Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of pressure overload on cardiac gene expression in wild-type and CHIP(-/-) mice

ABSTRACT: Wild-type mice or mice lacking the expression of CHIP (Stub1) were subjected to either sham surgery (Sham) or trans-aortic banding (TAB). After one week, RNA was extracted from heart and run on the Agilent 4x44K gene expression array to look at differences in the cardiac transcriptional response to pressure overload-induced hypertrophy in the absence of CHIP. Four-condition experiment: WT vs. CHIP(-/-) with SHAM or TAB surgery. Biological replicates: 4 per condition.

ORGANISM(S): Mus musculus

SUBMITTER: Jonathan Schisler

PROVIDER: E-GEOD-24209 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Effect of pressure overload on cardiac gene expression in wild-type and CHIP(-/-) mice

Project description:Wild-type mice or mice lacking the expression of CHIP (Stub1) were subjected to either sham surgery (Sham) or trans-aortic banding (TAB). After one week, RNA was extracted from heart and run on the Agilent 4x44K gene expression array to look at differences in the cardiac transcriptional response to pressure overload-induced hypertrophy in the absence of CHIP.

2011-05-01 | GSE24209 | GEO

Effect of neonatal right ventricular pressure overload on gene expression and regions of open chromatin during postnatal heart development

Project description:To investigate the effect of pressure overload (PO) during postnatal right ventricular (RV) development, we established the RV PO model by conducting pulmonary artery banding (PAB) surgery on neonatal Sprague-Dawley (SD) rats. We then performed gene expression and chromatin openness profiling analysis using data obtained from RNA-seq and ATAC-seq of RV free walls from PO and sham-operated rats at postnatal day 21 (P21).

2024-05-17 | GSE210180 | GEO

Altered expression of uc.323 during aortic banding-induced cardiac hypertrophy in mice

Project description:To investigate the changes in T-UCR (transcribed ultraconserved regions) transcription during aortic banding-induced cardiac hypertrophy, we performed lncRNA microarray analysis on the hearts of mice subjected to sham or aortic banding surgery.

2019-11-30 | GSE141165 | GEO

Transcriptomic analysis of pulmonary vein under pathological pulmonary vein stenosis

Project description:We reported the RNAseq analyses of pulmonary vein tissues at the age of postnatal day 21 (P21) on SD rats with or without pulmonary vein stenosis. Pulmonary vein stenosis was induced by performing pulmonary vein banding surgery within 24 hours postnatally. RNAseq analyses of the pulmonary vein tissues was generated at P21 from 3 sham-operated rats and 3 pulmonary vein banding rats. The results revealed that there were 1124 differentially expressed genes between PAB and sham group at P7, among which 714 were upregulated and 410 were downregulated.

2024-07-10 | GSE267175 | GEO

Postnatal lung development under the influence of pulmonary hypoperfusion

Project description:We reported the RNAseq analyses of lungs tissues in neonatal SD rats with or without reduced pulmonary blood flow. Lung hypoperfution was induced by causing the supravalvular pulmonary stenosis through performing pulmonary artery banding surgery within 24 hours postnatally (P1). RNAseq analyses of the upper lobe of the right lung tissues was generated at P7 from 5 sham-operated rats and 4 pulmonary artery banding rats (1 rat dead before sample collection). The results revealed that there were 2666 differentially expressed genes between PAB and sham group at P7, among which 1255 were upregulated and 1411 were downregulated.

2023-01-18 | GSE206972 | GEO

Cardiopulmonary Phenotyping of Sex-Based Differences in a Feline Model of HFpEF

Project description:In order to better understand sex-related differences of heart failure with preserved ejection fraction (HFpEF), male and female kittens underwent aortic contriction surgery (banding) or sham surgery (normal). Slow progressive pressure overload was then compared between male and female kittens, analyzing structural and functional phenotypes. Transcriptional differences between male and female kittens were investigated via single nuclear RNA sequencing (snRNA-seq) within left ventricle tissue.

2022-09-16 | GSE184328 | GEO

Cyclosporin ameliorates right ventricular remodeling of postnatal mice with volume overload.

Project description:We reported the RNAseq analyses of right ventricular free wall of myocardium in three groups of mice（3 in each group）at postnatal day 14 (P14). The mice in volume overload (VO) group underwent an abdominal surgery by puncture from aorta to inferior vena cava at P7, mice in Sham group underwent the same surgery except for the puncture. The mice in CsA group were VO mice who were also injected with cyclosporin A(CsA) for seven days. The results revealed that there were differentially expressed genes between VO and sham group at P14, Inhibiting the immune response with CsA caused the gene expression profile of VO mice to shift towards that of sham mice.

2024-02-01 | GSE254207 | GEO

CHF1/Hey2 Promotes Physiological Hypertrophy in response to Pressure Overload

Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways.

2010-01-20 | GSE13031 | GEO

ARID-DNA interactions are essential for SWI/SNF function

Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.

2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress

Differential regulation of extracellular matrix constituents in compensated versus decompensated heart failure following pressure overload

Project description:The aim of the present study was to examine potential differences in the regulation of myocardial ECM constituents, in mice that develop hypertrophy only (ABnonHF) and in mice that develop overt heart failure (ABHF) as response to pressure overload. Seven weeks old male C57BL/6 mice were subjected to aortic banding (AB) or sham operation (sAB), with sacrifice 4 weeks after banding. Prior to sacrifice, cardiac function and geometry were evaluated by echocardiography. Animals with comparable gradients over the banded ascending aorta, comparable cardiac output and heart rate were divided into two groups: ABnonHF and ABHF. Our criterion for dividing AB animals into these two groups was based on lung weight and left atrial diameter (LAD), as an increase in these parameters most likely is due to pulmonary congestion. Heart failure (HF) was defined as an increase in lung weight and LAD defining ABnonHF as lung weight/tibia length M-bM-^IM-$ 10.5 mg/mm and LAD M-bM-^IM-$ 2.0 mm and ABHF as lung weight/tibia length M-bM-^IM-% 15 mg/mm and LAD M-bM-^IM-% 2.4 mm. Microarray screening was performed in 7 mice from each AB group and in 5 sAB mice. Sham was used as control.

2012-11-01 | E-GEOD-36074 | biostudies-arrayexpress

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