病理
载脂蛋白E
医学
结缔组织
动脉树
主动脉
骨桥蛋白
内科学
组织病理学
载脂蛋白B
脂肪条纹
肉芽组织
弹性蛋白
主动脉弓
发病机制
生物
解剖
病变
伤口愈合
胆固醇
免疫学
疾病
作者
Yutaka Nakashima,Andrew S. Plump,Elaine W. Raines,Jan L. Breslow,Russell Ross
出处
期刊:Arteriosclerosis and thrombosis
[Ovid Technologies (Wolters Kluwer)]
日期:1994-01-01
卷期号:14 (1): 133-140
被引量:1393
标识
DOI:10.1161/01.atv.14.1.133
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI