Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
PLoS One. 2014 Feb 20;9(2):e88274. doi: 10.1371/journal.pone.0088274. eCollection 2014.
Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6 background (129-apoE). To explore atherosclerosis-responsible genetic regions, we performed a quantitative trait locus (QTL) analysis using 172 male and 137 female F2 derived from an intercross between DBA-apoE and 129-apoE mice. A genome-wide scan identified two significant QTL for the size of lesions at the root: one is Ath44 on Chromosome (Chr) 1 at 158 Mb, and the other Ath45 on Chr 2 at 162 Mb. Ath44 co-localizes with but appears to be independent of a previously reported QTL, Ath1, while Ath45 is a novel QTL. DBA alleles of both Ath44 and Ath45 confer atherosclerosis-susceptibility. In addition, a QTL on Chr 14 at 73 Mb was found significant only in males, and 129 allele conferring susceptibility. Further analysis detected female-specific interactions between a second QTL on Chr 1 at 73 Mb and a QTL on Chr 3 at 21 Mb, and between Chr 7 at 84 Mb and Chr 12 at 77 Mb. These loci for the root atherosclerosis were independent of QTLs for plasma total cholesterol and QTLs for triglycerides, but a QTL for HDL (Chr 1 at 126 Mb) overlapped with the Ath44. Notably, haplotype analysis among 129S6, DBA/2J and C57BL/6 genomes and their gene expression data narrowed the candidate regions for Ath44 and Ath45 to less than 5 Mb intervals where multiple genome wide associations with cardiovascular phenotypes have also been reported in humans. SNPs in or near Fmo3, Sele and Selp for Ath44, and Lbp and Pkig for Ath45 were suggested for further investigation as potential candidates underlying the atherosclerosis susceptibility.
载脂蛋白 E 基因敲除小鼠在 DBA/2J 遗传背景(DBA-apoE)下,主动脉根部的动脉粥样硬化易感性明显高于 129S6 遗传背景(129-apoE)。为了探索动脉粥样硬化相关的遗传区域,我们使用来自 DBA-apoE 和 129-apoE 小鼠杂交的 172 只雄性和 137 只雌性 F2 进行了定量性状基因座(QTL)分析。全基因组扫描鉴定出两个与根部病变大小相关的显著 QTL:一个位于 158 Mb 的染色体(Chr)1 上的 Ath44,另一个位于 162 Mb 的 Chr2 上的 Ath45。Ath44 与先前报道的 Ath1 共定位,但似乎是独立的,而 Ath45 是一个新的 QTL。Ath44 和 Ath45 的 DBA 等位基因均赋予动脉粥样硬化易感性。此外,在 73 Mb 的 Chr14 上发现了一个仅在雄性中显著的 QTL,129 等位基因赋予易感性。进一步的分析检测到 Chr1 上 73 Mb 的第二个 QTL 与 Chr3 上 21 Mb 的 QTL 之间,以及 Chr7 上 84 Mb 与 Chr12 上 77 Mb 的 QTL 之间的雌性特异性相互作用。这些根部动脉粥样硬化的 QTL 与血浆总胆固醇的 QTL 和甘油三酯的 QTL 无关,但一个高密度脂蛋白(HDL)的 QTL(Chr1 上的 126 Mb)与 Ath44 重叠。值得注意的是,在 129S6、DBA/2J 和 C57BL/6 基因组及其基因表达数据之间的单倍型分析,将 Ath44 和 Ath45 的候选区域缩小到小于 5 Mb 的间隔,人类也报道了与心血管表型相关的多个全基因组关联。Ath44 中的 Fmo3、Sele 和 Selp 附近或附近的 SNPs,以及 Ath45 中的 Lbp 和 Pkig 被认为是动脉粥样硬化易感性的潜在候选基因。