Identification of Potential Abnormal Methylation-Modified Genes in Coronary Artery Ectasia.

IF 2.6 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

International Journal of Genomics Pub Date : 2023-01-01 DOI:10.1155/2023/4969605

Xiuchun Yang, Yijun Zong, Zhentian Zhang, Yan Zhao, Xueying Gao, Jie Zhang, Qian Hou, Renyi Li, Bing Xiao

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引用次数: 0

Abstract

Background: Coronary artery ectasia (CAE) is an easily recognized abnormality of coronary artery anatomy and morphology. However, its pathogenesis remains unclear.

Objectives: This study aimed to identify abnormal methylation-modified genes in patients with CAE, which could provide a research basis for CAE.

Methods: Peripheral venous blood samples from patients with CAE were collected for RNA sequencing to identify differentially expressed genes (DEGs), followed by functional enrichment. Then, the DNA methylation profile of CAE was downloaded from GSE87016 (HumanMethylation450 BeadChip data, involving 11 cases and 12 normal controls) to identify differentially methylated genes (DMGs). Finally, after taking interaction genes between DEGs and DMGs, abnormal methylation-modified genes were identified, followed by protein-protein interaction analysis and expression validation using reverse transcriptase polymerase chain reaction.

Results: A total of 152 DEGs and 4318 DMGs were obtained from RNA sequencing and the GSE87016 dataset, respectively. After taking interaction genes, 9 down-regulated DEGs due to hypermethylation and 11 up-regulated DEGs due to hypomethylation were identified in CAE. A total of 10 core abnormal methylation-modified genes were identified, including six down-regulated DEGs due to hypermethylation (netrin G1, ADAM metallopeptidase domain 12, immunoglobulin superfamily member 10, sarcoglycan dela, Dickkopf WNT signaling pathway inhibitor 3, and GATA binding protein 6), and four up-regulated DEGs due to hypomethylation (adrenomedullin, ubiquitin specific peptidase 18, lymphocyte antigen 6 family member E, and MX dynamin-like GTPase 1). Some signaling pathways were identified in patients with CAE, including cell adhesion molecule, O-glycan biosynthesis, and the renin-angiotensin system.

Conclusions: Abnormal methylation-modified DEGs involved in signaling pathways may be involved in CAE development.

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冠状动脉扩张中潜在异常甲基化修饰基因的鉴定。

背景:冠状动脉扩张(CAE)是一种容易识别的冠状动脉解剖形态异常。然而，其发病机制尚不清楚。目的:本研究旨在鉴定CAE患者甲基化修饰异常基因，为CAE的研究提供依据。方法:采集CAE患者外周静脉血样本进行RNA测序，鉴定差异表达基因(DEGs)，并进行功能富集。然后，从GSE87016 (HumanMethylation450 BeadChip数据，涉及11例病例和12例正常对照)中下载CAE的DNA甲基化谱，以鉴定差异甲基化基因(dmg)。最后，取deg与dmg相互作用基因后，鉴定异常甲基化修饰基因，进行蛋白-蛋白相互作用分析，并利用逆转录酶聚合酶链反应进行表达验证。结果:从RNA测序和GSE87016数据集中分别获得152个deg和4318个dmg。取相互作用基因后，在CAE中鉴定出9个因高甲基化而下调的DEGs和11个因低甲基化而上调的DEGs。共鉴定出10个核心异常甲基化修饰基因，包括6个因高甲基化而下调的deg (netrin G1、ADAM金属肽酶结构域12、免疫球蛋白超家族成员10、肌糖聚糖dela、Dickkopf WNT信号通路抑制剂3和GATA结合蛋白6)，以及4个因低甲基化而上调的deg(肾上腺髓质素、泛素特异性肽酶18、淋巴细胞抗原6家族成员E、GATA结合蛋白6)。和MX动力蛋白样GTPase 1)。在CAE患者中发现了一些信号通路，包括细胞粘附分子、o聚糖生物合成和肾素-血管紧张素系统。结论:参与信号通路的异常甲基化修饰的deg可能参与CAE的发展。

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来源期刊

International Journal of Genomics BIOCHEMISTRY & MOLECULAR BIOLOGY-BIOTECHNOLOGY & APPLIED MICROBIOLOGY

CiteScore

5.40

自引率

0.00%

发文量

审稿时长

17 weeks

期刊介绍： International Journal of Genomics is a peer-reviewed, Open Access journal that publishes research articles as well as review articles in all areas of genome-scale analysis. Topics covered by the journal include, but are not limited to: bioinformatics, clinical genomics, disease genomics, epigenomics, evolutionary genomics, functional genomics, genome engineering, and synthetic genomics.