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PROVIDER: PRJDB20132 | ENA |
REPOSITORIES: ENA
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Project description:The molecular mechanisms of progressive right heart failure are incompletely understood. We systematically examined transcriptomic changes occurring over months in isolated cardiomyocytes or whole heart tissues from failing right and left ventricles in rat models of pulmonary artery (PAB) or aortic banding (AOB). Detailed bioinformatics analyses resulted in the identification of gene signatures, protein, and transcription factor networks specific to ventricles and compensated or decompensated disease states. Proteomic and RNA-FISH analyses confirmed PAB-mediated regulation of key genes (including proenkephalin) and revealed spatially heterogeneous mRNA expression in the heart. Intersection of rat PAB-specific gene sets with transcriptome data sets from human patients with chronic thromboembolic pulmonary hypertension led to the identification of more than 50 genes whose expression levels correlated with the severity of right heart disease, including multiple matrix-regulating and secreted factors. These data define a conserved, differentially regulated genetic network associated with right heart failure in rats and humans
2024-04-11 | PXD047022 | Pride
Project description:Heart failure is among the leading causes of death globally. Ventricular failure progresses through a hypertrophic compensatory phase followed by failure of the ventricle function through rapid decompensation. In order to unravel right heart specific mechanisms of disease, rat animal models were established that (i) reflect the slowly progressive mode of compensation / decompensation and (ii) allow comparative analyses of left versus right heart failure in the same experimental set up. Differential gene expression analysis was performed for all three treatment groups (sham, AOB, PAB), at both time points (compensation, decompensation) and for both ventricles as well as the septum
2024-04-15 | GSE216264 | GEO
Project description:Proteomic analysis of the changes in kidney upon chronic heart failure in a rat model. Heart failure develops due to surgically created aorto-venoufistula.
2018-09-24 | PXD009296 | Pride
Project description:Heart failure is among the leading causes of death globally. Ventricular failure progresses through a hypertrophic compensatory phase followed by failure of the ventricle function through rapid decompensation. In order to unravel right heart specific mechanisms of disease, rat animal models were established that (i) reflect the slowly progressive mode of compensation / decompensation and (ii) allow comparative analyses of left versus right heart failure in the same experimental set up. Non-restrictive clips around the pulmonary artery (pulmonary artery banding, PAB) or the aorta (aortic banding, AOB) were surgically implanted into weanling rats. Upon animal growth the clips become increasingly constrictive, leading to a compensatory, hypertrophic state at around 6 weeks and heart failure at 21 (PAB) or 24 weeks (AOB). Disease progression was monitored functionally and by sonography. Differential gene expression analysis was performed for all three treatment groups (sham, AOB, PAB), at both time points (compensation, decompensation) and for both ventricles.
2024-04-15 | GSE216263 | GEO
Project description:In our chemogenetic rat heart failure model, LV and RV transcriptomic analysis was performed by RNA-seq
2022-02-06 | GSE195913 | GEO
Project description:We aimed to identify gene variants associated with heart failure by using a rat model of the human disease. We performed invasive cardiac hemodynamic measurements in F2 crosses between spontaneously hypertensive heart failure rats (SHHF) and reference strains. We combined linkage analyses with genome-wide expression profiling .
2008-09-01 | E-TABM-418 | biostudies-arrayexpress
Project description:Epigenetic status has been linked to cardiac hypertrophy and heart failure. Histone deacetylase inhibitors are promising drugs for preventing cardiac remodeling. We previously demonstrated very different patterns of histone H3 lysine 9 trimethylation (H3K9me3) and histone H3 lysine 4 trimethylation (H3K4me3) in failing hearts compared to control hearts in both animal models and clinical heart specimens. Here, we focused on a heart failure-specific histone modification, H3K9me3, and investigated the prognostic efficacy of administering a histone H3K9 methyltransferase inhibitor, chaetocin, to Dahl salt-sensitive rats, an animal model of heart failure. Chaetocin delayed the timing of transition from cardiac hypertrophy to heart failure, and prolonged survival in this animal model. Mitochondrial dysfunction was improved with inhibitor use in the failing heart. ChIP-seq analysis demonstrated that heart failure caused an increase in H3K9me3 alignments in thousands of repetitive elements, including regions neighboring mitochondrial genes, and a corresponding reduction of this effect with inhibitor use. However, at 35 loci, heart failure was conversely associated with a reduction in H3K9me3 alignments, and inhibitor use reversed this effect. These data suggest that excessive heterochromatinization of repetitive elements in the failing heart might impair pumping function with mitochondrial gene silencing. H3K9 methyltransferase inhibitors may be a promising novel therapy for chronic heart failure.
2015-05-31 | GSE69194 | GEO
Project description:Array-based CGH analysis of developmental disorder (CBX127)
| PRJDB20093 | ENA
Project description:Full Title: Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat: Structure, Function, and Transcript Analysis Gene expression changes and left ventricular remodeling associated with the transition to systolic heart failure (HF) were determined in the spontaneously hypertensive rat (SHR). By combining transcriptomics of left ventricles from six SHR with HF with changes in function and structure we aimed to better understand the molecular events underlying the onset of systolic HF compared to six age-matched, SHR with compensated hypertrophy. Left ventricle (LV) ejection fraction was depressed (82±4 to 52±3 %) in compensated vs. failing animals. Systolic blood pressure decreased and LV end-diastolic and systolic volume increased with HF. Failing SHR hearts also demonstrated increases in left and right ventricular mass relative to non-failing SHRs.  LV papillary muscle force development and shortening velocity decreased, β-adrenergic responsiveness was depressed, myocardial stiffness and myocardial fibrosis increased with HF relative to non-failing animals. Initial micro-array analysis revealed that 1,431 transcripts were differentially expressed with HF compared to non-failing SHR (p<0.05). Of the identified transcripts, lipopolysaccharide binding protein, the most highly expressed transcript with HF, was negatively correlated to myocardial force while elevated expression of the collagen cross-linking enzyme lysyl oxidase correlated positively with muscle stiffness. Besides these individual transcripts, gene set enrichment analysis (GSEA) identified multiple enriched pathways with HF, most prominent of the altered signaling pathways involved TGF-β and insulin signaling. GESA analysis additionally identified altered gene sets involving inflammation, oxidative stress, cell degradation and cell death, among others (all p<0.01). In contrast to diastolic HF where few transcripts are reported to be altered, our data indicate multiple genes and pathways involved in a variety of biological processes characterize the onset of systolic HF, consistent with many functional and structural changes present in the failing hypertensive heart. Comprehensive gene expression profiling of heart failure Rat model vs control.
2010-02-21 | E-GEOD-19210 | biostudies-arrayexpress
Project description:Heart failure is a leading cause of death in US. Hypertension is one of the most important risk factor of heart failure. In the presence of high blood pressure, the heart manifests hypertrophic growth to ameliorate ventricular wall stress. This once adaptive response may progress into decompensation and heart failure. The precise mechanisms governing this transition remain elusive. Here, we aimed to identify novel signaling pathways in cardiac hypertrophic growth. Primary neonatal rat ventricular myocytes (NRVMs) were isolated from 1-2 days old rats and treated with phenylephrine or IGF-1. Total RNA was isolated for RNA-seq analysis.
2020-11-16 | GSE153763 | GEO