ER stress activates the NLRP3 inflammasome via an UPR-independent pathway.

Détails

Ressource 1Télécharger: BIB_B8334B683F4E.P001.pdf (516.12 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_B8334B683F4E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
ER stress activates the NLRP3 inflammasome via an UPR-independent pathway.
Périodique
Cell Death and Disease
Auteur(s)
Menu P., Mayor A., Zhou R., Tardivel A., Ichijo H., Mori K., Tschopp J.
ISSN
2041-4889 (Electronic)
Statut éditorial
Publié
Date de publication
2012
Volume
3
Pages
e261
Langue
anglais
Résumé
Uncontrolled endoplasmic reticulum (ER) stress responses are proposed to contribute to the pathology of chronic inflammatory diseases such as type 2 diabetes or atherosclerosis. However, the connection between ER stress and inflammation remains largely unexplored. Here, we show that ER stress causes activation of the NLRP3 inflammasome, with subsequent release of the pro-inflammatory cytokine interleukin-1β. This ER-triggered proinflammatory signal shares the same requirement for reactive oxygen species production and potassium efflux compared with other known NLRP3 inflammasome activators, but is independent of the classical unfolded protein response (UPR). We thus propose that the NLRP3 inflammasome senses and responds to ER stress downstream of a previously uncharacterized ER stress response signaling pathway distinct from the UPR, thus providing mechanistic insight to the link between ER stress and chronic inflammatory diseases.
Mots-clé
Animals, Carrier Proteins/genetics, Carrier Proteins/metabolism, Cell Differentiation/drug effects, Cell Line, Endoplasmic Reticulum Stress, Gene Expression/drug effects, Humans, Inflammasomes/immunology, Inflammasomes/metabolism, Inflammation/immunology, Inflammation/metabolism, Interleukin-1beta/biosynthesis, Interleukin-1beta/immunology, Lentivirus, Mice, Mice, Knockout, Potassium/metabolism, RNA, Small Interfering/genetics, Reactive Oxygen Species/metabolism, Signal Transduction/drug effects, Tetradecanoylphorbol Acetate/pharmacology, Tunicamycin/pharmacology, Unfolded Protein Response
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/12/2012 10:23
Dernière modification de la notice
20/08/2019 15:26
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