J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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Originally published In Press as doi:10.1194/jlr.M700409-JLR200 on December 3, 2007

Papers In Press, published online ahead of print March 1, 2008
J. Lipid Res., doi:10.1194/jlr.M700409-JLR200
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Journal of Lipid Research, Vol. 49, 588-596, March 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

A common VLDLR polymorphism interacts with APOE genotype in the prediction of carotid artery disease riskboxs

Dana C. Crawford*, Alex S. Nord{dagger}, Michael D. Badzioch{dagger}, Jane Ranchalis{dagger}, Laura A. McKinstry{dagger}, Magdalena Ahearn§, Caterina Bertucci§, Cynthia Shephard§, Michelle Wong§, Mark J. Rieder§, Gerard D. Schellenberg**, Deborah A. Nickerson§, Patrick J. Heagerty{dagger}{dagger}, Ellen M. Wijsman{dagger},{dagger}{dagger} and Gail P. Jarvik1,{dagger}

* Department of Molecular Physiology and Biophysics, Center for Human Genetics Research, Vanderbilt University, Nashville, TN
{dagger} Department of Medicine, Division of Medical Genetics, University of Washington, Seattle, WA
§ Department of Genome Sciences, University of Washington, Seattle, WA
{dagger}{dagger} Department of Biostatistics, University of Washington, Seattle, WA
** Departments of Medicine, Neurology, and Pharmacology, University of Washington, and Geriatrics Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of two tables.

Published, JLR Papers in Press, December 3, 2007.

1 To whom correspondence should be addressed. e-mail: pair{at}u.washington.edu

The genetic factors associated with carotid artery disease (CAAD) are not fully known. Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLR was resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5' flanking region of VLDLR was associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR 1226 and APOE genotype for predicting CAAD case status. These findings may further our understanding of VLDLR function, its ligand APOE, and ultimately the pathogenesis of CAAD in the general population.

Supplementary key words very low density lipoprotein receptor • apolipoprotein E • body mass index • triglycerides


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