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Single cell RNA transcriptome analysis of Epicardial Derived Cells in the Desmoplakin haplo-insufficient Arrhythmogenic Cardiomyopathy mouse

ABSTRACT: Single cell RNA transcriptome analysis of Epicardial Derived Cells in the Desmoplakin haplo-insufficient Arrhythmogenic Cardiomyopathy mouse

PROVIDER: PRJNA634559 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11832973_1.fastq.gz	Fastqsanger.gz
	SRR11832973_2.fastq.gz	Fastqsanger.gz
	SRR11832974_1.fastq.gz	Fastqsanger.gz
	SRR11832974_2.fastq.gz	Fastqsanger.gz
	SRR11832975_1.fastq.gz	Fastqsanger.gz

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Exercise Reverses Dysregulated Gene Expression in a Desmoplakin Haplo-insufficient Mouse Model of Arrhythmogenic Cardiomyopathy

Project description:Exercise Reverses Dysregulated Gene Expression in a Desmoplakin Haplo-insufficient Mouse Model of Arrhythmogenic Cardiomyopathy

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Single cell RNA transcriptome analysis of Epicardial Derived Cells in the Desmoplakin haplo-insufficient Arrhythmogenic Cardiomyopathy mouse

Project description:To delineate the role of the epicardium, the initial site of presentation of the ACM phenotype, the Dsp gene, encoding desmosome protein desmoplakin (DSP) was conditionally deleted in the mouse epicardial cells under the transcriptional regulation of Wilms tumor 1 (Wt1) locus. Single cell RNA sequencing (scRNA-Seq) of ~ 40,000 tagged epicardial-derived cells (EDCs), isolated using the dual reporter R26mT/mG mice, showed an increased number of EDCs expressing unique molecular identifiers of fibroblasts as well as a unique subset of epicardial-derived fibroblasts expressing pro-fibrotic genes in the Wt1-Cre: R26mT/mG: Dsp mice. Analysis of pseudo-bulk RNA-Seq data identified ~ 800 differentially expressed genes (DEGs), which were predominantly involved in epithelial-mesenchymal transition (EMT). The DEGs were the targets of TGFB1 among other trophic/mitotic factors, whose activation was verified by immunohistochemistry and quantification of transcript levels of selected TGBF1 pathway genes. Retro-mapping of the DEGs to the cell clusters, identified by scRNA-Seq, denoted epicardial-derived fibroblasts and to a lesser extent the epithelial cells as the main sources of paracrine factors in the myocardium of Wt1-Cre: R26mT/mG: Dsp mice.

2021-04-13 | GSE151084 | GEO

Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [scRNA-seq]

Project description:We performed single cell RNA sequencing (scRNAseq) on epicardial cells generated from human induced pluripotent stem cells (hiPSCs) of an arrhythmogenic cardiomyopathy patient and their PKP2 reverted isogenic control. The goal of this experiment was to analyze the process of epicardial to fibro-fatty celluar differentiation in diseased cells and compare the cellular transcirptomes of diseased and healthy cells.

2021-06-20 | GSE149331 | GEO

Exercise Reverses Dysregulated Gene Expression in a Desmoplakin Haplo-insufficient Mouse Model of Arrhythmogenic Cardiomyopathy

Project description:Mutations in desmosome genes cause arrhyythmogenic cardiomyopathy (ACM). Using desmoplakin haploinsufficient mouse model of ACM, we evaluated the effects of treadmill exercise on cardiac myocyte transcritional profile. Strand specific, ribosome depleted paired end RNA sequencing of cardiac myocytes from wild type and Myh6-Cre:DspW/F were generate using Illumina HiSeq 4000.

2020-04-29 | GSE129962 | GEO

Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [bulk RNA-seq]

Project description:We performed bulk cell RNA sequencing (RNAseq) on epicardial cells generated from human induced pluripotent stem cells (hiPSCs) of an arrhythmogenic cardiomyopathy patient and their PKP2 reverted isogenic control. The goal of this experiment was to compare the transcriptomes of diseased and healthy cells.

2021-06-20 | GSE152669 | GEO

Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy

Project description:Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy

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Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [scRNA-seq]

Project description:Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [scRNA-seq]

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Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [bulk RNA-seq]

Project description:Epicardial Differentiation Drives Fibro-fatty Remodeling in Arrhythmogenic Cardiomyopathy [bulk RNA-seq]

| PRJNA640043 | ENA

Reduced desmoplakin immunofluorescence signal in arrhythmogenic cardiomyopathy with epicardial right ventricular outflow tract tachycardia.

Project description: Not available

| S-EPMC6379492 | biostudies-literature

EPAS1 induction drives myocardial degeneration in Desmoplakin-cardiomyopathy [TOMO-seq]

Project description:Arrhythmogenic cardiomyopathy (ACM) is frequently attributed to desmosomal mutations, such as those in the desmoplakin (DSP) gene. Patients with DSP- cardiomyopathy are predisposed to myocardial degeneration and arrhythmias. Despite advancements, the underlying molecular mechanisms remain incompletely understood, thus limiting therapeutic options. Here, we employed spatial transcriptomics on an explanted heart from a patient with a pathogenic DSP variant. Our transcriptional analysis revealed endothelial PAS domain-containing protein 1 (EPAS1) as a potential regulator of mitochondrial homeostasis in stressed cardiomyocytes. Elevated EPAS1 levels were associated with mitochondrial dysfunction and hypoxic stress in both human-relevant in vitro ACM models and additional explanted hearts with genetic cardiomyopathy. Collectively, cardiomyocytes bearing pathogenic DSP variants exhibit mitochondrial dysfunction, increased apoptosis, and impaired contractility, which are linked to the increased EPAS1 levels. These findings implicate EPAS1 as a key regulator of myocardial degeneration in DSP-cardiomyopathy, which expand to other forms of ACM.

2025-02-15 | GSE289630 | GEO

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