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Papers In Press, published online ahead of print August 1, 2003
J. Lipid Res., doi:10.1194/jlr.M300097-JLR200

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Journal of Lipid Research, Vol. 44, 1566-1573, August 2003
Copyright © 2003 by American Society for Biochemistry and Molecular Biology

ApoE genotype-specific inhibition of apoptosis

Robert M. DeKroon^1,*, Mirta Mihovilovic^1,*, Zoe V. Goodger^*, Jennifer B. Robinette^*, Patrick M. Sullivan^*, Ann M. Saunders^2,* and Warren J. Strittmatter^3,*,

^* Deane Laboratory, Division of Neurology, Duke University Medical Center, Durham, NC 27710
Department of Medicine, and Department of Neurobiology, Duke University Medical Center, Durham, NC 27710

³ To whom correspondence should be addressed. e-mail: warren{at}neuro.duke.edu

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.

Supplementary key words apolipoprotein E • high density lipoprotein • very low density lipoprotein • low density lipoprotein • atherosclerosis • endothelial cell

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