J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on July 1, 2005

Papers In Press, published online ahead of print April 1, 2005
J. Lipid Res., doi:10.1194/jlr.M400382-JLR200
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Submitted on October 4, 2004
Revised on March 2, 2005
Accepted on March 21, 2005

Genome-wide linkage analyses and candidate gene fine mapping for HDL3 cholesterol: the Framingham study

Qiong Yang, Chao-Qiang Lai, Laurence Parnell, L. Adrienne Cupples, Xian Adiconis, Yueping Zhu, Peter W. F. Wilson, David E. Housman, Amanda M. Shearman, Ralph B. D'Agostino, and Jose M. Ordovas

Boston University, Boston, MA 02118

Corresponding Author: qyang{at}bu.edu

Background: High Density Lipoprotein (HDL) cholesterol (C) has been found to be inversely associated with coronary heart disease and has a genetic component; however few studies have reported conclusive linkage evidence. It has been hypothesized that the subfractions of HDL such as HDL3-C may be better phenotypes for linkage studies. Study Design: Using HDL3-C levels measured on 907 Framingham Heart Study subjects from 330 families around 1987, we conducted a genome-wide variance components linkage analysis with 401 microsatellite markers spaced about 10 cM apart. Traditional risk factors were adjusted in a sex-specific regression model prior to the linkage analysis. Nine candidate genes were identified and annotated using a bioinformatics approach in the region of the highest linkage peak. Twenty-eight single nucleotide polymorphisms (SNPs) were selected from these candidate genes, and linkage and family-based association fine mapping were conducted with these SNPs adding to the existing microsatellite marker map. Results and Conclusions: The highest multipoint LOD from the initial linkage analysis score was 3.7 at 133 cM on chromosome 6. Linkage analyses with additional SNPs yielded the highest LOD score of 4.0 at 129 cM on chromosome 6. Family-based association analysis revealed that SNP rs2257104 in PLAGL1 at approximate 143 cM was associated with multivariable adjusted HDL3 (p-value=0.03). Further study of the linkage region and exploration of other variants in PLAGL1 are warranted to more clearly define potential functional variants of HDL-C metabolism.


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