Quantitative trait loci analysis for plasma HDL-cholesterol concentrations and atherosclerosis susceptibility between inbred mouse strains C57BL/6J and 129S1/SvImJ
Quantitative trait loci analysis for plasma HDL-cholesterol concentrations and atherosclerosis susceptibility between inbred mouse strains C57BL/6J and 129S1/SvImJ
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DOI：
10.1161/01.atv.0000104027.52895.d7
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发表时间：
2004-01-01
影响因子：
8.7
通讯作者：
Paigen, B
中科院分区：
文献类型：
--
作者：
Ishimori, N;Li, RH;Paigen, B
目的：C57BL/6 （B6）和129小鼠近交系在高脂饮食后血浆高密度脂蛋白胆固醇浓度和动脉粥样硬化易感性方面存在显著差异。为了确定控制这些性状的位点，我们进行了数量性状位点（QTL）分析。方法与结果：对294例（B6x129S1/SvImJ）F-2型女性喂食高脂饲料14周，测定血浆HDL浓度和主动脉脂肪条纹病变大小，对F-2型女性进行基因分型，并进行QTL分析。HDL浓度受6个位点的影响：1号染色体上的Hdlq14和Hdlq15（峰值cM 80和cM 104，比值对数[LOD]分别为5.3和9.7）；8号染色体Hdlq16 (cM 44, LOD 2.6)；9号染色体Hdlq17 (cM 24, LOD 2.9)；12号染色体Hdlq18 (cM 20, LOD 5.9)；2号染色体（cM 90）上的Hdlq19与Hdlq15相互作用。动脉粥样硬化易感性受5个位点影响：10号染色体上的Ath17 (cM 34, LOD 6.6)；12号染色体上的Ath18 (cM 16, LOD 3.7)；Ath19(11号染色体，cM 60)，与Ath18相互作用；和与Ath21（12号染色体，cM 50）相互作用的Ath20（10号染色体，cM 10）。结论：我们在（B6x129S1/SvImJ） F-2交叉中发现了6个与HDL相关的位点和5个与动脉粥样硬化易感性相关的位点。
Objective-The C57BL/6 (B6) and 129 mouse inbred strains differ markedly in plasma HDL-cholesterol concentrations and atherosclerosis susceptibility after a high-fat diet consumption. To identify loci controlling these traits, we performed quantitative trait loci (QTL) analysis.Methods and Results-We fed a high-fat diet to 294 (B6x129S1/SvImJ)F-2 females for 14 weeks, measured plasma HDL concentrations and size of aortic fatty-streak lesions, genotyped F-2 females, and performed QTL analysis. HDL concentrations were affected by six loci: Hdlq14 and Hdlq15 on chromosome 1 (peaks cM 80 and cM 104, logarithm of odds [LOD] 5.3 and 9.7, respectively); Hdlq16 on chromosome 8 (cM 44, LOD 2.6); Hdlq17 on chromosome 9 (cM 24, LOD 2.9); Hdlq18 on chromosome 12 (cM 20, LOD 5.9); and Hdlq19 on chromosome 2 (cM 90), which interacted with Hdlq15. Atherosclerosis susceptibility was affected by five loci: Ath17 on chromosome 10 (cM 34, LOD 6.6); Ath18 on chromosome 12 (cM 16, LOD 3.7); Ath19 (chromosome 11, cM 60), which interacted with Ath18; and Ath20 (chromosome 10, cM 10), which interacted with Ath21 (chromosome 12, cM 50).Conclusions-We identified six loci for HDL and five loci for atherosclerosis susceptibility in a (B6x129S1/SvImJ) F-2 intercross.