Transcriptome-wide N6-methyladenosine methylation landscape of coronary artery disease

被引:16
|
作者
Deng, Keyong [1 ,2 ,3 ]
Ning, Xiaotong [1 ,2 ,3 ]
Ren, Xiaoxiao [1 ,2 ,3 ]
Yang, Bin [1 ,2 ,3 ]
Li, Jianxin [1 ,2 ,3 ]
Cao, Jie [1 ,2 ,3 ]
Chen, Jichun [1 ,2 ,3 ]
Lu, Xiangfeng [1 ,2 ,3 ]
Chen, Shufeng [1 ,2 ,3 ]
Wang, Laiyuan [1 ,2 ,3 ]
机构
[1] Chinese Acad Med Sci & Peking Union Med Coll, Fuwai Hosp, Natl Ctr Cardiovasc Dis, State Key Lab Cardiovasc Dis, 167 Beilishi Rd, Beijing 100037, Peoples R China
[2] Chinese Acad Med Sci & Peking Union Med Coll, Fuwai Hosp, Natl Ctr Cardiovasc Dis, Key Lab Cardiovasc Epidemiol, 167 Beilishi Rd, Beijing 100037, Peoples R China
[3] Chinese Acad Med Sci & Peking Union Med Coll, Fuwai Hosp, Natl Ctr Cardiovasc Dis, Dept Epidemiol, 167 Beilishi Rd, Beijing 100037, Peoples R China
基金
中国国家自然科学基金;
关键词
coronary artery disease; differentially methylated m(6)A sites; fat mass and obesity-associated protein; neointima formation; RNA m(6)A methylation; ATHEROSCLEROTIC PLAQUES; RNA; RISK; LONG; MOUSE; CELLS;
D O I
10.2217/epi-2020-0372
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Aim: To reveal transcriptome-wide N6-methyladenosine (m(6)A) methylome of coronary artery disease (CAD). Materials & methods: The m(6)A levels of RNA from peripheral blood mononuclear cells measured by colorimetry were significantly decreased in CAD cases. Transcriptome-wide m(6)A methylome profiled by methylated RNA immunoprecipitation sequencing (MeRIP-seq) identified differentially methylated m(6)A sites within both mRNAs and lncRNAs between CAD and control group. Results: Bioinformatic analysis indicated that differentially methylated genes were involved in the pathogenesis of atherosclerosis. MeRIP-quantitative real-time PCR assay confirmed the reliability of MeRIP-seq data. Finally, the rat carotid artery balloon injury model was performed to confirm the role of m(6)A demethylase FTO in neointima formation. Conclusion: Our study provided a resource of differentially methylated m(6)A profile for uncovering m(6)A biological functions in the pathogenesis of CAD.
引用
收藏
页码:793 / 808
页数:16
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