Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome.

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Serval ID
serval:BIB_6DB36CC14A46
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome.
Journal
Cell Death and Disease
Author(s)
Menu P., Pellegrin M., Aubert J.F., Bouzourene K., Tardivel A., Mazzolai L., Tschopp J.
ISSN
2041-4889 (Electronic)
Publication state
Published
Issued date
2011
Volume
2
Pages
e137
Language
english
Abstract
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.
Keywords
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
Yes
Create date
02/09/2011 9:00
Last modification date
20/08/2019 14:27
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