Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles in the hearts of WT and Bcl-xL S14A KI mice after TAC or Sham

ABSTRACT: Acute increase of blood pressure by transverse aortic constriction (TAC), pressure overload, stimulates hypertrophic signaling in the heart, which is suppressed in Bcl-xL Ser14Ala knock-in mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE199705 | GEO | 2023/08/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of left ventricular myocardium after sham or TAC surgery in BL/6N and BL/6J mice

Project description:The most commonly used inbred mouse strain, C57BL/6J, lacks a functional nicotinamide nucleotide transhydrogenase (Nnt) and thus, is protected from pressure-overload-induced oxidative stress and heart failure. We screened for differential gene expression in left ventricular myocardium after sham/transverse aortic constriction (TAC) surgery in 10-12 weeks old mice from BL/6N (functional Nnt) and BL/6J (non-functional Nnt, missense of exons 7-11) strains.

2015-06-21 | E-MTAB-2732 | biostudies-arrayexpress

Transcription profiling of mouse gene expression after transverse aortic constriction in mice: comparison of TAC vs. sham group at 2, 10 and 21 days to identify the differential expression of genes

Project description:Microarray analysis of gene expression after transverse aortic constriction in mice: comparison of TAC vs. sham group at 48 hours, 10 days, and 3 weeks.

2007-10-12 | E-GEOD-1621 | biostudies-arrayexpress

Myocardial gene expression in response to pressure overload

Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice. 10wk old male mice was subjected to transverse aortic constriction (TAC) to induce pressure overload or sham operation as control group. After 3 days, heart was removed and total RNA was extracted from apex and subjected for array analysis. Four animals in each group.

2015-07-01 | E-GEOD-61177 | biostudies-arrayexpress

Transcription profiling of hearts from FVB male mice subjected to cardiac pressure overload by transverse aortic constriction to study the quantitative relationships between gene expression and left ventricular hypertrophy

Project description:Expression profiling of hearts from FVB males subjected to cardiac pressure overload by transverse aortic constriction (TAC). TAC performed on 8-10 weeks month old males and females. Hearts examined 30 weeks after surgery.

2007-12-01 | E-GEOD-2459 | biostudies-arrayexpress

Pressure overload cardiac hypertrophy

2005-06-29 | GSE2459 | GEO

RNA-Seq analysis of mouse heart tissue

Project description:The purpose of the experiment is to assess the genes expression changes in the heart in response to transverse aortic constriction (TAC)-induced pressure overload, and to identify the genes which are involved in the pathogenesis of heart failure induced by hypertension; thereafter examining the individual gene function in the heart and discovering the novel drug targets to prevent heart failure. Wild-type C57 mice were subjected to transverse aortic constriction (TAC) for 12 weeks (sham as the control, Con). The hearts were collected and snap frozen for the following experiments.

2023-05-23 | E-MTAB-12979 | biostudies-arrayexpress

Differential expression of genes after 48 hrs, 10 d, and 3 wks of TAC

Project description:Microarray analysis of gene expression after transverse aortic constriction in mice: comparison of TAC vs. sham group at 48 hours, 10 days, and 3 weeks. Keywords: time-course

2004-07-31 | GSE1621 | GEO

Identification of differentially expressed genes in mice with chronic heart failure induced by pressure overload

Project description:To investigate the mechanism of chronic heart failure induced by pressure overload, we established an animal model in mice by transverse aortic constriction (TAC), with mice undergoing sham surgery as control.

2023-10-31 | GSE228199 | GEO

mRNA- and RISC-sequencing of mouse hearts overexpressing miR-133a

Project description:miR-133a-3p is a highly abundant cardiomyocyte-enriched microRNA whose expression is persistently decreased in response to pressure overload (or transverse aortic constriction, TAC) in mice. Overexpression of miR-133a in cardiomyocytes of mouse hearts in vivo (under the control of the Myh6 promoter) decreases pressure overload-induced apoptosis and fibrosis. In previous studies using microarray platforms, we detected numerous mRNAs whose transcript levels were altered by either or both of miR-133a overexpression and pressure overload. The data set presented here builds upon our previous study in these mice by examining mRNA-RISC associations (using Ago2-immunoprecipitated RNA) and global mRNA abundances via RNA-sequencing procedures, and tests the hypothesis that mRNAs targeted by overexpressed miR-133a are dissimilar between sham and TAC contexts. Cardiac polyadenylated RNA (mRNA) profiles were generated from nontransgenic and transgenic mouse hearts of FVB/N background, on Illumina HiSeq 2000 instruments. Male mice 8-12 weeks of age were used in these studies, and subjected to sham surgery or 1 week of pressure-overload via transverse aortic constriction (TAC). 3 nontransgenic sham, 7 transgenic sham, 5 nontransgenic TAC, 4 transgenic TAC, each with mRNA-seq and RISC-seq (mRNA-seq of Ago2 immunoprecipitate) data.

2016-01-11 | E-GEOD-65141 | biostudies-arrayexpress

expression data from Zbtb17 cKO mouse heart after pressure overload

Project description:whole gene expression analysis for ZBTB17 cKO mice after transverse aortic constriction (TAC) We used microarrays to detail the global programme of gene expression underlying hypertrophy and heart failure process upon pressure overload

2013-09-06 | GSE50638 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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