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Papers In Press, published online ahead of print May 16, 2003
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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.
Revised on May 7, 2003
Accepted on May 15, 2003
Apolipoprotein E genotype: specific inhibition of apoptosis
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