Expression profile of circular RNAs in epicardial adipose tissue in heart failure

被引:0
|
作者
Zheng Mei-Li
Du Xiang-Peng
Zhao Lei
Yang Xin-Chun
机构
[1] Beijing Key Laboratory of Hypertension Research
[2] Beijing Chao-Yang Hospital
[3] Weihaiwei People’s Hospital
[4] Capital Medical University
[5] Heart Center
[6] Beijing 100020
[7] Shandong 264200
[8] Department of Cardiology
[9] China
关键词
CircRNA; Epicardial adipose tissue; Heart failure;
D O I
暂无
中图分类号
R541.6 [血液循环衰竭];
学科分类号
1002 ; 100201 ;
摘要
Background: Recent studies have reported circular RNA (circRNA) expression profiles in various tissue types; however, circRNA expression profile in human epicardial adipose tissue (EAT) remains undefined. This work aimed to compare circRNA expression patterns in EAT between the heart failure (HF) and non-HF groups.Methods: RNA-sequencing was carried out to compare circRNA expression patterns in EAT specimens from coronary artery disease cases between the HF and non-HF groups. Quantitative real-time polymerase chain reaction was performed for validation. Comparisons of patient characteristics between the two groups were usingt test, Mann-WhitneyU test, and Chi-squared test.Results: A total of 141 circRNAs substantially different between the HF and non-HF groups (P < 0.05; fold change >2) were detected, including 56 up-regulated and 85 down-regulated. Among them, hsairc005565 stood out, for it had the highest fold change and was significantly increased in HF patients in quantitative real-time polymerase chain reaction validation. The top highly expressed EAT circRNAs corresponded to genes involved in cell proliferation and inflammatory response, including GSE1, RHOBTB3, HIPK3, UBXN7, PCMTD1, N4BP2L2, CFLAR, EPB41L2, FCHO2, FNDC3B, and SPECC1. The top enriched Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway were positive regulation of metabolic processes and insulin resistance, respectively.Conclusion: These data indicate EAT circRNAs may contribute to the pathogenesis of metabolic disorders causing HF.
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收藏
页码:2565 / 2572
页数:8
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