Abstract
Coronary heart disease (CHD) is one of the most common severe cardiovascular diseases. Competitive endogenous RNAs (ceRNA) play critical roles in complex diseases. However, our understanding of the dysregulated functions of ceRNAs in CHD remains limited. Here, we systematically analyzed the alterations of ceRNAs and identified the specific functions based on dysregulated modules from the ceRNA network. A total of 2457 significantly differential expressed genes and 212 differential expressed lncRNAs were identified. We got 76679 regulator relationship between different expression genes and miRNAs and 336 regulator relationship between differential expressed lncRNAs and miRNAs. We constructed the ceRNA network and selected five dysregulated modules. Furthermore, CHD specific functions based on dysregulated modules from the ceRNA network were identified, including histone acetylation, platelet degranulation, cAMP-dependent protein kinase complex, xenobiotic transport and so on. Our results will provide novel insight for a better understanding of the mechanism of ceRNAs and facilitate the identification of novel diagnostic and therapeutic biomarkers in CHD.
Highlights
Coronary heart disease (CHD) is one of the most common severe cardiovascular diseases [1]
MicroRNAs are a type of small noncoding RNA composed of 21–22 nucleotides [8, 9]. ey exert their biological effects by silencing genes posttranscriptionally via binding to miRNA response elements (MREs) in the target mRNA [10, 11]. e report suggested that miR-451 is upregulated in CHD and is associated with the PI3K-Akt-mTOR pathway; the data indicated that miR-451 might be a novel biomarker for CHD [12]
One study observed that the direct binding between Long noncoding RNAs (lncRNAs)-MEG3 and miR-26a was confirmed via dual-luciferase reporter assay, which Journal of Healthcare Engineering indicated that lncRNA-MEG3 could sponge miR-26a as a Competitive endogenous RNAs (ceRNA) in CHD [23]. e other study provided evidence that lncRNA HIF1A-AS1 could act as ceRNA to adsorb miR-204 to suppress miR-204 expression and elevate SOCS2 expression in a mouse model, which was established by left coronary artery occlusion [24]
Summary
Coronary heart disease (CHD) is one of the most common severe cardiovascular diseases [1]. Studies have shown that more than 400 genes are associated with the incidence, pathogenesis, and progression of CHD [6, 7]. Ey exert their biological effects by silencing genes posttranscriptionally via binding to miRNA response elements (MREs) in the target mRNA [10, 11]. Some studies verified that the abnormal expression of lncRNA in CHD [14–16]. Liu et al reported that lncRNAANRIL is expressed low in the serum of patients with CHD, and it has high predictive value both for effective treatment and for poor prognosis of them. Numerous studies have highlighted that lncRNAs can bind to miRNA sites as ceRNAs, thereby affecting and regulating the expression of mRNAs and target genes [21, 22]. One study observed that the direct binding between lncRNA-MEG3 and miR-26a was confirmed via dual-luciferase reporter assay, which
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