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J. Lipid Res.
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A more recent version of this article appeared on August 1, 2003

Papers In Press, published online ahead of print May 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300097-JLR200
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Submitted on February 28, 2003
Revised on May 7, 2003
Accepted on May 15, 2003

Apolipoprotein E genotype: specific inhibition of apoptosis

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

Department of Medicine, Duke University Medical Center, Durham, NC 27710

Corresponding Author: warren{at}neuro.duke.edu

Endothelial cell apoptosis can be initiated by withdrawing growth factors or serum, and is inhibited by high-density lipoproteins (HDL). Our results show that the total lipoprotein population from apolipoprotein E 4/4 (APOE 4/4) sera is less anti-apoptotic than total lipoproteins from other APOE genotypes, as measured by caspase 3/7 activity. Moreover, APOE 4/4 very low-density lipoprotein (VLDL) antagonizes the anti-apoptotic activity of HDL, by a mechanism requiring binding of apoE4 on VLDL particles to an LDL-family receptor. This ability of APOE 4/4 VLDL to inhibit the anti-apoptotic effects of HDL presents a potential mechanism by which the expression of several diseases, including atherosclerosis, is enhanced by the APOE4 genotype.


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