Dysregulated lncRNAs are involved in the progress of myocardial infarction by constructing regulatory networks

被引:0
作者
Yang, Jingqi [2 ]
Yang, Ming [1 ]
Sheng, Guotai [2 ]
机构
[1] Jiangxi Prov Peoples Hosp, Nanchang Med Coll, Dept Cardiovasc Med, Affiliated Hosp 1, 152 Aiguo Road, Nanchang 330000, Peoples R China
[2] Jiangxi Prov Peoples Hosp, Nanchang Med Coll, Dept Cardiovasc Med, Affiliated Hosp 1, Nanchang 330000, Peoples R China
来源
OPEN MEDICINE | 2023年 / 18卷 / 01期
关键词
long noncoding RNA; myocardial infarction; immune system; inflammation; regulatory networks; NONCODING RNAS; ANNOTATION; EXPRESSION; EVOLUTION;
D O I
10.1515/med-2023-0657
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Long noncoding RNAs (lncRNAs) mediate important epigenetic regulation in a wide range of biological processes. However, the effect of all dysregulated lncRNAs in myocardial infarction (MI) is not clear. Whole transcriptome sequencing analysis was used to characterize the dynamic changes in lncRNA and mRNA expression. A gene network was constructed, and genes were classified into different modules using WGCNA. In addition, for all dysregulated lncRNAs, gene ontology analysis and cis-regulatory analysis were applied. The results demonstrated that a large number of the differentially co-expressed genes were primarily linked to the immune system process, inflammatory response, and innate immune response. The functional pathway analysis of the MEblue module included immune system process and apoptosis, and MEbrown included the T-cell receptor signal pathway by WGCNA. In addition, through cis-acting analysis of lncRNA regulation, the cis-regulated mRNAs were mainly enriched in immune system processes, innate immune responses, and VEGF signal pathways. We found that lncRNA regulation of mRNAs plays an important role in immune and inflammatory pathways. Our study provides a foundation to further understand the role and potential mechanism of dysregulated lncRNAs in the regulation of MI, in which many of them could be potential targets for MI.
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页数:13
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