Cited by 1,693Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismLipoproteins and Cardiovascular Health

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ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.

Nakashima, Y, Plump, A S, Raines, E W, Breslow, J L, Ross, R·1994·Arteriosclerosis and Thrombosis: A Journal of Vascular Biology

DOI 10.1161/01.atv.14.1.133

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Abstract

Initial description of apolipoprotein (apo) E-deficient transgenic mice demonstrated the development of severe hypercholesterolemia due to probable delayed clearance of large atherogenic particles from the circulation. Examination of these mice demonstrated foam cell accumulation in the aortic root and pulmonary arteries by 10 weeks of age. In the present study, the animals were fed either chow or a high-fat, Western-type diet and examined at ages ranging from 6 to 40 weeks. Gross examination by dissection microscopy revealed a predilection for development of lesions in the aortic root, at the lesser curvature of the aortic arch, the principal branches of the aorta, and in the pulmonary and carotid arteries. Monocyte attachment to endothelial cells was observed by light and electron microscopic examination at 6 weeks, the earliest time point examined. Foam cell lesions developed as early as 8 weeks, and after 15 weeks advanced lesions (fibrous plaques) were observed. The latter consisted of a fibrous cap containing smooth muscle cells surrounded by connective tissue matrix that covered a necrotic core with numerous foamy macrophages. Mice fed the Western-type diet generally had more advanced lesions than those fed a chow diet. The apoE-deficient mouse contains the entire spectrum of lesions observed during atherogenesis and is the first mouse model to develop lesions similar to those in humans. This model should provide numerous opportunities to study the pathogenesis and therapy of atherosclerosis in a small, genetically defined animal.

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Authors: Nakashima, Y., Plump, A. S., Raines, E. W., Breslow, J. L., & Ross, R.
Affiliations: University of Washington (US)
ORCID: Nakashima, Y
Breslow, J L
Venue: Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1994-01
Volume: 14
Issue: 1
Pages: 133-140
ISSN: 1049-8834 (ISSN-L)
DOI: 10.1161/01.atv.14.1.133
OpenAlex: W1964814612
Cited by: 1,693
References: 28
Citations by year: 2026: 18 · 2025: 32 · 2024: 40 · 2023: 42 · 2022: 54 · 2021: 60 · 2020: 47 · 2019: 57 · 2018: 45 · 2017: 66 · 2016: 50 · 2015: 69 · 2014: 71 · 2013: 73 · 2012: 78
FWCI: 14.99
Type: journal article
Language: en
Open access: closed
Locations: Arteriosclerosis and Thrombosis A Journal of Vascular Biology (publishedVersion)
PubMed (publishedVersion)
Funders: Bristol-Myers Squibb
National Institutes of Health (5r01hl033714-17, 18645, HL 18645)
National Heart, Lung, and Blood Institute (HL-18645, HL 33714, R01HL032435, HL32435, P01HL018645)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
Keywords: apolipoprotein E deficiency, atherosclerosis, atherosclerotic plaque development, Western diet, hypercholesterolemia, fibrous cap, necrotic core, aortic root lesions, mouse model of atherosclerosis, atherogenesis
MeSH terms: Animals, Aorta, Aorta, Thoracic, Apolipoproteins E, Arteriosclerosis, Carotid Arteries, Coronary Vessels, Diet, Endothelium, Vascular, Hypercholesterolemia, Leukocytes, Mononuclear, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Pulmonary Artery, Mice

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ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.

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