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PMID: 21451572 Published · epublish English Journal Article Research Support, Non-U.S. Gov't

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

Cell death & disease ·Vol. 2 ·2011-03-31 ·Pages e137

Menu P, Pellegrin M, Aubert JF, Bouzourene K, Tardivel A, Mazzolai L, Tschopp J

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.

MeSH Terms
Animals Apolipoproteins E/deficiency,genetics,immunology Atherosclerosis/genetics,immunology,pathology Carrier Proteins/genetics,immunology Disease Models, Animal Disease Progression Female Humans Inflammasomes/genetics,immunology Male Mice Mice, Inbred C57BL Mice, Knockout NLR Family, Pyrin Domain-Containing 3 Protein
Chemicals
Apolipoproteins E Carrier Proteins Inflammasomes NLR Family, Pyrin Domain-Containing 3 Protein Nlrp3 protein, mouse
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Menu P
Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Pellegrin M
Aubert J-F
Bouzourene K
Tardivel A
Mazzolai L
Tschopp J
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Article Info
Journal
Cell death & disease
Abbr.
Cell Death Dis
ISSN
2041-4889
Published
2011-03-31
Epub
2011-00-31
Pages
e137
Language
English
Region
England
NLM ID
101524092
PMCID
PMC3101814
Subset
IM
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