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Transcriptome Analysis of Oxytocin-Treated Human Induced Pluripotent Stem Cell-Derived Epicardial Cells

ABSTRACT: Transcriptome Analysis of Oxytocin-Treated Human Induced Pluripotent Stem Cell-Derived Epicardial Cells

PROVIDER: PRJNA819986 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18484574.fastq.gz	Fastqsanger.gz
	SRR18484575.fastq.gz	Fastqsanger.gz
	SRR18484576.fastq.gz	Fastqsanger.gz
	SRR18484577.fastq.gz	Fastqsanger.gz
	SRR18484578.fastq.gz	Fastqsanger.gz

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Transcriptome Analysis of Oxytocin-Treated Human Induced Pluripotent Stem Cell-Derived Epicardial Cells

Project description:Cardiovascular disease (CVD) is one of the leading causes of mortality worldwide, and frequently leads to massive heart injury and the loss of billions of cardiac muscle cells and associated vasculature. Critical work in the last two decades demonstrated that these lost cells can be partially regenerated by the epicardium, the outermost mesothelial layer of the heart, in a process that highly recapitulates its role in heart development. Upon cardiac injury, mature epicardial cells activate and undergo an epithelial-mesenchymal transition (EMT) to form epicardial-derived progenitor cells (EpiPCs), multipotent progenitors that can differentiate into several important cardiac lineages, including cardiomyocytes and vascular cells. In mammals, this process alone is insufficient for significant regeneration, but it may be possible to prime it by administering specific reprogramming factors, leading to enhanced EpiPC function. Here, we compared changes in gene expression induced by oxytocin in epicardial cells to determine potential pro-regenerative effects.

2022-09-01 | GSE199427 | GEO

Human induced-Pluripotent Stem Cells-derived Preepicardial Cells

Project description:Bulk RNA Sequencing to Characterize Human induced-Pluripotent Stem Cells-derived Pre-epicardial Cells,the extended culture at Passage 1 and the donated H9 ESC-lined derived epicardial cells (Bao et al., 2016)

2021-06-16 | GSE148543 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Human Primary and Pluripotent Stem Cell-Derived Epicardial Cell Transcriptomes

Project description:Next-generation sequencing (NGS) has significantly advanced the elucidation of developmental signaling mechanisms that are important for different cell lineage formation from human pluripotent stem cells (hPSCs). We report here the application of RNA-sequencing technology for transcriptome profile of human primary and hPSC-derived epicardial cell, and compare to those of other cell lineages including hPSCs, mesoderm, cardiomcyotyes. Eight epicaridal cell samples from four different hPSC lines and four different donors were performed in IIIumina HiSeq2500. The resulting sequence reads (about 20 million reads per sample) were mapped to human genome (hg19) using HISAT, and the RefSeq transcript levels (RPKMs) were quantified using the python script rpkmforgenes.py. Our RNA-seq data confirmed the stable expression of key epicardial cell markers including WT1, TBX18, TCF21, ALDH1A2 and ZO1, and the gene set enrichment analysis (GSEA) showed enrichment in extracellular matrix related pathways and keratinocyte (epithelial) differentiation. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to epicardial function. This study represents the first detailed analysis of epicardial transcriptomes generated by RNA-seq technology, providing insight into the mechanisms underlying the differentiation of hPSCs into epicardial cells.

2016-12-05 | GSE84085 | GEO

Nonmuscle myosin IIB regulates epicardial integrity and epicardium-derived mesenchymal cell maturation

Project description:Nonmuscle myosin IIB (NMIIB; heavy chain encoded by MYH10) is essential for cardiac myocyte cytokinesis. The role of NMIIB in other cardiac cells is not known. Here, we show that NMIIB is required in epicardial formation and functions to support myocardial proliferation and coronary vessel development. Ablation of NMIIB in epicardial cells results in disruption of epicardial integrity with a loss of E-cadherin at cell-cell junctions and a focal detachment of epicardial cells from the myocardium. NMIIB-knockout and blebbistatin-treated epicardial explants demonstrate impaired mesenchymal cell maturation during epicardial epithelial-mesenchymal transition. This is manifested by an impaired invasion of collagen gels by the epicardium-derived mesenchymal cells and the reorganization of the cytoskeletal structure. Although there is a marked decrease in the expression of mesenchymal genes, there is no change in Snail (also known as Snai1) or E-cadherin expression. Studies from epicardium-specific NMIIB-knockout mice confirm the importance of NMIIB for epicardial integrity and epicardial functions in promoting cardiac myocyte proliferation and coronary vessel formation during heart development. Our findings provide a novel mechanism linking epicardial formation and epicardial function to the activity of the cytoplasmic motor protein NMIIB.

2017-07-21 | GSE101701 | GEO

CDH18 is an epicardial biomarker regulating epicardial specification and differentiation towards vascular smooth muscle cells

Project description:The epicardium is a mesothelial layer covering the myocardium and contributes to different cardiac lineage descendants during cardiogenesis. Fine-tuned balanced signaling defines epicardial specification and regulates cell plasticity and cell-fate decisions of epicardial-derived cells (EPCDs) by epicardial-to-mesenchymal transition (EMT). However, powerful tools to investigate epicardial cell function, including markers with pivotal roles in developmental signaling, are still lacking. Here, we recapitulated embryonic epicardiogenesis using human induced pluripotent stem cells (hiPSCs) and identified type II classical cadherin CDH18 as a novel biomarker defining lineage specification in human developing epicardium. The loss of CDH18 led to the onset of EMT and specific differentiation towards cardiac smooth muscle cells. Furthermore, GATA4 regulated epicardial CDH18 expression. These results demonstrate the production and enrichment of hiPSC-derived epicardial cells via the tracing of CDH18 expression, providing a model for investigating epicardial function in human development and disease and enabling new possibilities for regenerative medicine.

2022-02-18 | GSE165450 | GEO

Fetal cortical transcriptomic changes after oxytocin induced aberrant uterine contractility

Project description:We report changes in the fetal brain cortical transcriptome after oxytocin-induced aberrant uterine contractility using unbiased RNA-seq analysis.

2020-03-02 | GSE146155 | 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

comparison of primary epicardium explant derived CDCs and primary Epicardial cells

Project description:The analysis showed differences of transcriptomes between primary epicardium explant derived CDCs and primary Epicardial cells directly isolated from the heart epicardium.SB-431542 was an effective TGF-b pathway inhibitor that could obviously inhibit the epicardial cells Epithelial-mesenchymal transition. SB-432542 treatment could produce some epithelial clones in the CDCs,which showed epicardiac specific expression profile, compared with the CDCs.

2022-02-18 | GSE189275 | GEO

RNA-seq of Pluripotent stem cell derived cardiac cells

Project description:Cardiac fibroblasts (CFBs) support heart function by secreting extracellular matrix and paracrine factors, respond to stress associated with injury and disease, and therefore are an increasingly important therapeutic target to treat heart disease. Here, we profile how developmental lineage of human pluripotent stem cell-derived CFBs, epicardial (EpiC-FB) and second heart field (SHF-FB) impacts their transcriptome. We compared this to human pluripotent stem cell derived cardiomyocytes, primary fetal cardiac fibroblasts, primary adult left ventricular fibroblasts, and primary adult dermal fibroblasts.

2021-08-11 | GSE168380 | GEO

Maternal oxytocin treatment at birth increases epigenetic age in male offspring [array]

Project description:Rates of oxytocin use to induce or augment labor are increasing in the United States with little understanding of the impact on offspring development. Using a prairie vole animal model, we have shown that oxytocin administered to mothers can reach offspring brains with long lasting impacts on the development of social behaviors. Here, we examine the epigenetic and transcriptomic consequences of oxytocin exposure during birth in juvenile male offspring. First, we show that male offspring exposed to oxytocin at birth have increased epigenetic age compared to the saline exposed group. We also find 900 differentially methylated CpG sites (annotated to 589 genes), with 2 CpG sites (2 genes) remaining significant after correction for multiple comparisons. Differentially methylated CpG sites are involved in regulation of gene expression and neurodevelopment. Using RNA-sequencing we find 217 nominally differentially expressed genes (p<0.05) in nucleus accumbens, a brain region involved in reward circuitry and social behavior, including 6 genes that remain significantly differentially expressed after corrections for multiple comparisons. Finally, we show that maternal oxytocin administration leads to widespread alternative splicing in the nucleus accumbens. These results indicate that oxytocin exposure during birth has long lasting epigenetic consequences in the brain and warrant further investigation of how oxytocin administration impacts development and behavior throughout the lifespan.

2024-04-03 | GSE240833 | GEO

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