Ribosomal Protein L13a Deficiency in Macrophages Promotes Atherosclerosis by Limiting Translation Control-Dependent Retardation of Inflammation | Zendy

Abhijit Basu | Zendy; Darshana Poddar | Zendy; Peggy Robinet | Zendy; Jonathan D. Smith | Zendy; Maria Febbraio | Zendy; William M. Baldwin | Zendy; Barsanjit Mazumder | Zendy

Open Access

Ribosomal Protein L13a Deficiency in Macrophages Promotes Atherosclerosis by Limiting Translation Control-Dependent Retardation of Inflammation

Author(s) -

Abhijit Basu,

Darshana Poddar,

Peggy Robinet,

Jonathan D. Smith,

Maria Febbraio,

William M. Baldwin,

Barsanjit Mazumder

Publication year - 2014

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.113.302573

Subject(s) - knockout mouse , inflammation , apolipoprotein b , macrophage , pathogenesis , apolipoprotein e , lipopolysaccharide , biology , macrophage polarization , immunology , gene silencing , endocrinology , medicine , cholesterol , gene , genetics , in vitro , disease

Unresolved inflammatory response of macrophages plays a pivotal role in the pathogenesis of atherosclerosis. Previously we showed that ribosomal protein L13a-dependent translational silencing suppresses the synthesis of a cohort of inflammatory proteins in monocytes and macrophages. We also found that genetic abrogation of L13a expression in macrophages significantly compromised the resolution of inflammation in a mouse model of lipopolysaccharide-induced endotoxemia. However, its function in the pathogenesis of atherosclerosis is not known. Here, we examine whether L13a in macrophage has a protective role against high-fat diet-induced atherosclerosis.

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