Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of Endothelial and Mesenchymal cell transitions in heart failure and recovery thereafter

ABSTRACT: Role of Endothelial and Mesenchymal cell transitions in heart failure and recovery thereafter

PROVIDER: PRJNA676178 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13037771.fastq.gz	Fastqsanger.gz
	SRR13037771_1.fastq.gz	Fastqsanger.gz
	SRR13037771_2.fastq.gz	Fastqsanger.gz
	SRR13037772.fastq.gz	Fastqsanger.gz
	SRR13037772_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 87

Similar Datasets

Role of Endothelial and Mesenchymal cell transitions in heart failure and recovery thereafter

Project description:Role of Endothelial and Mesenchymal cell transitions in heart failure and recovery thereafter

2021-07-01 | GSE161309 | GEO

Defining cardiac functional recovery in end-stage heart failure at single cell resolution

Project description:Recovery of cardiac function is the ultimate goal of heart failure therapy yet is infrequently observed and remains poorly understood. Here we characterize the cellular landscape and predictors of cardiac recovery by performing single nucleus RNA-sequencing (snRNA-seq) from 40 heart failure patients who recovered LV systolic function following left ventricular assist device (LVAD) implantation and patients who did not recover and non-diseased donors. We identify cell type specific transcriptional signatures of recovery in all cell types, most prominently in macrophages and fibroblasts. Pro-inflammatory macrophages and inflammatory signalling in fibroblasts were negative predictors of recovery, while downregulation of RUNX1 transcriptional activity in macrophages and fibroblasts was associated with recovery. In silico perturbation of RUNX1 in macrophages and fibroblasts recapitulated the transcriptional state of recovery. In a mouse model of cardiac recovery mediated by BRD4 inhibition, we observed a decrease in macrophage and fibroblast Runx1 expression, diminished chromatin accessibility within a Runx1 intronic peak, and acquisition of human recovery signatures. These findings suggest that cardiac recovery is a unique biological state and identify RUNX1 as a possible therapeutic target to facilitate cardiac recovery.

2023-02-28 | GSE226314 | GEO

Role of Endothelial and Mesenchymal Cell Transitions in Heart Failure and Recovery Thereafter.

Project description:Background: Mechanisms of myocardial recovery are not well elucidated. Methods: 3-month-old C57/BL6 mice were treated with Angiotensin-II infusion and N (w)-nitro-L-arginine methyl ester in drinking water to induce HF at 5 weeks. These agents were discontinued, and animals studied with echocardiographic, histological and genetic assessment every 2 weeks until week 19. mRNA was extracted from these samples and human pre-post LVAD samples. Results: Histologic and echo characteristics showed progressive worsening of cardiac function by week 5 and normalization by week 19 accompanied by normalization of the transcriptional profile. Expression of 1,350 genes were upregulated and 3,050 genes down regulated in HF compared to controls; during recovery, this altered gene expression was largely reversed. We focused on genes whose expression was altered during HF but reverted to control levels by Week 19. A gene ontology (GO) analysis of this cohort of genes implicated pathways involved in EndoMT and MEndoT. The cohort of genes that were differentially regulated in heart failure recovery in the murine model, were similarly regulated in human myocardial samples obtained pre- and post-placement of a left ventricular assist device (LVAD). Human end stage HF myocardial samples showed cells with dual expressed VE-Cadherin and FSP-1 consistent with cell fate transition. Furthermore, we observed a reduction in fibrosis, and an increase in endothelial cell density, in myocardial samples pre- and post-LVAD. Conclusions: Cell fate transitions between endothelial and mesenchymal types contribute to the pathophysiology of heart failure followed by recovery.

| S-EPMC7874124 | biostudies-literature

INO80 and heart failure.

Project description:INO80 and heart failure.

| PRJNA1002579 | ENA

Defining cardiac functional recovery in end-stage heart failure at single cell resolution

Project description:Defining cardiac functional recovery in end-stage heart failure at single cell resolution

| PRJNA939636 | ENA

Heart Failure with Preserved Ejection Fraction - Mouse Heart and Lung Tissue & Comorbidities

Project description:FASILOX analysis of heart and lung tissue form mice with heart failure with preserved ejection fraction and several comorbidities.

2024-10-02 | PXD056447 | JPOST Repository

Heart failure patients' peripheral blood mononuclear cell gene expression profiles before mechanical circulatory support

Project description:This data represents whole transcriptome total RNA gene expression profiles of peripheral blood mononuclear cells collected from 29 advanced heart failure patients on the day before undergoing mechanical circulatory support surgery. Keywords = Advanced Heart Failure. Keywords = Mechanical Circulatory Support. Keywords = Biological Age. Keywords = PBMC. Keywords = Immune Response. Keywords = Peripheral Blood. Keywords =Organ Function. Keywords = Recovery. Organism: Homo sapiens. Type: Expression profiling by array. Platforms: Illumina HiSeq 2500.

2018-02-13 | GSE104423 | GEO

Cardiomayocyte specific translating RNA sequencing from mice in heart failure

Project description:Mammalian organs vary widely in regenerative capacity, and poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in in considerable mortality and early demise. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. We show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischemic heart failure after myocardial infarction induced a reparative genetic program characterized by increased scar border vascularity, reduced fibrosis, and recovery of pumping function to that of sham-operated controls. To isolate cardiomyocyte specific translating mRNA we used TRAP (translating ribosomal affinity purification) followed by RNA sequencing. Hippo deficient cardiomyocytes had increased expression of proliferative, and stress response genes. Interestingly the mitochondrial quality control gene, Park2 was among the stress response genes. Further genetic studies indicated that Park2 was essential for heart repair in both the neonatal mouse and the adult Salv conditional knockout mouse. Thus, suggesting a requirement for mitochondrial quality control in the regenerating myocardium. Our findings indicate that the failing heart has a previously unrecognized capacity for repair involving more than cardiomyocyte renewal.

2017-10-04 | GSE100532 | GEO

Heart Failure Network - Xanthine Oxidase Inhibition for Hyperuricemic Heart Failure Patients (HFN EXACT-BioLINCC)

Project description:Heart Failure Network - Xanthine Oxidase Inhibition for Hyperuricemic Heart Failure Patients (HFN EXACT-BioLINCC)

| PRJNA1068760 | ENA

Heart Failure Network - Xanthine Oxidase Inhibition for Hyperuricemic Heart Failure Patients (HFN EXACT-BioLINCC)

Project description:Heart Failure Network - Xanthine Oxidase Inhibition for Hyperuricemic Heart Failure Patients (HFN EXACT-BioLINCC)

| PRJNA1068761 | ENA