Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

52 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of H11 Kinase/Hsp22 deletion in response to cardiac stress

ABSTRACT: The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress. We used microarray to examine differential gene expression by Hsp22 deletion at baseline and 3-day pressure overload. Left ventricles from wild type and Hsp22 knockout mice were selected from basal condition (each, n=3) and TAC surgery (each, n=4).

ORGANISM(S): Mus musculus

SUBMITTER: Jiyeon Park

PROVIDER: E-GEOD-24489 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Effect of H11 Kinase/Hsp22 deletion in response to cardiac stress

Project description:The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress.

2010-12-31 | GSE24489 | GEO

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

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

Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy. We applied TAC to wild type and MAFbx KO mice, and extracted total RNA one week after the surgery. The gene expression profiles were examined by Affymetrix Mouse Gene ST Array.

2011-05-01 | E-GEOD-24372 | biostudies-arrayexpress

Myocardial gene expression in response to pressure overload

2015-07-01 | GSE61177 | GEO

Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

2011-05-01 | GSE24372 | GEO

Ro5-4864, a Ligand of the Mitochondrial Translocator Protein, Protects Against Heart Failure in Mice

Project description:The 18-kDa mitochondrial translocator protein (TSPO), likely through its interaction with the voltage-dependent anion channel (VDAC), has been shown to modulate mitochondrial function and the cardiac response to pressure overload. We have previously shown that conditional knockout of TSPO limited the development of heart failure in the murine model of transverse aortic constriction (TAC). In this study, we tested the hypothesis that similar protection could be achieved by a ligand of TSPO, Ro5-4864 (Ro5), in in-vivo animal model of pressure-overload induced heart failure. To elucidate mechanisms, we performed proteomic and western blot analysis of cardiac tissue after 8 weeks of TAC in mice treated and untreated with Ro5.

2024-10-15 | MSV000096098 | MassIVE

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

Project description: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.

2023-08-10 | GSE199705 | GEO

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