Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice
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Zhihui Chang1,2, Chaoji Huangfu1,3, Andrew T. Grainger4, Jingang Zhang3, Qiyong Guo2 and Weibin Shi1,4
1Department of Radiology & Medical Imaging, University of Virginia, Charlottesville, Virginia, USA
2Department of Radiology, Shengjing Hospital of China Medical University, Shenyang, China
3Beijing Key Laboratory of Blood Safety and Supply Technologies, Beijing Institute of Transfusion Medicine, Beijing, China
4Biochemistry & Molecular Genetics, University of Virginia, Charlottesville, Virginia, USA
Weibin Shi, email: email@example.com
Keywords: atherosclerosis; hyperlipidemia; neovessel; foam cell; mice
Received: August 31, 2017 Accepted: November 05, 2017 Published: November 25, 2017
Complete ligation of the common carotid artery near its bifurcation induces neointimal formation due to smooth muscle cell proliferation in normolipidemic wild-type mice, but it was unknown what would happen to hyperlipidemic apolipoprotein E-deficient (Apoe-/-) mice. Examination of these mice revealed rapid development of atherosclerotic lesions in completely ligated carotid arteries within 4 weeks. Mice were fed a Western diet, starting 1 week before ligation, or a chow diet. Foam cell lesions formed as early as 1 week after ligation in mice fed the Western diet and 2 weeks in mice fed the chow diet. Fibrous lesions comprised of foam cells and smooth muscle cells and more advance lesions containing neovessels occurred at 2 and 4 weeks after ligation, respectively, in the Western diet group. Lesions were larger and more advanced in the Western diet group than the chow group. Neutrophil infiltration was observed in growing intimal lesions in both diet groups, while CD8+ T cells were found in lesions of chow-fed mice. This study demonstrates that Apoe-/- mice develop the entire spectrum of atherosclerosis in ligated carotid arteries in an accelerated manner and this model could be a valuable tool for investigating the development and therapy of atherosclerosis.
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