Similar Datasets
Project description:Plasma lncRNA expression profiles were acquired by using a human lncRNA microarray.
2020-12-29 | GSE143786 | 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 | 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:Hypertrophic cardiomyopathy (HCM) is the most common inherited myocardial disease with significant genetic and phenotypic heterogeneity. To search for novel biomarkers, which could increase the accuracy of HCM diagnosis and possibly improve understanding of its phenotype formation, we analyzed the levels of circulating microRNAs (miRNAs) − stable non-coding regulatory RNAs. Performed high throughput sequencing of miRNAs in plasma of HCM patients and controls pinpointed miR-499a-5p as one of 35 miRNAs dysregulated in HCM.
2022-01-29 | GSE195436 | GEO
Project description:Circulating ceRNAs associated with hypertrophic cardiomyopathy
| PRJNA625111 | ENA
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:Circulating long noncoding RNAs associated with hypertrophic cardiomyopathy
| PRJNA601680 | ENA
Project description:BackgroundHypertrophic cardiomyopathy (HCM) is caused by mutations in the genes coding for proteins essential in normal myocardial contraction. However, it remains unclear through which molecular pathways gene mutations mediate the development of HCM. The objectives were to determine plasma protein biomarkers of HCM and to reveal molecular pathways differentially regulated in HCM.MethodsWe conducted a multicenter case-control study of cases with HCM and controls with hypertensive left ventricular hypertrophy. We performed plasma proteomics profiling of 1681 proteins. We performed a sparse partial least squares discriminant analysis to develop a proteomics-based discrimination model with data from 1 institution (ie, the training set). We tested the discriminative ability in independent samples from the other institution (ie, the test set). As an exploratory analysis, we executed pathway analysis of significantly dysregulated proteins. Pathways with false discovery rate <0.05 were declared positive.ResultsThe study included 266 cases and 167 controls (n=308 in the training set; n=125 in the test set). Using the proteomics-based model derived from the training set, the area under the receiver operating characteristic curve was 0.89 (95% CI, 0.83-0.94) in the test set. Pathway analysis revealed that the Ras-MAPK (mitogen-activated protein kinase) pathway, along with its upstream and downstream pathways, was upregulated in HCM. Pathways involved in inflammation and fibrosis-for example, the TGF (transforming growth factor)-β pathway-were also upregulated.ConclusionsThis study serves as the largest-scale investigation with the most comprehensive proteomics profiling in HCM, revealing circulating biomarkers and exhibiting both novel (eg, Ras-MAPK) and known (eg, TGF-β) pathways differentially regulated in HCM.
| S-EPMC8292216 | biostudies-literature
Project description:Arrhythmogenic cardiomyopathy (ACM) and hypertrophic cardiomyopathy (HCM) are genetically and phenotypically distinct disorders of the myocardium. Here we describe for the first time co-inheritance of mutations in genes associated with ACM or HCM in two families with recurrence of both cardiomyopathies. Among the double heterozygotes for mutations in desmoplakin (DSP) and myosin binding protein C (MYBPC3) genes identified in Family A, two were diagnosed with ACM and two with HCM. In Family B, one patient was identified to carry mutations in ?-T-catenin (CTTNA3) and ?-myosin (MYH7) genes, but he does not fulfill the current diagnostic criteria neither for ACM nor for HCM. Interestingly, the double heterozygotes showed a variable clinical expression of both cardiomyopathies and they do not exhibit a more severe phenotype than family members carrying only one of the two mutations.
| S-EPMC5602010 | biostudies-other
Project description:Hypertrophic cardiomyopathy (HCM) is one of the most commonly inherited heart diseases and the leading cause of sudden cardiac death among adolescents and young adults. Circulating long noncoding RNAs (lncRNAs) have demonstrated potential as diagnostic and therapeutic targets in several cardiovascular diseases. However, the circulating extracellular lncRNA expression profile of patients with HCM remains unclear. Plasma lncRNA expression was evaluated in patients with HCM and healthy controls using a human lncRNA microarray. A weighted correlation network analysis (WGCNA) and linear models for microarray data (Limma) were used. GSE68316 data from cardiac tissue in the Gene Expression Omnibus database were analysed for further validation. Using WGCNA, two modules (referred to as the magenta and the light?yellow module) were identified that were positively associated with HCM. Gene Ontology analysis revealed that lncRNAs in the magenta module targeted 'heart growth'. Using Limma, a total of 290 lncRNAs were differentially expressed (210 upregulated and 80 downregulated) in the plasma of HCM patients, compared with controls. Moreover, combined WGCNA and Limma analysis demonstrated that 27 hub lncRNAs in the magenta module and 13 hub lncRNAs in the light?yellow module were significantly upregulated, compared with the controls. Moreover, of the 40 differentially expressed hub lncRNAs identified in the two modules, three circulating lncRNAs (lnc?P2RY6?1:1, ENST00000488040 and ENST00000588047) were also significantly upregulated in the HCM cardiac tissue validation dataset. These lncRNAs may serve as biomarkers and therapeutic targets for precise diagnosis and treatment of HCM.
| S-EPMC7646839 | biostudies-literature