Next Generation Sequencing Facilitates Quantitative Analysis of Hypertrophic Cardiomyopathy/Healthy control Left Ventricular Transcriptomes
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE191120 | GEO | 2025/07/02
REPOSITORIES: GEO
Similar Datasets
Project description:Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopath that caused by mutations in genes encoding proteins of the cardiac sarcomere. Although multiple efforts have been made to understand the pathogenesis of HCM, the mechanisms of how long noncoding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network result in HCM still unkown. Herein, we acquired the different expression profiles of lncRNAs (DElncRNAs) and messenger RNAs (mRNA, DEGs) by using microarray, microRNAs (DEmiRNAs) by sequencing in plasma of HCM patients and healthy controls. LncRNA-miRNA pairs were predicted using miRcode and starBase, and crossed with DEmiRNAs. MiRNA-mRNA pairs were retrieved from miRanda and TargetScan, and crossed with DEGs. Combined these pairs, the ceRNA network was constructed and hub nodes were then analyzed to reconstruct subnetwork. Gene Ontology and KEGG pathways were used to analyse the mRNAs in the ceRNA. Total 520 DElncRNAs, 33 DEmiRNAs, and 371 DEGs were identified. By coexpression analysis, 682 lncRNA-mRNA pairs were identified with a coefficient ≥ 0.9 and p < 0.05. The ceRNA network with 8 lncRNAs, 3 miRNAs and 22 mRNAs was constructed visualized by Cytoscape. LncRNA RP11-66N24.4 and LINC00310 are among the top 10% nodes and the associated ceRNA subnetwork may be the center of the whole ceRNA network. Furthermore, the qRT-PCR results showed that LINC00310 was signifcantly decreased in HCM patients. For LINC00310, GO analysis revealed that the biological processes was enriched in cardiovascular system development, sprouting angiogenesis, circulatory system development and so on, and Pathway analysis was mainly enriched in cGMP-PKG signaling pathway. Our study reveals the novel lncRNA-related ceRNA network in HCM and the identified lncRNA LINC00310 may be roles in the pathogenesis mechanisms of HCM, which could provide further insight into the pathogenesis of HCM.
2022-09-28 | GSE197218 | GEO
Project description:Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopath that caused by mutations in genes encoding proteins of the cardiac sarcomere. Although multiple efforts have been made to understand the pathogenesis of HCM, the mechanisms of how long noncoding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network result in HCM still unkown. Herein, we acquired the different expression profiles of lncRNAs (DElncRNAs) and messenger RNAs (mRNA, DEGs) by using microarray, microRNAs (DEmiRNAs) by sequencing in plasma of HCM patients and healthy controls. LncRNA-miRNA pairs were predicted using miRcode and starBase, and crossed with DEmiRNAs. MiRNA-mRNA pairs were retrieved from miRanda and TargetScan, and crossed with DEGs. Combined these pairs, the ceRNA network was constructed and hub nodes were then analyzed to reconstruct subnetwork. Gene Ontology and KEGG pathways were used to analyse the mRNAs in the ceRNA. Total 520 DElncRNAs, 33 DEmiRNAs, and 371 DEGs were identified. By coexpression analysis, 682 lncRNA-mRNA pairs were identified with a coefficient ≥ 0.9 and p < 0.05. The ceRNA network with 8 lncRNAs, 3 miRNAs and 22 mRNAs was constructed visualized by Cytoscape. LncRNA RP11-66N24.4 and LINC00310 are among the top 10% nodes and the associated ceRNA subnetwork may be the center of the whole ceRNA network. Furthermore, the qRT-PCR results showed that LINC00310 was signifcantly decreased in HCM patients. For LINC00310, GO analysis revealed that the biological processes was enriched in cardiovascular system development, sprouting angiogenesis, circulatory system development and so on, and Pathway analysis was mainly enriched in cGMP-PKG signaling pathway. Our study reveals the novel lncRNA-related ceRNA network in HCM and the identified lncRNA LINC00310 may be roles in the pathogenesis mechanisms of HCM, which could provide further insight into the pathogenesis of HCM.
2022-09-28 | GSE197191 | GEO
Project description:Approximately 1426 lncRNAs (965 up-regulated and 461 down-regulated) and 1715 mRNAs (896 up-regulated and 819 down-regulated) were aberrantly expressed in HCM patients with fold change > 2.0 Myocardial tissues were obtained from 7 HCM patients and 5 disease-free individuals, and lncRNA and mRNA expression profiles were analyzed using the CapitalBio Human LncRNA Microarray v2.0.
2015-05-08 | E-GEOD-68316 | biostudies-arrayexpress
Project description:Left ventricular hypertrophy, myocardial disarray and interstitital fibrosis are the hallmarks of hypertrophic cardiomyopathy (HCM). Access to the myocardium for diagnostic purposes is limited. Circulating biomolecules reflecting the myocardial disease processes could improve early detection of HCM. Circulating miRNAs have been found to reflect disease processes in several cardiovascular diseases. Circulating miR-1, miR-495-3p and miR-4454 levels are elevated in plasma of HCM patients. miR-4454 is suggested as a potential biomarker for fibrosis in these patients.
2021-11-20 | GSE188324 | GEO
Project description:Background: Of Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC), 85%-90% of cases develop from liver cirrhosis, and circular RNAs (circRNAs) have important roles in this process; however, differences in serum circRNA expression profiles between patients with HBV-related cirrhosis and those with HCC have not been studied. Methods: Serum RNA was extracted from patients with HCC and cirrhosis (n = 5 per group) and used for microarray analysis of circRNA expression profiles. Bioinformatics analyses, including clustering, differential expression, and construction of a ceRNA network, were performed. Quantitative real-time reverse transcription PCR validation analysis was conducted using samples from patients with HBV-related cirrhosis (n = 88) and HCC (n = 73). Further, statistical analyses were used to analyze the potential function and value of selected circRNAs with expression differing between the HBV-related cirrhosis and HCC groups. Results: Cluster analysis revealed 8 up-regulated and 80 down-regulated circRNAs. Further, qRT-PCR analysis showed that circRNA_0000367 expression was consistent with that detected by microarray experiments, with significantly lower levels in patients with HBV-related HCC than those with HBV-related cirrhosis. CircRNA_0000367 expression levels were also significantly lower in patients with drug-resistant HBV and those with HBV-related cirrhosis with Model for End-Stage Liver Disease score < 10. Further, circRNA_00000367 expression levels were lower in patients with HBV-related cirrhosis who progressed to HCC. Analysis of the lncRNA-miRNA-mRNA ceRNA network identified 39 miRNAs and 24 mRNAs involved in circRNA_00000367 networks; these target genes were involved in various biological processes and signaling pathways. Conclusion: Serum cicrRNA_0000367 is a potential HCC biomarker in patients with HBV-related cirrhosis, where down-regulation of cicrRNA_0000367 in HBV-related cirrhosis may be associated with progression to HCC.
2025-02-10 | E-MTAB-12717 | biostudies-arrayexpress
Project description:Approximately 1426 lncRNAs (965 up-regulated and 461 down-regulated) and 1715 mRNAs (896 up-regulated and 819 down-regulated) were aberrantly expressed in HCM patients with fold change > 2.0
2015-05-08 | GSE68316 | GEO
Project description:BACKGROUND: MYBPC3 is one of the most mutated gene known to cause hypertrophic cardiomyopathy (HCM). However, the molecular mechanisms of how mutations in MYBPC3 lead to the onset and progression of HCM are poorly understood. Thus, advancing in-vitro studies to define these mechanisms of mutations leading to HCM are still warranted. Thus, the primary objective of this study was to investigate the molecular mechanisms underlying the pathogenesis of HCM associated with MYBPC3 mutation utilizing isogenic human-induced pluripotent stem cell (hiPSC)-derived cardiac organoids (hCOs).
2025-01-28 | GSE262876 | GEO
Project description:Purpose: Immunoglobulin A nephropathy (IgAN) is immune-mediated primary glomerulonephritis, which is the most common reason leading to renal failure worldwide, the exact pathogenesis of IgAN is not well defined. Accumulating evidence indicates that circular RNAs (circRNAs) play crucial roles in the immune disease by involving in the competing endogenous RNA (ceRNA) network mechanism. At present, the studies of the circRNA profiles and circRNA-associated ceRNA networks in the IgAN are still scarce. This study aimed to elucidate the potential roles of circRNA, microRNA (miRNA), and messenger RNA (mRNA) ceRNA network in peripheral blood mononuclear cells (PBMCs) of IgAN. Methods: CircRNA sequencing was used to identify the differential expressed circRNAs (DEcircRNAs) of PBMCs in IgAN and healthy controls. A circRNA-miRNA-mRNA ceRNA network was constructed to further investigate the mechanisms of IgAN. Results: A total of 145 circRNAs were differentially expressed in IgAN compared with controls (|log2 (FC)|>1 and P-value <0.05). Combined with the data from GSE73953 and GSE25590 in GEO database, a ceRNA network was constructed which contained 16 DEcircRNAs, 72 differential expressed mRNAs (DEmRNAs) and 11 differential expressed miRNAs (DEmiRNAs). Conclusion: Our study identified a novel circRNA-mediated ceRNA regulatory network mechanisms in the pathogenesis of IgAN.
2020-11-08 | GSE154046 | GEO
Project description:Background: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder, characterized by cardiomyocyte hypertrophy, cardiomyocyte disarray and fibrosis, which has a prevalence of ~1:200-500 and predisposes individuals to sudden death and heart failure. The mechanisms through which diverse HCM-causing mutations cause cardiac dysfunction remain mostly unknown and their identification may reveal new therapeutic avenues. MicroRNAs have emerged as critical regulators of gene expression and disease phenotype in various pathologies. We explored whether miRNAs could play a role in HCM pathogenesis and offer potential therapeutic targets. Methods and Results: Using high-throughput miRNA expression profiling and qPCR analysis in two distinct mouse models of HCM, we found that miR-199a-3p expression levels are upregulated in mutant mice compared to age- and treatment-matched wild-type mice. We also found that miR-199a-3p expression is enriched in cardiac non-myocytes compared to cardiomyocytes. When we expressed miR-199a-3p mimic in cultured primary cardiac non-myocytes and analyzed the conditioned media by proteomics, we found that several ECM proteins (e.g., TSP2, FBLN3, COL11A1, LYOX) were differentially expressed. We confirmed our proteomics findings by qPCR analysis of selected mRNAs and demonstrated that miR-199a-3p mimic expression in cardiac non-myocytes drives upregulation of ECM genes including Tsp2, Fbln3, Pcoc1, Col1a1 and Col3a1. To examine the role of miR-199a-3p in vivo, we inhibited its function using lock-nucleic acid (LNA)-based inhibitors (antimiR-199a-3p) in an HCM mouse model. Our results revealed that progression of cardiac fibrosis is attenuated when miR-199a-3p function is inhibited in mild-to-moderate HCM. Finally, guided by computational target prediction algorithms, we identified mRNAs Cd151 and Itga3 as direct targets of miR-199a-3p and have shown that miR-199a-3p mimic expression negatively regulates AKT activation in cardiac non-myocytes. Conclusions: Altogether, our results suggest that miR-199a-3p may contribute to cardiac fibrosis in HCM through its actions in cardiac non-myocytes. Thus, inhibition of miR-199a-3p in mild-to-moderate HCM may offer therapeutic benefit in combination with complementary approaches that target the primary defect in cardiac myocytes.
2024-01-26 | PXD042904 | Pride
Project description:Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disorder characterized by ventricular wall hypertrophy and diastolic dysfunction. Most patients with HCM are often a slowly progressive disease and may be asymptomatic; however, some progress to the dilated phase of HCM (D-HCM), and have a poorer prognosis. This study established disease-specific human induced pluripotent stem cells (iPSCs) from a patient with D-HCM harboring a truncating mutation in MYBPC3, and compared transcriptomes of iPSCs-derived cardiomyocytes between healthy control and D-HCM.
2025-04-06 | GSE263980 | GEO