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

To reveal transcriptome-wide N6-methyladenosine (m A) methylome of coronary artery disease (CAD). The m A levels of RNA from peripheral blood mononuclear cells measured by colorimetry were significantly decreased in CAD cases. Transcriptome-wide m A methylome profiled by methylated RNA immunoprecipi...

Full description

Saved in:
Bibliographic Details
Published in:Epigenomics 2021-05, Vol.13 (10), p.793-808
Main Authors: Deng, Keyong, Ning, Xiaotong, Ren, Xiaoxiao, Yang, Bin, Li, Jianxin, Cao, Jie, Chen, Jichun, Lu, Xiangfeng, Chen, Shufeng, Wang, Laiyuan
Format: Article
Language:English
Subjects:
A methylation
A sites
Adenosine - analogs & derivatives
Adenosine - genetics
Animals
Computational Biology
coronary artery disease
Coronary Artery Disease - genetics
differentially methylated m
fat mass and obesity-associated protein
Humans
Male
Methylation
neointima formation
Rats
Rats, Sprague-Dawley
RNA m
Transcriptome
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:To reveal transcriptome-wide N6-methyladenosine (m A) methylome of coronary artery disease (CAD). The m A levels of RNA from peripheral blood mononuclear cells measured by colorimetry were significantly decreased in CAD cases. Transcriptome-wide m A methylome profiled by methylated RNA immunoprecipitation sequencing (MeRIP-seq) identified differentially methylated m A sites within both mRNAs and lncRNAs between CAD and control group. 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 A demethylase in neointima formation. Our study provided a resource of differentially methylated m A profile for uncovering m A biological functions in the pathogenesis of CAD.
ISSN:1750-1911
1750-192X
DOI:10.2217/epi-2020-0372