Effect of knockdown of Snai1 on gene expression of EndoFP during in a mouse model of pressure overload.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE217528 | GEO | 2022/11/14
REPOSITORIES: GEO
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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
Project description:The goal of this study was to reveal SNAI1 function in angiogenesis. SNAI1 is up-regulated by VEGF stimulus. Using RNASeq method (single-ended 150-bp sequencing on Illumina Hi-seq 3000 instrument), we measured the transcriptional difference between siSNAI1 or NC-transfected HUVECs.
2019-03-04 | GSE111386 | GEO
Project description:Pressure overload (PO) leads first to cardiac hypertrophy and later to heart failure. In mice, PO leads to sex differences in cardiac morphology and function. However, early sex differences in gene regulation that precede sex differences in function have not yet been identified. To identify such changes, we developed a model of PO that is characterized by compensated hypertrophy without sex differences after 2 weeks and by heart failure with sex differences after 9 weeks. We used transverse aortic constriction (TAC) or sham-operation in male and female mice and analyzed gene expression by microarray experiments. Experiment Overall Design: The gene expression induced by pressure overload in female and male mice in comparison to sham operated control mice was investigated. For each of these four conditions four biological replicates were performed and the individual samples were hybridized seperately on Affymetrix RAE 430A GeneChip Arrays.
2008-06-15 | E-GEOD-6970 | biostudies-arrayexpress
Project description:Effect of knockdown of Snai1 on gene expression of EndoFP during in a mouse model of pressure overload.
| PRJNA899476 | ENA
Project description:BACKGROUND: Heart failure (HF) is one of the leading causes of mortality worldwide. Extracellular vesicles (EVs) including small EVs, or exosomes and their molecular cargo are known to modulate cell to cell communication during multiple cardiac diseases. However, the role of systemic EV biogenesis inhibition in the models of HF is not well documented and remains unclear. METHODS: We investigated the role of circulating exosomes during cardiac dysfunction and remodeling in a mouse transverse aortic constriction (TAC) model of HF. Importantly, we investigate the efficacy of Tipifarnib (Tip), a recently identified exosome biogenesis inhibitor that targets the critical proteins (Rab27a, nSmase2 and Alix) involved in exosome biogenesis for this mouse model of HF. In this study, 10-week-old male mice underwent TAC surgery, were randomly assigned to groups with and without Tip treatment (10 mg/kg three times/week) and monitored for 8 weeks and a comprehensive assessment was conducted through performed echocardiographic, histological, and biochemical studies. RESULTS: TAC significantly elevated circulating plasma exosomes and markedly increased cardiac left ventricular (LV) dysfunction, cardiac hypertrophy, and fibrosis. Furthermore, injection of plasma exosomes from TAC mice induced LV dysfunction and cardiomyocyte hypertrophy in uninjured mice without TAC. On the contrary, treatment of Tip in TAC mice reduced circulating exosomes to baseline and remarkably improved LV functions, hypertrophy, and fibrosis. Tip treatment also drastically altered the miRNA profile of circulating post-TAC exosomes, including miR331-5p which was highly downregulated both in TAC circulating exosomes and in TAC cardiac tissue. Mechanistically, miR331-5p is crucial for inhibiting fibroblast-to-myofibroblast transition by targeting HOXC8, a critical regulator of fibrosis. Tipifarnib treatment in TAC mice upregulated the expression of miR331-5p that acts as potent repressor for one of the fibrotic mechanisms mediated by HOXC8. CONCLUSIONS: Our study underscores the pathological role of exosomes in HF and fibrosis in response to pressure overload. Tipifarnib mediated inhibition of exosome biogenesis and cargo sorting may serve as a viable strategy to prevent progressive cardiac remodeling to HF.
2024-05-07 | GSE266185 | GEO
Project description:Trans-aortic constriction (TAC) is a widely used murine model to study pressure overload-induced cardiac hypertrophy and heart failure. Despite its high prevalence during aortic stenosis or chronic arterial hypertension, the global alterations in cardiac proteome and phospho-proteome dynamics following TAC remain incompletely characterised. Here, we present a comprehensive database of detailing the phospho-proteomic signature of the mouse heart one day and seven days after TAC. Utilising proteomic and phosphor-proteomic analyses, we identified and quantified thousands of proteins and phosphorylation sites, revealing hundreds of differential phosphorylation events that are significantly altered in the cardiac response to pressure overload. Our analysis highlights significant changes in pathways related to hypertrophic signalling, metabolic remodelling, contractile function, and the stress response. We also present proteomic data from the main cardiac cell types (endothelial cells, fibroblasts and cardiomyocytes) after TAC to reveal the cellular localization of the detected phosphoproteins. The dataset offers insights into temporal and site-specific phosphorylation events, facilitating the potential discovery of novel therapeutic targets and biomarkers. By making this resource publicly available, we aim to enable further exploration of the molecular basis of cardiac remodelling and advance translational research in heart failure.
2025-05-26 | PXD061784 | Pride
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
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 16 male mice, 4 mice per group, were selected at 8-10 weeks old for 4 weeks of TAC and SHAM and collected samples for RNA extraction and hybridization on Affymetrix microarrays. We included corresponding controls.
2013-09-06 | E-GEOD-50638 | biostudies-arrayexpress
Project description:This study employs a factorial design to delineate the combinatorial effects of cardiac-specific conditional gene knockout and pressure overload-induced cardiac hypertrophy via transverse aortic constriction (TAC). Four experimental cohorts were established: (1) conditional knockout mice subjected to TAC (CKO_TAC), (2) knockout controls with Sham surgery (CKO_Sham), (3) floxed control mice receiving TAC (ff_TAC), and (4) floxed Sham-operated controls (ff_Sham). Following a 5-week pressure overload (TAC), myocardial tissue underwent parallel proteomic and phosphoproteomic profiling using TMT-based quantitative mass spectrometry. This dual-omics approach specifically interrogates: (a) the intrinsic genetic perturbation effect (CKO_ Sham vs ff_ Sham), (b) the pure pressure overload response (ff_TAC vs ff_Sham), and critically, (c) the genotype-by-environment interaction through synergistic/antagonistic divergence between observed versus predicted additive effects in CKO_TAC relative to genetic and surgical controls. Phosphoproteomic data further resolve signaling pathway dynamics underlying phenotypic modulation.
2025-09-25 | PXD067213 | Pride
Project description:SNAI1 knockdown under VEGF stimulus in HUVECs
| PRJNA436851 | ENA