Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq Identifies Novel Myocardial Gene Expression Signatures of Heart Failure [microarray]

ABSTRACT: We have utilized the RNA-Seq technology to identify genes with distinct expression patterns between failing and non-failing hearts. In an era of next-generation sequencing studies, our study demonstrates how knowledge gained from a small set of samples with accurately measured gene expressions using RNA-Seq can be leveraged as a complementary strategy to discern the genetics of complex disorders. Identify the signature genes based on RNA-seq come from six Heart Failure and healthy individuals. Validation is based on Affymetrix microarray of a total of 313 individuals with/without Heart Failure.

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Morley

PROVIDER: E-GEOD-57338 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

miR-302-367 regulates cardiomycyte proliferation and differentiation during development

Project description:To define the role of miR-302-367 cluster in cardiac development, we overexpressed miR-302-367 cluster in mouse heart by using R26R-miR-302-367; Nkx2.5-Cre mice. This data set contains the microarrays examining gene expression in the hearts of R26R-miR-302-367; Nkx2.5-Cre mice at postnatal day 14. We overexpressed miR-302-367 cluster in developing mouse heart using Nkx2.5-Cre mouse line

2015-01-01 | E-GEOD-54988 | biostudies-arrayexpress

E-MTAB-9361

Project description:Heart RNA-seq of therapeutic RBM20 antisense oligonucleotide (ASO) treatment in a mouse model of heart failure with preserved ejection fraction (HFpEF)

2020-07-22 | E-MTAB-9361 | ExpressionAtlas

E-GEOD-36761

Project description:RNA-seq of heart right ventricle from 22 patients with Tetralogy of Fallot and healthy individuals

2025-01-24 | E-GEOD-36761 | ExpressionAtlas

E-TABM-418

Project description:Transcription profiling of spontaneously hypertensive heart failure rats (SHHF) and a reference strain to identify heart failure susceptibility genes

2015-11-02 | E-TABM-418 | ExpressionAtlas

Affymetrix array of postnatal day 4 mouse atria exposed to room air or hyperoxia

Project description:It is unclear why preterm birth increases risk of cardiovascular disease later in life. Studies in mice indicate excess oxygen typically used to treat preterm infants causes pulmonary hypertension, cardiac failure, and shortens lifespan. We previously reported neonatal hyperoxia causes pulmonary hypertension in aged mice as defined pathologically by pulmonary capillary rarefaction, dilation of pulmonary arterioles and veins, right ventricular hypertrophy, and reduced lifespan. These changes were preceded by a pronounced growth inhibition of cardiomyocytes lining the pulmonary vein and extending into the left atria, resulting in diastolic heart failure as the mice aged. To identify transcriptional changes by which hyperoxia suppresses proliferation of these cardiomyocytes, newborn mice were exposed to room air or 100% oxygen between birth and postnatal day 4. RNA was then isolated from atria of 3 room air and 4 hyperoxia-exposed mice and used to probe Affymetrix mouse array 430 versus 2.0

2021-02-23 | E-MTAB-9008 | biostudies-arrayexpress

Left ventricular samples from humans with ischemic heart failure and non-failing controls

Project description:LCMS files from tryptic digests of ~1-4 mg piece of heart ventricular tissue from human with ischemic heart failure and non-failing controls. Specimen number correspond to .raw files as follows: Ischemic Heart failure - 54687.1; HF_1_phos.raw 53148.1; HF_2_phos.raw 53589.2; HF_3_phos.raw 54146.1; HF_4_phos.raw 52935.1; HF_5_phos.raw Non-failing - 52941.1; NHF_1_phos.raw 52777.1; NHF_2_phos.raw 53019.2; NHF_3_phos.raw 53058.1; NHF_4_phos.raw 52621.1; NHF_5_phos.raw

2022-12-07 | MSV000090858 | MassIVE

Genome-wide maps of H3K9me3 and H3K4me3 state in failing heart with or without chaetocin in animal model

Project description:Epigenetic status has been linked to cardiac hypertrophy and heart failure. Histone deacetylase inhibitors are promising drugs for preventing cardiac remodeling. We previously demonstrated very different patterns of histone H3 lysine 9 trimethylation (H3K9me3) and histone H3 lysine 4 trimethylation (H3K4me3) in failing hearts compared to control hearts in both animal models and clinical heart specimens. Here, we focused on a heart failure-specific histone modification, H3K9me3, and investigated the prognostic efficacy of administering a histone H3K9 methyltransferase inhibitor, chaetocin, to Dahl salt-sensitive rats, an animal model of heart failure. Chaetocin delayed the timing of transition from cardiac hypertrophy to heart failure, and prolonged survival in this animal model. Mitochondrial dysfunction was improved with inhibitor use in the failing heart. ChIP-seq analysis demonstrated that heart failure caused an increase in H3K9me3 alignments in thousands of repetitive elements, including regions neighboring mitochondrial genes, and a corresponding reduction of this effect with inhibitor use. However, at 35 loci, heart failure was conversely associated with a reduction in H3K9me3 alignments, and inhibitor use reversed this effect. These data suggest that excessive heterochromatinization of repetitive elements in the failing heart might impair pumping function with mitochondrial gene silencing. H3K9 methyltransferase inhibitors may be a promising novel therapy for chronic heart failure.

2015-05-31 | GSE69194 | GEO

Functional Roles of Hdac1/2 in lung development

Project description:Hdac1/2 are important epigenetic factors, yet their functional roles in specific tissues inluding lung is not determined. We used the conditional knockout model of Hdac1/2 to determine their roles in lung development. To explore the genes that are regulated by Hdac1/2 during lung development, we performed microarray analysis of Shhcre control and Hdac1/2DKO lungs at E11.5 embryos.

2013-12-31 | E-GEOD-39946 | biostudies-arrayexpress

Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

2015-02-04 | E-GEOD-60660 | biostudies-arrayexpress

Characterization of proteomic changes in human heart failure

Project description:The microtubule (MT) cytoskeleton can provide a mechanical resistance that can impede the motion of contracting cardiomyocytes. Yet a role of the MT network in human heart failure is unexplored. Here we utilize mass spectrometry to characterize changes to the cytoskeleton in human heart failure. Proteomic analysis of left ventricle tissue reveals a consistent upregulation and stabilization of intermediate filaments and MTs in human heart failure. This dataset includes left ventricular (LV) myocardium from 34 human hearts – either non-failing (NF) or failing hearts. NF hearts are subdivided into normal or compensated hypertrophy (cHyp), while failing hearts are subdivided into ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), and hypertrophic cardiomyopathy with preserved or reduced ejection fraction (HCMpEF and HCMrEF, respectively). Further details on patient classification and in vivo parameters on each heart are listed in sample details.txt.

2018-06-06 | PXD008934 | 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