title: ApoE genotype-specific inhibition of apoptosis.
abstract: Endothelial cell apoptosis can be initiated by withdrawing growth factors or serum, and is inhibited by HDL. Our results show that the total lipoprotein population from apolipoprotein E 4/4 (APOE4/4) sera is less anti-apoptotic than total lipoproteins from other APOE genotypes, as measured by caspase 3/7 activity. Moreover, APOE4/4 VLDL antagonizes the antiapoptotic activity of HDL by a mechanism requiring binding of apoE4 on VLDL particles to an LDL family receptor. This ability of APOE4/4 VLDL to inhibit the antiapoptotic effects of HDL presents a potential mechanism by which the expression of several diseases, including atherosclerosis, is enhanced by the APOE4 genotype.
authors.affiliation: Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: DeKroon
authors.forename: Mirta
authors.initials: M
authors.lastname: Mihovilovic
authors.forename: Zoe V
authors.initials: ZV
authors.lastname: Goodger
authors.forename: Jennifer B
authors.initials: JB
authors.lastname: Robinette
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Sullivan
authors.forename: Ann M
authors.initials: AM
authors.lastname: Saunders
authors.forename: Warren J
authors.initials: WJ
authors.lastname: Strittmatter
mesh_terms: D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism*; D017209:Apoptosis; D020169:Caspases / Q000378:metabolism; D002460:Cell Line; D008076:Cholesterol, HDL / Q000378:metabolism; D005838:Genotype; D006801:Humans; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008246:Lysophospholipids / Q000097:blood
chemical_list: D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008079:Lipoproteins, VLDL; D008246:Lysophospholipids; D020169:Caspases