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Activation of Aryl Hydrocarbon Receptor Induces Vascular Inflammation and Promotes Atherosclerosis in Apolipoprotein E−/− Mice
Author(s) -
Dalei Wu,
Noriko Nishimura,
Victoria Kuo,
Oliver Fiehn,
Sevini Shahbaz,
Laura S. Van Winkle,
Fumio Matsumura,
Christoph F.A. Vogel
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.110.220202
Subject(s) - aryl hydrocarbon receptor , inflammation , apolipoprotein e , macrophage , chemistry , receptor , chemokine , endocrinology , medicine , immunology , biology , in vitro , biochemistry , transcription factor , disease , gene
Exposure to dioxins has been shown to contribute to the development of inflammatory diseases, such as atherosclerosis. Macrophage-mediated inflammation is a critical event in the initiation of atherosclerosis. Previously, we showed that treatment of macrophages with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to aryl hydrocarbon receptor (AhR)-dependent activation of inflammatory mediators and the formation of cholesterol-laden foam cells. However, the mechanisms responsible for the formation of atherosclerotic lesions mediated through AhR have not been identified.

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