Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

50 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

SUBMITTER: Virginia Hebl

PROVIDER: E-GEOD-36961 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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. Case (n = 107)-Control (n=20) study comparing the microRNA transcriptome of cardiac tissues from patients with hypertrophic cardiomyopathy to the microRNA transcriptome of control donor cardiac tissues.

2012-09-01 | E-GEOD-36946 | biostudies-arrayexpress

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

MicroRNA Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

2012-09-01 | GSE36946 | GEO

Human Hypertrophic Cardiomyopathy mRNA Profiling.

Project description:Cardiac biopsies were obtained from hypertrophic cardiomyopathy (HCM) patients and controls and subjected to mRNA profiling.

2024-11-12 | GSE249925 | GEO

miRNA expression profiles in the serum of cats with hypertrophic cardiomyopathy compared to healthy cats

Project description:MicroRNAs negatively regulate gene expression and may serve as biomarkers for human cardiomyopathy. In the domestic cat, hypertrophic cardiomyopathy (HCM) represents the most common primary cardiomyopathy. In humans, the etiology of HCM is linked to mutations in genes of contractile muscle proteins, while in cats a clear proof for causal mutations is missing. The etiology of feline HCM is uncertain. Diagnosis is made by heart ultrasound examination and measuring the serum level of N-terminal pro B-type natriuretic peptide. The purpose of this study was to investigate whether microRNA profiles in the serum of cats with HCM are different from the profiles of healthy cats and whether specific miRNAs can be detected to serve as potential biomarkers for feline HCM or may help in understanding the etiology of this disease Blood was drawn from two groups of cats: 12 healthy cats and 11 cats suffering from hypertrophic cardiomyopathy. After clotting, samples were centrifuged and total mRNA was extracted from serum. These 23 serum samples were analyzed and the groups were compared

2015-07-22 | E-GEOD-49427 | biostudies-arrayexpress

Untargeted lipidomics of hypertrophic cardiomyopathy (part II)

Project description:Hypertrophic cardiomyopathy (HCM) is a complex disease partly explained by the effects of individual gene variants on sarcomeric protein biomechanics. At the cellular level, HCM mutations most commonly enhance force production, leading to higher energy demands. Despite significant advances in elucidating sarcomeric structure-function relationships, there is still much to be learned about the mechanisms that link altered cardiac energetics to HCM phenotypes. In this work, we test the hypothesis that changes in cardiac energetics represent a common pathophysiologic pathway in HCM.

2021-07-13 | ST001887 | MetabolomicsWorkbench

Untargeted metabolomics of hypertrophic cardiomyopathy (part I)

2021-07-13 | ST001886 | MetabolomicsWorkbench

Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

Project description:To understand the interplay between cardiomyocyte and nonmyocyte cell types in human obstructive and non-obstructive hypertrophic cardiomyopathy, single nuclei RNA-sequencing was performed on 2 unused donor hearts, 1 obstructive HCM specimen, and 6 non-obstructive HCM specimens.

2022-01-01 | GSE181764 | GEO

Base Editing Correction of a Hypertrophic Cardiomyopathy-Causing MYH7 Mutation in Human Cardiomyocytes and Humanized Mice

Project description:The most common form of genetic heart disease is hypertrophic cardiomyopathy (HCM), which is caused by mutations in cardiac sarcomeric genes and leads to abnormal heart muscle thickening. Complications of HCM include heart failure, arrhythmia, and sudden cardiac death. The dominant-negative c.1208 G>A (p.R403Q) mutation in b-myosin (MYH7) is a common and well-studied mutation that leads to increased cardiac contractility and HCM onset. Here we identify an adenine base editor (ABE) and single-guide RNA system that can efficiently correct this human pathogenic mutation with minimal off-target and bystander editing. We show that delivery of base editing components rescues pathological manifestations of HCM in iPSC-cardiomyocytes derived from HCM patients and in a humanized mouse model of HCM. Our findings demonstrate the use of base editing to treat inherited cardiac diseases and prompt the further development of ABE-based therapies to correct a variety of monogenic mutations causing cardiac disease.

2022-10-25 | GSE201755 | GEO

Alteration in Tyrosine Phosphorylation of Cardiac Proteome and EGFR Pathway Contribute to Hypertrophic Cardiomyopathy

Project description:Alterations of serine/threonine phosphorylation of the cardiac proteome are a hallmark of heart failure. However, the contribution of tyrosine phosphorylation (pTyr) to the pathogenesis of cardiac hypertrophy remains unclear. We use global mapping to discover and quantify site-specific pTyr in two cardiac hypertrophic mouse models, i.e., cardiac overexpression of ErbB2 (TgErbB2) and myosin heavy chain R403Q (R403Q-aMyHC Tg), compared to control hearts. From this, there are significant phosphoproteomic alterations in TgErbB2 mice in right ventricular cardiomyopathy, hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM) pathways. On the other hand, R403Q-aMyHC Tg mice indicated that the EGFR1 pathway is central for cardiac hypertrophy, along with angiopoietin, ErbB, growth hormone, and chemokine signaling pathways activation. Surprisingly, most myofilament proteins have downregulation of pTyr rather than upregulation. Kinase-substrate enrichment analysis (KSEA) shows a marked downregulation of MAPK pathway activity downstream of k-Ras in TgErbB2 mice and activation of EGFR, focal adhesion, PDGFR, and actin cytoskeleton pathways. In vivo ErbB2 inhibition by AG-825 decreases cardiomyocyte disarray. Serine/threonine and tyrosine phosphoproteome confirms the above-described pathways and the effectiveness of AG-825 treatment. Thus, altered pTyr may play a regulatory role in cardiac hypertrophic models.

2023-03-10 | PXD036506 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data