First Author | Zhang SH | Year | 1992 |
Journal | Science | Volume | 258 |
Issue | 5081 | Pages | 468-71 |
PubMed ID | 1411543 | Mgi Jnum | J:16573 |
Mgi Id | MGI:64642 | Doi | 10.1126/science.1411543 |
Citation | Zhang SH, et al. (1992) Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258(5081):468-71 |
abstractText | 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. |