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Novel QTLs for HDL levels identified in mice by controlling for Apoa2 allelic effects: confirmation of a chromosome 6 locus in a congenic strain

¹ Division of Molecular Medicine, Department of Medicine
² Institute of Human Nutrition, Columbia University, New York, New York 10032
³ Departments of Medicine
⁴ Microbiology and Molecular Genetics
⁵ Molecular Biology Institute, University of California, Los Angeles, California 90095
⁶ Department of Atherosclerosis, Pasteur Institute, Lille 59019, France
⁷ University of Florida, Gainesville, Florida 32610

Atherosclerosis is a complex disease resulting from the interaction of multiple genes, including those causing dyslipidemia. Relatively few of the causative genes have been identified. Previously, we identified Apoa2 as a major determinant of high-density lipoprotein cholesterol (HDL-C) levels in the mouse model. To identify additional HDL-C level quantitative trait loci (QTLs), while controlling for the effect of the Apoa2 locus, we performed linkage analysis in 179 standard diet-fed F₂ mice derived from strains BALB/cJ and B6.C-H25^c (a congenic strain carrying the BALB/c Apoa2 allele). Three significant QTLs and one suggestive locus were identified. A female-specific locus mapping to chromosome 6 (Chr 6) also exhibited effects on plasma non-HDL-C, apolipoprotein AII (apoAII), apoB, and apoE levels. A Chr 6 QTL was independently isolated in a related congenic strain (C57BL/6J vs. B6.NODc6: P = 0.003 and P = 0.0001 for HDL-C and non-HDL-C levels, respectively). These data are consistent with polygenic inheritance of HDL-C levels in the mouse model and provide candidate loci for HDL-C and non-HDL-C level determination in humans.

atherosclerosis; lipoprotein; quantitative trait locus

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