RGD Reference Report - Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. - Rat Genome Database

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Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.

Authors: Zhang, SH  Reddick, RL  Piedrahita, JA  Maeda, N 
Citation: Zhang SH, etal., Science 1992 Oct 16;258(5081):468-71.
RGD ID: 734968
Pubmed: PMID:1411543   (View Abstract at PubMed)

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.



Disease Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Apoe  (apolipoprotein E)

Genes (Mus musculus)
Apoe  (apolipoprotein E)

Genes (Homo sapiens)
APOE  (apolipoprotein E)


Additional Information