Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of p53 on cardiac hypertrophy and its mechanism

ABSTRACT: This study aims to investigate the role of p53 in cardiac hypertrophy. We constructed a cardiac hypertrophy model using both wild-type (WT) and p53 knockout (KO) mice subjected to transverse aortic constriction (TAC). After six weeks, cardiac tissues from the hypertrophied left ventricle were collected from both mouse groups. These tissues were analyzed using single-cell RNA sequencing to observe differential gene expression in hypertrophied cardiomyocytes and identify the key pathways enriched in these cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE289882 | GEO | 2025/02/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE289882_RAW.tar	Raw
	filelist.txt	Txt

Items per page:

1 - 3 of 3

Similar Datasets

Ribo-seq of murine left ventricular tissues

Project description:To evaluate the genome-wide changes in gene translational efficiency during the development of heart failure, we performed transverse aortic constriction(TAC) in male C57BL/6 mice. According to our experience, hypertrophy of the left ventricle was observed 2 weeks after TAC. Cardiac decompensation was observed at 5 weeks. We collected left ventricular tissues at 0, 2, 5 weeks after TAC and then performed ribosome footprinting and sequencing.

2023-10-31 | E-MTAB-8552 | biostudies-arrayexpress

Aberrantly expressed microRNAs participate in cardiac hypertrophy by modulating multiple signaling pathways

Project description:The expressed difference of aberrant microRNAs was successfully constructed through detection in a rat model of cardiac hypertrophy,which had been subjected to transverse aortic constriction surgery. In this study, the expressed situation of aberrant microRNAs was measured in a rat model of cardiac hypertrophy. The survey was contucted in the rats 5, 10, 15 or 20 days later after TAC surgery.

2012-06-08 | E-GEOD-38599 | biostudies-arrayexpress

Gene and exon expression change in cardiac hypertrophy with pressure overload

2011-05-01 | GSE24242 | GEO

Gene and exon expression change in cardiac hypertrophy with pressure overload

Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).

2011-05-01 | E-GEOD-24242 | biostudies-arrayexpress

OTUD1 aggravates pathological cardiac hypertrophy through activation of PGAM5-ASK1 signaling pathways

Project description:Deubiquitinating enzymes have gained more and more attention in the field of pathological cardiac hypertrophy. In this study, we explored the role of a deubiquitinase, OTUD1, in the transverse aortic constriction (TAC) induced cardiac hypertrophy. We found the upregulation of OTUD1 in heart tissues of TAC mice. OTUD1 overexpression promoted cardiac hypertrophy, cardiac fibrosis and apoptosis. Conversely, OTUD1 depletion alleviated these pathological changes both in vivo and in vitro. Mechanistically, ASK1 was identified as one substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. Interestingly, OTUD1 didn’t deubiquitinate ASK1, but increased the phosphorylation level of ASK1 during the process of cardiac hypertrophy. We found that PGAM5, the upper stream regulator of ASK1, was stabilized by OTUD1 in a K63 ubiquitin chain dependent way, which reminded us OTUD1 increased the phosphorylation level of ASK1 by deubiquitinating PGAM5. This study identified the OTUD1-ASK1 axis as a potential therapeutic target for pathological cardiac hypertrophy.

2023-09-05 | GSE241809 | GEO

Transcriptome analysis of mouse cardiac hypertrophy

Project description:RNA-Seq analysis of mouse cardiac transcriptome. Transverse aortic contraction was used to induce cardiac hypertrophy (TAC). To compare wild type and physiological cardiac hypertrophy 'Sendetary' (feeding mouse during 4 weeks) and 'Swim (exercise training to induce the cardiac hypertrophy) samples were analysed.

2012-05-11 | E-MTAB-727 | 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

Loss of ADAM15 exacerbates transition to decompensated hypertrophy through activation of calcineurin pathway

Project description:Label-free quantification of cardiac tissue following transverse aortic constriction (TAC) in a WT and ADAM15-/- mouse model.

2022-03-07 | MSV000089016 | MassIVE

Pressure overload cardiac 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. Keywords: ordered

2005-06-29 | GSE2459 | GEO

Role of SIRT5 in Inhibition of Myocardial Hypertrophy

Project description:SIRT5 is one of the seven members of the NAD+-dependent sirtuin family of protein deacylase that is mainly present in mitochondria and regulates metabolism. In heart, SIRT5 is highly expressed and responsible for succinylation on metabolic enzymes. Although the role of SIRT5 in maintaining cardiac homeostasis under physiological stress and few potential substrates of SIRT5 have been preliminarily revealed, the regulatory network and key cellular signaling pathways involving SIRT5 in myocardial hypertrophy remain largely unknown. Here, we used an established murine model of pressure overload-induced myocardial hypertrophy caused by transverse aortic constriction (TAC) to outline the network and pathway involving SIRT5 in cardiac stress responses. Remarkably, SIRT5 KO mice had enhanced myocardial hypertrophy after TAC surgery compared with wild-type mice.

2024-10-05 | GSE186985 | 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