Homozygosity for an Allele Encoding Deacetylated FoxO1 Protects Macrophages From Cholesterol-Induced Inflammation Without Increasing Apoptosis | Zendy

Kyoichiro Tsuchiya | Zendy; Alexander S. Banks | Zendy; Chien-Ping Liang | Zendy; Ira Tabas | Zendy; Alan R. Tall | Zendy; Domenico Accili | Zendy

Open Access

Homozygosity for an Allele Encoding Deacetylated FoxO1 Protects Macrophages From Cholesterol-Induced Inflammation Without Increasing Apoptosis

Author(s) -

Kyoichiro Tsuchiya,

Alexander S. Banks,

Chien-Ping Liang,

Ira Tabas,

Alan R. Tall,

Domenico Accili

Publication year - 2011

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.110.219477

Subject(s) - allele , inflammation , apoptosis , cholesterol , macrophage , cancer research , genetics , biology , microbiology and biotechnology , immunology , chemistry , medicine , gene , biochemistry , in vitro

Insulin resistance renders macrophages more prone to cholesterol-induced apoptosis by promoting nuclear localization of transcription factor forkhead box transcription factor (Fox) O1. However, FoxO1 also decreases macrophage inflammation, raising the question of how the balance between proapoptotic and antiinflammatory effects is determined. We sought to identify the mechanism whereby FoxO1 dampens inflammation without promoting apoptosis. We hypothesized that nutrient-dependent FoxO1 acetylation plays a role in this process.

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