Poly(I:C) Induces Human Lung Endothelial Barrier Dysfunction by Disrupting Tight Junction Expression of Claudin-5.
Identifieur interne : 000D60 ( Main/Exploration ); précédent : 000D59; suivant : 000D61Poly(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
Affiliations:
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Proteins, Vesicular Transport (metabolism)</term><term>Chemokines (metabolism)</term><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><term>Poly I-C (metabolism)</term><term>Poly I-C (pharmacology)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Tight Junctions (drug effects)</term><term>Tight Junctions (metabolism)</term><term>Toll-Like Receptor 3 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Cellules endothéliales (cytologie)</term><term>Cellules endothéliales (métabolisme)</term><term>Chimiokines (métabolisme)</term><term>Claudine-5 (génétique)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Jonctions serrées ()</term><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></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Claudin-5</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Vesicular Transport</term><term>Chemokines</term><term>Interferon Regulatory Factor-3</term><term>NF-kappa B</term><term>Poly I-C</term><term>RNA, Messenger</term><term>Toll-Like Receptor 3</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Down-Regulation</term><term>Permeability</term><term>Signal Transduction</term><term>Tight Junctions</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Claudine-5</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Tight Junctions</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Cellules endothéliales</term><term>Chimiokines</term><term>Facteur de transcription NF-kappa B</term><term>Facteur-3 de régulation d'interféron</term><term>Jonctions serrées</term><term>Poly I-C</term><term>Protéines adaptatrices du transport vésiculaire</term><term>Récepteur de type Toll-3</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Poly I-C</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Poly I-C</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Jonctions serrées</term><term>Perméabilité</term><term>Régulation négative</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><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></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Huang, Li Yun" sort="Huang, Li Yun" uniqKey="Huang L" first="Li-Yun" last="Huang">Li-Yun Huang</name></region><name sortKey="D Agnillo, Felice" sort="D Agnillo, Felice" uniqKey="D Agnillo F" first="Felice" last="D'Agnillo">Felice D'Agnillo</name><name sortKey="Golding, Basil" sort="Golding, Basil" uniqKey="Golding B" first="Basil" last="Golding">Basil Golding</name><name sortKey="Stuart, Christine" sort="Stuart, Christine" uniqKey="Stuart C" first="Christine" last="Stuart">Christine Stuart</name><name sortKey="Takeda, Kazuyo" sort="Takeda, Kazuyo" uniqKey="Takeda K" first="Kazuyo" last="Takeda">Kazuyo Takeda</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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