title: Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.
abstract: Apolipoprotein E (apoE) is a ligand for receptors that clear remnants of chylomicrons and very low density lipoproteins. Lack of apoE is, therefore, expected to cause accumulation in plasma of cholesterol-rich remnants whose prolonged circulation should be atherogenic. ApoE-deficient mice generated by gene targeting were used to test this hypothesis and to make a mouse model for spontaneous atherosclerosis. The mutant mice had five times normal plasma cholesterol, and developed foam cell-rich depositions in their proximal aortas by age 3 months. These spontaneous lesions progressed and caused severe occlusion of the coronary artery ostium by 8 months. The severe yet viable phenotype of the mutants should make them valuable for investigating genetic and environmental factors that modify the atherogenic process.
authors.affiliation: Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.
authors.forename: S H
authors.initials: SH
authors.lastname: Zhang
authors.forename: R L
authors.initials: RL
authors.lastname: Reddick
authors.forename: J A
authors.initials: JA
authors.lastname: Piedrahita
authors.forename: N
authors.initials: N
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D006937:Hypercholesterolemia / Q000235:genetics* / Q000473:pathology; D008074:Lipoproteins / Q000378:metabolism; D051379:Mice; D008817:Mice, Mutant Strains; D016254:Mutagenesis, Insertional; D014280:Triglycerides / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol