A susceptibility biomarker identification strategy based on significantly differentially expressed ceRNA triplets for ischemic cardiomyopathy

Zou, Yongxin; Wang, Yahui; Rong, Zherou; Wei, Benliang; Liu, Yang; Song, Zhaona; Li, Wenshuai; Hu, Erqiang; Deng, Gui; He, Yuehan; Liu, Jun-Jie; Chen, Lina; Li, Wan

doi:10.1042/bsr20191731

Cited by 5 publications

(4 citation statements)

References 43 publications

(40 reference statements)

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“…Long noncoding RNA can act as a molecular sponge for miRNA to release the downstream target mRNA (Zhou et al 2018;Zhang et al 2020;Zou et al 2020). We anticipated that SOX2-OT regulated H9c2 cell injury by this pattern.…”

Section: Sox2-ot Worked As a Sponge For Mir-215-5pmentioning

confidence: 99%

Long Non-Coding RNA SOX2 Overlapping Transcript Aggravates H9c2 Cell Injury via the miR-215-5p/ZEB2 Axis and Promotes Ischemic Heart Failure in a Rat Model

Zhang

et al. 2021

Tohoku J. Exp. Med.

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Heart failure is a common cardiovascular disease, which has been regarded as one of the highest health care costs with high morbidity and mortality in the western countries. Long noncoding RNAs have been widely reported to regulate the initiation or progression of cardiovascular diseases. However, the specific role of SOX2 overlapping transcript (SOX2-OT) in ischemic heart failure remains uncharacterized. The present study aimed to explore the function and mechanism of SOX2-OT in ischemic heart failure. The starBase website was used to predict potential miRNAs or target mRNAs. Western blot assay was implemented to test collagen protein levels. Functional assays were conducted to evaluate the effects of SOX2-OT on H9c2 cell viability and apoptosis. RNA pull down and luciferase reporter assays were used to confirm the combination between miR-215-5p and SOX2-OT. We found out that SOX2-OT level was increased by oxygen glucose deprivation/reoxygenation treatment in H9c2 cells. Silencing of SOX2-OT ameliorated cell injury by promoting cell viability, inhibiting cell apoptosis and reducing productions of collagens. Mechanistically, miR-215-5p was confirmed to bind with SOX2-OT after prediction and screening. In addition, we discovered that miR-215-5p negatively regulated zinc finger E-box binding homeobox 2 (ZEB2) protein level by directly binding with ZEB2 3′ untranslated region. Finally, we verified that SOX2-OT aggravated cell injury by targeting ZEB2 in H9c2 cells. In conclusion, SOX2-OT aggravated heart failure in vivo and promoted H9c2 cell injury via the miR-215-5p/ZEB2 axis in vitro, implying a novel insight into heart failure treatment.

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Section: Sox2-ot Worked As a Sponge For Mir-215-5pmentioning

confidence: 99%

Long Non-Coding RNA SOX2 Overlapping Transcript Aggravates H9c2 Cell Injury via the miR-215-5p/ZEB2 Axis and Promotes Ischemic Heart Failure in a Rat Model

Zhang

et al. 2021

Tohoku J. Exp. Med.

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“…IL-6 in vascular endothelial cells can increase the expression of platelet-derived growth factor (PDGF), which stimulates the proliferation and migration of vascular smooth of muscle cells and fibroblasts, acts as a chemotactic factor, and has a chemotactic effect on monocytes and neutrophils, inducing them to produce inflammatory factors ( 32 ). IL-6 can also increase the permeability of vascular endothelial cells and promote the occurrence of vasculitis and atherosclerosis ( 33 ). Endothelial cells can synthesize and release nitric oxide (NO) through L-arginine to regulate vascular resistance of coronary artery and adjacent vessels.…”

Section: Discussionmentioning

confidence: 99%

Screening and identification of hub genes for ischemic cardiomyopathy and construction and validation of a clinical prognosis model using bioinformatics analysis

Wang,

Tang,

Bai

et al. 2024

J Thorac Dis

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Background Myocardial ischemia and hypoxia may result in myocardial cell necrosis, scar formation, and hyperplasia. We aim to explore the differentially expressed genes (DEGs) in ischemic cardiomyopathy (ICM), construct and identify a clinical prognosis model using bioinformatics methods, so as to screen potential biomarkers of ICM to provide a basis for the early diagnosis and treatment of ICM. Methods Based on the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database, R language was used to screen DEGs in healthy myocardial (n=5) and ICM myocardial tissues (n=12). DEGs were analyzed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI). Receiver operating characteristic (ROC) curves were drawn to verify the target genes. Results A total of 259 genes with significantly changed fold change (FC) values were obtained through conditional screening, including up-regulated genes and down-regulated genes. The first two hub genes [interleukin-6 ( IL-6 ) and Ras homologous gene family member A ( RHOA )] with the largest degree value among the above up-regulated and down-regulated genes were selected and their expression values were combined in the gene chip to draw the ROC curve based on the pROC package of R language. The area under the ROC curve (AUC) values of IL-6 and RHOA were 0.956 and 0.995, respectively. The expression levels of Sqstm1, Nos2, IL-6, RHOA , and Zfp36 genes in the ICM group are lower than those in the blank control group and the difference was statistically significant (P<0.05). RHOA and Stat3 were identified as the key genes controlling the occurrence and development of ICM. Conclusions ICM is closely related to the changes of extracellular matrix (ECM) and oxidoreductase activity. The IL-6 and RHOA are expected to become potential targets for ICM treatment.

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“…So far, several studies have used microarray [ 24 ] and RNA-sequencing [ 25 ] to analyze the transcription of lncRNAs in the heart tissues of patients with ICM, and differentially expressed lncRNAs were identified as potential biomarkers for further analysis. Identifying DEGs is important for transcriptome analysis as DEGs are often highly associated with disease status.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and Experimental Analyses Reveal Immune-Related LncRNA–mRNA Pair AC011483.1-CCR7 as a Biomarker and Therapeutic Target for Ischemic Cardiomyopathy

Jin

Gong

et al. 2022

IJMS

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Ischemic cardiomyopathy (ICM), which increases along with aging, is the leading cause of heart failure. Currently, immune response is believed to be critical in ICM whereas the roles of immune-related lncRNAs remain vague. In this study, we aimed to systematically analyze immune-related lncRNAs in the aging-related disease ICM. Here, we downloaded publicly available RNA-seq data from ischemic cardiomyopathy patients and non-failing controls (GSE116250). Weighted gene co-expression network analysis (WGCNA) was performed to identify key ICM-related modules. The immune-related lncRNAs of key modules were screened by co-expression analysis of immune-related mRNAs. Then, a competing endogenous RNA (ceRNA) network, including 5 lncRNAs and 13 mRNAs, was constructed using lncRNA–mRNA pairs which share regulatory miRNAs and have significant correlation. Among the lncRNA–mRNA pairs, one pair (AC011483.1-CCR7) was verified in another publicly available ICM dataset (GSE46224) and ischemic cell model. Further, the immune cell infiltration analysis of the GSE116250 dataset revealed that the proportions of monocytes and CD8+ T cells were negatively correlated with the expression of AC011483.1-CCR7, while plasma cells were positively correlated, indicating that AC011483.1-CCR7 may participate in the occurrence and development of ICM through immune cell infiltration. Together, our findings revealed that lncRNA–mRNA pair AC011483.1-CCR7 may be a novel biomarker and therapeutic target for ICM.

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A susceptibility biomarker identification strategy based on significantly differentially expressed ceRNA triplets for ischemic cardiomyopathy

Cited by 5 publications

References 43 publications

Long Non-Coding RNA SOX2 Overlapping Transcript Aggravates H9c2 Cell Injury via the miR-215-5p/ZEB2 Axis and Promotes Ischemic Heart Failure in a Rat Model

Long Non-Coding RNA SOX2 Overlapping Transcript Aggravates H9c2 Cell Injury via the miR-215-5p/ZEB2 Axis and Promotes Ischemic Heart Failure in a Rat Model

Screening and identification of hub genes for ischemic cardiomyopathy and construction and validation of a clinical prognosis model using bioinformatics analysis

Bioinformatics and Experimental Analyses Reveal Immune-Related LncRNA–mRNA Pair AC011483.1-CCR7 as a Biomarker and Therapeutic Target for Ischemic Cardiomyopathy

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