Loss of Heterozygosity in DNA Mismatch Repair Genes in Human Atherosclerotic Plaques

George A. Flouris , Demetrios A. Arvanitis , John T. Parissis , Demetrios L. Arvanitis , Demetrios A. Spandidos
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引用次数: 24

Abstract

To detect the incidence of loss of heterozygosity (LOH) in DNA mismatch repair genes (MMR) occurring in atherosclerosis, fifty human autopsy cases of atherosclerosis were examined for LOH using 19 microsatellite markers, in three single and four tetraplex microsatellite assays. The markers used are located on or close to MMR genes. Fourteen specimens (28%) showed allelic imbalance in at least one locus. Loci hMSH2 (2p22.3–p16.1), hPMS1 (2q24.1–q32.1), and hMLH1 (3p21.32–p21.1) exhibited LOH (10, 10, and 12% respectively). We found that loss of heterozygosity on hMSH2, hPMS1, and hMLH1, occurs in atherosclerosis. The occurrence of such genomic alterations may represent important events in the development of atherosclerosis.

人类动脉粥样硬化斑块DNA错配修复基因杂合性缺失
为了检测动脉粥样硬化中DNA错配修复基因(MMR)杂合性缺失(LOH)的发生率,我们使用19个微卫星标记,在3个单星和4个四星微卫星试验中检测了50例动脉粥样硬化尸检患者的LOH。所使用的标记位于MMR基因上或靠近MMR基因。14例(28%)至少有一个位点存在等位基因不平衡。基因座hMSH2 (2p22.3-p16.1)、hPMS1 (2q24.1-q32.1)和hMLH1 (3p21.32-p21.1)表现出LOH(分别为10%、10%和12%)。我们发现,hMSH2、hPMS1和hMLH1的杂合性缺失发生在动脉粥样硬化中。这种基因组改变的发生可能代表了动脉粥样硬化发展中的重要事件。
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