of NF-κB and IRF3 confirming the Poly(I:C)-responsiveness of these cells. Poly(I:C) increased endothelial monolayer permeability with a corresponding dose- and time-dependent decrease in the expression of claudin-5, a transmembrane tight junction protein and reduction of CLDN5 mRNA levels. Immunofluorescence experiments revealed disappearance of membrane-associated claudin-5 and co-localization of cytoplasmic claudin-5 with lysosomal-associated membrane protein 1. Chloroquine and Bay11-7082, inhibitors of TLR3 and NF-κB signaling, respectively, protected against the loss of claudin-5. Together, these findings provide new insight on how dsRNA-activated signaling pathways may disrupt vascular endothelial function and contribute to vascular leakage pathologies. </div>
</front>
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