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

被引：211

作者：

Menu, P. ^{[1
]}

Pellegrin, M. ^{[2
]}

Aubert, J-F ^{[2
]}

Bouzourene, K. ^{[2
]}

Tardivel, A. ^{[1
]}

Mazzolai, L. ^{[2
]}

Tschopp, J. ^{[1
]}

机构：

[1] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland

[2] Univ Lausanne, Serv Angiol, CHUV, Lausanne, Switzerland

来源：

CELL DEATH & DISEASE | 2011年 / 2卷

基金：

瑞士国家科学基金会;

关键词：

atherosclerosis; interleukin-1; beta; NLRP3; inflammasome; ApoE-/-; mice; INTERLEUKIN-1 RECEPTOR ANTAGONIST; ATHEROGENESIS; METABOLISM; CRYSTALS;

D O I：

10.1038/cddis.2011.18

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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-1 beta 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. Cell Death and Disease (2011) 2, e137; doi: 10.1038/cddis.2011.18; published online 31 March 2011

引用

页码：e137 / e137

页数：4

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