Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome.
Détails
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_6DB36CC14A46
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome.
Périodique
Cell Death and Disease
ISSN
2041-4889 (Electronic)
Statut éditorial
Publié
Date de publication
2011
Volume
2
Pages
e137
Langue
anglais
Résumé
The interleukin-1 (IL-1) family of cytokines has been implicated in the pathogenesis of atherosclerosis in previous studies. The NLRP3 inflammasome has recently emerged as a pivotal regulator of IL-1β maturation and secretion by macrophages. Little is currently known about a possible role for the NLRP3 inflammasome in atherosclerosis progression in vivo. We generated ApoE-/- Nlrp3-/-, ApoE-/- Asc-/- and ApoE-/- caspase-1-/- double-deficient mice, fed them a high-fat diet for 11 weeks and subsequently assessed atherosclerosis progression and plaque phenotype. No differences in atherosclerosis progression, infiltration of plaques by macrophages, nor plaque stability and phenotype across the genotypes studied were found. Our results demonstrate that the NLRP3 inflammasome is not critically implicated in atherosclerosis progression in the ApoE mouse model.
Mots-clé
Animals, Apolipoproteins E/deficiency, Apolipoproteins E/genetics, Atherosclerosis/genetics, Atherosclerosis/immunology, Carrier Proteins/genetics, Carrier Proteins/immunology, Disease Models, Animal, Disease Progression, Female, Humans, Inflammasomes/genetics, Inflammasomes/immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/09/2011 9:00
Dernière modification de la notice
12/05/2023 5:55
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