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

Expression data from human heart right ventricular wall

ABSTRACT: Gene expression in the right ventricle is different in control patients as compared to either idiopathic dilated cardiomyopathy or pulmonary arterial hypertension Two human hearts obtained at autopsy from each of control, pulmonary hypertension, and dilated cardiomyopathy

ORGANISM(S): Homo sapiens

SUBMITTER: James West

PROVIDER: E-GEOD-67492 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Evidence for right ventricular lipotoxicity in heritable pulmonary arterial hypertension.

Hemnes Anna R AR Brittain Evan L EL Trammell Aaron W AW Fessel Joshua P JP Austin Eric D ED Penner Niki N Maynard Karen B KB Gleaves Linda L Talati Megha M Absi Tarek T Disalvo Thomas T West James J

American journal of respiratory and critical care medicine 20140201 3

<h4>Rationale</h4>Shorter survival in heritable pulmonary arterial hypertension (HPAH), often due to BMPR2 mutation, has been described in association with impaired right ventricle (RV) compensation. HPAH animal models are insulin resistant, and cells with BMPR2 mutation have impaired fatty acid oxidation, but whether these findings affect the RV in HPAH is unknown.<h4>Objectives</h4>To test the hypothesis that BMPR2 mutation impairs RV hypertrophic responses in association with lipid deposition ...[more]

PMID: 24274756

Similar Datasets

Expression data from human heart right ventricular wall

Project description:Gene expression in the right ventricle is different in control patients as compared to either idiopathic dilated cardiomyopathy or pulmonary arterial hypertension

2015-04-02 | GSE67492 | GEO

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

Project description:Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy primarily of the right ventricle characterized through fibrofatty replacement of cardiomyocytes. The genetic etiology in ARVC patients is most commonly caused by dominant inheritance and high genetic heterogeneity. Though histological examinations of ARVC affected human myocardium reveals fibrolipomatous replacement, the molecular mechanisms leading to loss of cardiomyocytes are largely unknown. We therefore analyzed the transcriptomes of 6 ARVC specimen derived from heart transplantation candidates and compared our findings to 6 non-failing donor hearts (NF) which could not be transplanted for technical reasons. In addition, we compared our findings to 7 hearts from patients with idiopathic dilated cardiomyopathy. From each heart left (LV) and right ventricular (RV) myocardial samples were analyzed by Affymetrix HG-U133 Plus 2.0 arrays, adding up to six sample groups. Unsupervised cluster analyses of the six sample groups revealed a clear separation of NF and cardiomyopathy samples. However, in contrast to the other samples, unsupervised cluster analyses revealed no distinct expression pattern in LV and RV samples from ARVC-hearts. We further identified differentially expressed transcripts using t-tests and found transcripts separating diseased and NF ventricular myocardium. Of note, in failing myocardium only about 15-16% of the genes are commonly regulated compared to NF samples. In addition both cardiomyopathies are clearly distinct on the transcriptome level. Comparison of the expression patterns between the failing RV and LV using a paired t-test revealed a lack of major differences between LV and RV gene expression in ARVC hearts. Microarrays were used to elucidate the differences between non-failing control hearts and those, suffering from arrhythmogenic right ventricular cardiomyopathy (ARVC).

2011-11-30 | E-GEOD-29819 | biostudies-arrayexpress

WNK463 Inhibition on Right Ventricular metabolomics

Project description:We investigated the effects of WNK463 treatment on right ventricular metabolism in monocrotaline-induced pulmonary artery hypertension.

2021-07-13 | ST001869 | MetabolomicsWorkbench

Expression data from human heart

Project description:Global gene expression is altered in heart failure. This syndrome can be caused by cardiovascular diseases, including dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), hypertrophic cardiomyopathy, viral or toxic myocarditis, hypertension, and valvular diseases. We used microarrays to evaluate the impact of heart failure on human nucleocytoplasmic transport-related genes examining simultaneoulsly both dilated and ischemic human cardiomyopathies compared to normal hearts.

2013-10-17 | GSE42955 | GEO

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

2011-11-30 | GSE29819 | GEO

Right ventricular failure due to pulmonary banding

Project description:Right ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treatmed with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding. 11 pigs. Samples at the following time periods: 1) Baseline 2) Right ventricular failure 3) Treatment with modified Glenn-shunt/Control. After Right ventricular failure, pigs were divided into two groups a) Treatment with modified Glenn-shunt or b) Control group

2013-06-11 | E-GEOD-47814 | biostudies-arrayexpress

CLINICAL SYMPTOMS OF RIGHT VENTRICULAR FAILURE IN EXPERIMENTAL CHRONIC PRESSURE LOAD ARE ASSOCIATED WITH PROGRESSIVE DIASTOLIC DYSFUNCTION

Project description:Right ventricular failure (RVF) due to pressure load is a major cause of death in congenital heart diseases and pulmonary hypertension. The mechanisms of RVF are yet unknown. Research is hampered by the lack of a good RVF model. Our aim was to study the pathophysiology of RVF in a rat model of chronic pressure load. Wistar rats (n=19) were subjected to pulmonary artery banding (PAB, 1.1mm) or sham surgery (CON). All PAB rats developed RVF (reduced cardiac output, RV stroke volume, TAPSE, increased end diastolic pressure, all p<0.05 vs. CON) but clinical symptoms of RVF (inactivity, ruffled fur, dyspnea, ascites) necessitating termination ensued in a subset (5/12) of rats (RVF+) after a period of 52Â±5 days. Rats with RVF+ had significantly worse RV function and pericardial effusion and liver congestion compared to RVF rats without symptoms (all p<0.05), despite similar pressure load (p=NS RVF vs. RVF+). Chronic pulmonary artery banding invariably leads to RV failure in rats, and a subset transitions to advanced clinical RVF. RVF is characterized by enhanced contractility, progressive diastolic dysfunction and derangement of energy metabolism, thus improving diastolic function and targeting RV metabolism may be the keys to treating RVF. Total RNA optainded ( Heart) of 7 Controls ,5 RVF+ and 4 RVF samples where used for this array study

2014-12-08 | E-GEOD-46863 | biostudies-arrayexpress

Right ventricular failure due to pulmonary banding

2013-06-11 | GSE47814 | GEO

Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy: left ventricle DCM

Project description:We wanted to see whether the set of affected genes in ischemic cardiomyopathy (ICM) is the same or different as compared to dilated cardiomyopathy (DCM). To find this out, we placed the single DCM sample on the same microarray slide with the ICM samples. Analysis of microarray data with ICM samples only showed 63 affected genes, while that carried out with 2 ICM samples PLUS one DCM sample reduced this number to just four genes. From this result we conclude that ICM and DCM affect different sets of genes in ventricular myocytes. Keywords: Expression profiling by array From the associated publication: To find out whether the splice microarray results reported in Table 3 are disease-type specific, we supplemented the same splice microarray of ICM ventricular myocytes with one additional sample prepared from left ventricle of a 41-years old dilated cardiomyopathy male donor. The top-list ANOVA gene score annotation for combined altered CE&P genes in ventricular myocytes (Table 3) was reduced from 63 to just 4 genes (FXYD1 (Gfold = +2.4), HCN2 (-1.5), GLRA1 (-1.8) and GJC1 (-2.3)).

2010-06-17 | E-GEOD-17530 | biostudies-arrayexpress

Rat right ventricular proteomes after cell therapy

Project description:We utilized an animal model of RV pressure overload created by banding the pulmonary artery (PAB). Two weeks post-banding, bone marrow-derived mesenchymal stromal cells (MSCs) and 3 populations of CPCs (nCPCs, cCPCs, ES-CPCs) were delivered to the RV free wall. RV function and cellular retention were measured for four weeks post-injection, at which point hearts were extracted and the RV was excised for liquid chromatography and tandem mass spectrometry. Resulting RV proteomes were compared and analyzed using systems biology and bioinformatics.

2024-10-17 | PXD051582 | 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