转录组
脱甲基酶
N6-甲基腺苷
生物
甲基化
DNA甲基化
发病机制
表观遗传学
癌症研究
差异甲基化区
计算生物学
基因
甲基转移酶
分子生物学
生物信息学
基因表达
冠状动脉疾病
遗传学
内科学
免疫学
医学
作者
Keyong Deng,Xiaotong Ning,Xiaoxiao Ren,Bin Yang,Jianxin Li,Jie Cao,Jichun Chen,Xiangfeng Lu,Shufeng Chen,Laiyuan Wang
出处
期刊:Epigenomics
[Future Medicine]
日期:2021-05-01
卷期号:13 (10): 793-808
被引量:12
标识
DOI:10.2217/epi-2020-0372
摘要
Aim: To reveal transcriptome-wide N6-methyladenosine (m6A) methylome of coronary artery disease (CAD). Materials & methods: The m6A levels of RNA from peripheral blood mononuclear cells measured by colorimetry were significantly decreased in CAD cases. Transcriptome-wide m6A methylome profiled by methylated RNA immunoprecipitation sequencing (MeRIP-seq) identified differentially methylated m6A 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 m6A demethylase FTO in neointima formation. Conclusion: Our study provided a resource of differentially methylated m6A profile for uncovering m6A biological functions in the pathogenesis of CAD.
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