Fibronectin Splicing Variants Containing Extra Domain A Promote Atherosclerosis in Mice Through Toll-Like Receptor 4
Author(s) -
Prakash Doddapattar,
Chintan Gandhi,
Prem Prakash,
Nirav Dhanesha,
Isabella M. Grumbach,
Michael E. Dailey,
Steven R. Lentz,
Anil K. Chauhan
Publication year - 2015
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.115.306474
Subject(s) - apolipoprotein e , inflammation , endocrinology , apolipoprotein b , medicine , aortic sinus , biology , m2 macrophage , macrophage , immunology , aorta , cholesterol , in vitro , disease , biochemistry
Cellular fibronectin containing extra domain A (EDA(+)-FN) is abundant in the arteries of patients with atherosclerosis. Several in vitro studies suggest that EDA(+)-FN interacts with Toll-like receptor 4 (TLR4). We tested the hypothesis that EDA(+)-FN exacerbates atherosclerosis through TLR4 in a clinically relevant model of atherosclerosis, the apolipoprotein E-deficient (Apoe(-/-)) mouse.
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