Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

ABSTRACT: To investigate the role of CITED4 in a murine model of cardiac pressure overload

ORGANISM(S): Mus musculus

PROVIDER: GSE150293 | GEO | 2020/05/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

Project description:Rationale: Cardiac CITED4 is induced by exercise and is sufficient to cause physiological hypertrophy and mitigate adverse ventricular remodeling after ischemic injury. However, the role of endogenous CITED4 in response to physiological or pathological stress is unknown. Objective: To investigate the role of CITED4 in murine models of exercise and pressure overload. Methods and Results: We generated cardiomyocyte-specific CITED4 knockout mice (C4KO) and subjected them to an intensive swim exercise protocol as well as transverse aortic constriction (TAC). Echocardiography, western blotting, qPCR, immunohistochemistry, immunofluorescence, and transcriptional profiling for mRNA and miRNA expression were performed. Cellular crosstalk was investigated in vitro. CITED4 deletion in cardiomyocytes did not affect baseline cardiac size or function in young adult mice. C4KO mice developed modest cardiac dysfunction and dilation in response to exercise. After TAC, C4KOs developed severe heart failure with left ventricular dilation, impaired cardiomyocyte growth accompanied by reduced mammalian target of rapamycin (mTOR) activity and maladaptive cardiac remodeling with increased apoptosis, autophagy, and impaired mitochondrial signaling. Interstitial fibrosis was markedly increased in C4KO hearts after TAC. RNAseq revealed induction of a pro-fibrotic miRNA network. miR30d was decreased in C4KO hearts after TAC and mediated crosstalk between cardiomyocytes and fibroblasts to modulate fibrosis. miR30d inhibition was sufficient to increase cardiac dysfunction and fibrosis after TAC. Conclusions: CITED4 protects against pathological cardiac remodeling by regulating mTOR activity and a network of miRNAs mediating cardiomyocyte to fibroblast crosstalk. Our findings highlight the importance of CITED4 in response to both physiological and pathological stimuli.

2020-04-30 | GSE149584 | GEO

Proteome wide screening for ubiquitination, ISGylation and NEDDylation sites in wildtype and ISG15 knockout mouse hearts after transverse aortic constriction

Project description:Hearts(left ventricles) were harvested from control wildtype and ISG15 knockout mice and wildtype and ISG15 knockout mice 4 weeks after pressure overload induced by transverse aortic constriction. Nano LC-MS/MS analysis was performedon left ventricle tissue following protein extraction, trypsin digestion, peptide desalting, anti K-e-GG enrichment.

2023-05-10 | PXD032267 | Pride

miRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

Project description:miRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

| PRJNA631727 | ENA

Gene expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

Project description:Gene expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

| PRJNA629314 | ENA

mRNA Expression data from transverse aortic constriction hearts (cardiovascular disease) and sham hearts in mice.

Project description:We used transverse aortic constraction pressure overload hypertrophy mouse hearts as a model of cardiovascular disease to study the genetic changes between TAC and SHAM (normal) mouse hearts and over 1 circadian cycle (24h). This is one approach to identify diurnal genetic biomarkers of cardiovascular disease. The micorarray approach allowed to see the gene expression in all genes in cardiovascular disease and sham hearts. There are 36 samples of cardiovascular disease (TAC) and normal SHAM hearts. For TAC: There were 3 mice sacrificed at each time point as biological replicates, for 6 timepoints over 24 hrs. For SHAM: There were 3 mice sacrificed at each time point as biological replicates, for 6 timepoints over 24 hrs.

2013-03-15 | E-GEOD-36407 | biostudies-arrayexpress

mRNA Expression data from transverse aortic constriction hearts (cardiovascular disease) and sham hearts in mice.

2013-03-15 | GSE36407 | GEO

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

Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

Project description:A number of mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, protein synthesis, metabolism,autophagy, oxidative stress and inﬂammation. These mediators including nuclear transcription factor, microRNAs and long noncoding RNAs. However, the gene expression profiles signaling pathways in the pressure overload-induced cardiac hypertrophy remain unknown. All mice were randomly undertaken sham surgery or TAC for 2 weeks. Hearts were harvested 2 weeks following TAC and performed to further analysis.

2021-08-24 | GSE127954 | GEO

Expression data from murine cardiac fibroblasts and endothelial cells following Transverse Aortic Constriction

Project description:Accumulation of activated cardiac fibroblasts plays a key role in heart failure progression. These cells deposit excessive extracellular matrix that leads to mechanical stiffness, myocyte uncoupling and ischemia. To investigate whether two developmentally distinct cardiac fibroblast populations exhibit distinct expression profiles in response to cardiac injury, and therefore might necessitate distinct therapeutic targeting, we performed microarray analysis on FACS sorted cells. Tie2cre lineage traced CFs, non Tie2cre lineage traced cardiac fibroblasts and endothelial cells were isolated from left ventricle of SHAM operated and banded hearts at the onset of fibrosis, one week after surgery. We used microarrays to detail the global programme of gene expression in cardiac fibroblasts and endothelium following pressure overload. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 TAC operated adult male Black Swiss mice. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 Transaortic Constriction (TAC) operated adult male Black Swiss mice for RNA extraction and Affymetrix microarray analysis. Hypertrophy in TAC animals, an lack of hypertrophy in SHAM operated animals, was evaluated by hemodynamic measurements before surgery and one week after surgery. Cells were isolated one week after surgery.

2014-05-19 | E-GEOD-45820 | biostudies-arrayexpress

Expression data from murine cardiac fibroblasts and endothelial cells following Transverse Aortic Constriction

2014-05-19 | GSE45820 | GEO