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Single-cell RNA sequencing reveals the impact of CD34+ cells in heart failure

ABSTRACT: Single-cell RNA sequencing reveals the impact of CD34+ cells in heart failure

PROVIDER: PRJNA817182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18360300_1.fastq.gz	Fastqsanger.gz
	SRR18360300_2.fastq.gz	Fastqsanger.gz
	SRR18360301_1.fastq.gz	Fastqsanger.gz
	SRR18360301_2.fastq.gz	Fastqsanger.gz
	SRR18360302_1.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing reveals the impact of CD34+ cells in heart failure

Project description:CD34+ cells have been used to treat the patients with heart failure, but the outcome is variable. It is of great significance to scrutinize the fate and the mechanism of CD34+ cell differentiation in vivo during heart failure and explore its intervention strategy. By analyzing the transcriptomes of single cells from the Cd34-CreERT2;R26-tdTomato heart, we illustrated the dynamics of cell landscape during the progression of heart hypertrophy, including CD34+ cells, fibroblasts, endothelial cells and immune cells. And Our study also provides a cellular landscape of CD34+ cell-derived cells in the hypertrophy heart of animal models.

2022-10-06 | GSE198833 | GEO

Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

Project description:Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

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Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

Project description:Hyperlipidemia and hypertension might play a role in cardiac fibrosis, in which a heterogeneous population of fibroblasts seems important. However, it is unknown whether CD34+ cells are involved in the pathogenesis of cardiac fibrosis. This study aimed to investigate the mechanism of CD34+ cell differentiation in cardiac fibrosis during hyperlipidemia. By analyzing the transcriptomes of single cells from the Cd34-CreERT2;R26-tdTomato&ApoE-/- heart, we also demonstrated the dynamics of cell landscape during cardiac fibrosis in the hypertrophic heart with hyperlipidemia.

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Project description:Heart Failure Network: Functional Impact of GLP-1 for Heart Failure Treatment (HFN FIGHT-BioLINCC)

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Heart Failure Network: Functional Impact of GLP-1 for Heart Failure Treatment (HFN FIGHT-BioLINCC)

Project description:Heart Failure Network: Functional Impact of GLP-1 for Heart Failure Treatment (HFN FIGHT-BioLINCC)

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Single-cell RNA sequencing for heart failure heart with the history of hypertension

Project description:CD34+ stem cells have been used to treat the patients with heart failure, but the outcome is variable. It is of great significance to scrutinize the fate and the mechanism of CD34+ cell differentiation in vivo during heart failure and explore its intervention strategy.

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INO80 and heart failure.

Project description:INO80 and heart failure.

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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

Model of heart failure induced by mild thiol-blocking with cystamine

Project description:Depletion of cardiac ATP content is a characteristic feature of heart failure in patients and experimental animal models. To analyze the impact of insufficient ATP supply on heart function we inhibited cellular respiration by disulfide poisoning with the mild thiol-blocking agent, cystamine. We chose 4 month-old apolipoprotein E (apoE)-deficient mice, which are highly vulnerable to increased oxygen and ATP demands. After 4 weeks of cystamine treatment (300 mg/kg in drinking water), echocardiography and histology analyses demonstrated that apoE-deficient mice had developed heart failure with cardiac dilation. The microarray gene expression study of heart tissue from cystamine-treated apoE-deficient mice relative to untreated mice confirmed the development of heart failure showing up-regulation heart failure-specific genes by mild thiol-blocking with cystamine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) cystamine-treated 5 month-old apolipoprotein- (apoE)- deficient mice with symptoms of heart failure, (ii) untreated 5 month-old apoE- deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.

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Project description:The microtubule (MT) cytoskeleton can provide a mechanical resistance that can impede the motion of contracting cardiomyocytes. Yet a role of the MT network in human heart failure is unexplored. Here we utilize mass spectrometry to characterize changes to the cytoskeleton in human heart failure. Proteomic analysis of left ventricle tissue reveals a consistent upregulation and stabilization of intermediate filaments and MTs in human heart failure. This dataset includes left ventricular (LV) myocardium from 34 human hearts – either non-failing (NF) or failing hearts. NF hearts are subdivided into normal or compensated hypertrophy (cHyp), while failing hearts are subdivided into ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), and hypertrophic cardiomyopathy with preserved or reduced ejection fraction (HCMpEF and HCMrEF, respectively). Further details on patient classification and in vivo parameters on each heart are listed in sample details.txt.

2018-06-06 | PXD008934 | Pride

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