Genome-wide DNA Methylation Profiling of Blood from Monozygotic Twins Discordant for Myocardial Infarction

被引:11
|
作者
Koseler, Aylin [1 ]
Ma, Feiyang [2 ]
Kilic, Ismail Dogu [3 ]
Morselli, Marco [2 ]
Kilic, Oguz [3 ]
Pellegrini, Matteo [2 ]
机构
[1] Pamukkale Univ, Dept Biophys, Sch Med, Denizli, Turkey
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol Cell & Dev Biol, Box 951606, Los Angeles, CA 90095 USA
[3] Pamukkale Univ, Dept Cardiol, Sch Med, Denizli, Turkey
来源
IN VIVO | 2020年 / 34卷 / 01期
关键词
Cardiovascular disease; epigenetics; DNA methylation; CARDIOVASCULAR-DISEASE; RISK; ISLANDS;
D O I
10.21873/invivo.11782
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background/Aim: This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy. Patients and Methods: Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis. Results: According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acylCoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1 ), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds. Conclusion: This twin study may contribute significantly to the understanding of the genetic basis of CVD and resulting myocardial infarction. This approach may allow identification of possible target loci associated with aberrant epigenetic regulation in CVD.
引用
收藏
页码:361 / 367
页数:7
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