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Transcriptome Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

ABSTRACT: Using a high-throughput gene expression profiling technology, we have been able to develop new hypotheses regarding the molecular pathogenic mechanisms of human hypertrophic cardiomyopathy (HCM). It is hoped that these hypotheses, among others generated by this data, will fuel future research endeavors that will uncover novel biomarkers, prognostic indicators, and therapeutic targets to improve our ability to diagnose, counsel, and treat patients with this highly heterogeneous and potentially life-threatening condition. Case-control study comparing the messenger RNA transcriptome of cardiac tissues from patients with hypertrophic cardiomyopathy to the transcriptome of control donor cardiac tissues.

ORGANISM(S): Homo sapiens

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PROVIDER: S-DIXA-D-1125 | biostudies-other |

REPOSITORIES: biostudies-other

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Transcriptome Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

Project description:Using a high-throughput gene expression profiling technology, we have been able to develop new hypotheses regarding the molecular pathogenic mechanisms of human hypertrophic cardiomyopathy (HCM). It is hoped that these hypotheses, among others generated by this data, will fuel future research endeavors that will uncover novel biomarkers, prognostic indicators, and therapeutic targets to improve our ability to diagnose, counsel, and treat patients with this highly heterogeneous and potentially life-threatening condition.

2012-09-01 | GSE36961 | GEO

Transcriptome Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

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MicroRNA Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

Project description: Not available

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MicroRNA Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

Project description:Using a high-throughput gene expression profiling technology, we have illuminated novel potential microRNA (miRNA) components of the molecular disease process underlying human hypertrophic cardiomyopathy (HCM). It is hoped that this will fuel future research endeavors that will eventually uncover the role miRNAs may play in the phenotypic heterogeneity of the disease, and thus, provide potential tools for identifying patients with benign versus malignant forms of the disease.

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Novel Genes Involved in Hypertrophic Cardiomyopathy: Data of Transcriptome and Methylome Profiling.

Project description:Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease; its pathogenesis is still being intensively studied to explain the reasons for the significant genetic and phenotypic heterogeneity of the disease. To search for new genes involved in HCM development, we analyzed gene expression profiles coupled with DNA methylation profiles in the hypertrophied myocardia of HCM patients. The transcriptome analysis identified significant differences in the levels of 193 genes, most of which were underexpressed in HCM. The methylome analysis revealed 1755 nominally significant differentially methylated positions (DMPs), mostly hypomethylated in HCM. Based on gene ontology enrichment analysis, the majority of biological processes, overrepresented by both differentially expressed genes (DEGs) and DMP-containing genes, are involved in the regulation of locomotion and muscle structure development. The intersection of 193 DEGs and 978 DMP-containing genes pinpointed eight common genes, the expressions of which correlated with the methylation levels of the neighboring DMPs. Half of these genes (AUTS2, BRSK2, PRRT1, and SLC17A7), regulated by the mechanism of DNA methylation, were underexpressed in HCM and were involved in neurogenesis and synapse functioning. Our data, suggesting the involvement of innervation-associated genes in HCM, provide additional insights into disease pathogenesis and expand the field of further research.

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Plasma metabolomic profiling of hypertrophic cardiomyopathy patients before and after surgical myectomy suggests postoperative improvement in metabolic function.

Project description:BackgroundHypertrophic cardiomyopathy (HCM) is a common inherited heart disorder complicated by left ventricle outflow tract (LVOT) obstruction, which can be treated with surgical myectomy. To date, no reliable biomarkers for LVOT obstruction exist. We hypothesized that metabolomic biomarkers for LVOT obstruction may be detectable in plasma from HCM patients.MethodsWe conducted metabolomic profiling on plasma samples of 18 HCM patients before and after surgical myectomy, using a commercially available metabolomics platform.ResultsWe found that 215 metabolites were altered in the postoperative state (p-value < 0.05). 12 of these metabolites were notably significant after adjusting for multiple comparisons (q-value < 0.05), including bilirubin, PFOS, PFOA, 3,5-dichloro-2,6-dihydroxybenzoic acid, 2-hydroxylaurate, trigonelline and 6 unidentified compounds, which support improved organ metabolic function and increased lean soft tissue mass.ConclusionsThese findings suggest improved organ metabolic function after surgical relief of LVOT obstruction in HCM and further underscore the beneficial systemic effects of surgical myectomy.

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Plasma Proteomic Profiling in Hypertrophic Cardiomyopathy Patients before and after Surgical Myectomy Reveals Post-Procedural Reduction in Systemic Inflammation.

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DNA methylome and transcriptome profiling reveal key electrophysiology and immune dysregulation in hypertrophic cardiomyopathy.

Project description:Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease. However, a detailed DNA methylation (DNAme) landscape has not yet been elucidated. Our study combined DNAme and transcriptome profiles for HCM myocardium and identify aberrant DNAme associated with altered myocardial function in HCM. The transcription of methylation-related genes did not significantly differ between HCM and normal myocardium. Nevertheless, the former had an altered DNAme profile compared with the latter. The hypermethylated and hypomethylated sites in HCM tissues had chromosomal distributions and functional enrichment of correlated genes differing from those of their normal tissue counterparts. The GO analysis of network underlying the genes correlated with DNAme alteration and differentially expressed genes (DEGs) shows functional clusters centred on immune cell function and muscle system processes. In KEGG analysis, only the calcium signalling pathway was enriched either by the genes correlated with changes in DNAme or DEGs. The protein-protein interactions (PPI) underlying the genes altered at both the DNAme and transcriptional highlighted two important functional clusters. One of these was related to the immune response and had the estrogen receptor-encoding ESR1 gene as its node. The other cluster comprised cardiac electrophysiology-related genes. Intelliectin-1 (ITLN1), a component of the innate immune system, was transcriptionally downregulated in HCM and had a hypermethylated site within 1500 bp upstream of the ITLN1 transcription start site. Estimates of immune infiltration demonstrated a relative decline in immune cell population diversity in HCM. A combination of DNAme and transcriptome profiles may help identify and develop new therapeutic targets for HCM.

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