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Science. 1992 Oct 16;258(5081):468-71.

Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.

Author information

1
Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.

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.

PMID:
1411543
[Indexed for MEDLINE]

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