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

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

PROVIDER: PRJNA694632 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13521024.fastq.gz	Fastqsanger.gz
	SRR13521025.fastq.gz	Fastqsanger.gz
	SRR13521026.fastq.gz	Fastqsanger.gz
	SRR13521027.fastq.gz	Fastqsanger.gz
	SRR13521028.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

F-53B and PFOS treatments skew human cardiac differentiation towards epicardial cells by in part disrupting the WNT signaling pathway

Project description:F-53B and PFOS treatments skew human cardiac differentiation towards epicardial cells by in part disrupting the WNT signaling pathway

2020-02-16 | GSE129018 | GEO

CDH18 is a fetal epicardial biomarker regulating differentiation towards vascular smooth muscle cells.

Project description:The epicardium is a mesothelial layer covering the myocardium serving as a progenitor source during cardiac development. The epicardium reactivates upon cardiac injury supporting cardiac repair and regeneration. Fine-tuned balanced signaling regulates cell plasticity and cell-fate decisions of epicardial-derived cells (EPCDs) via epicardial-to-mesenchymal transition (EMT). However, powerful tools to investigate epicardial function, including markers with pivotal roles in developmental signaling, are still lacking. Here, we recapitulated epicardiogenesis using human induced pluripotent stem cells (hiPSCs) and identified type II classical cadherin CDH18 as a biomarker defining lineage specification in human active 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 highlight the importance of tracing CDH18 expression in hiPSC-derived epicardial cells, providing a model for investigating epicardial function in human development and disease and enabling new possibilities for regenerative medicine.

| S-EPMC8810917 | biostudies-literature

PRMT1-Mdm4-p53 pathway controls epicardial invasion and cell fate transition

Project description:Epicardial cells are progenitors giving rise to the majority of cardiac fibroblasts, coronary smooth muscle cells, and pericytes during cardiac development, and critically modulating heart morphogenesis and coronary development. An integral phase of epicardial cell fate transition is epithelial-to-mesenchymal transition (EMT), which confers motility and facilitates cell fate transition. We identify a pathway involving protein arginine methyltransferase 1 (PRMT1) and its downstream p53 signaling that drives epicardial EMT and invasion. We show that PRMT1 determines the half-life of p53 through regulating alternative splicing of Mdm4, which is a key controller of p53 degradation. Loss of PRMT1 promotes the expression of Mdm4 short form, which inhibits p53 degradation. Accumulation of p53 subsequently enhances Slug degradation and blocks epicardial EMT. We further demonstrated that the PRMT1-Mdm4-p53 pathway drives epicardial cell fate transition into cardiac fibroblasts, coronary smooth muscle cells and pericytes in vivo, and modulates ventricular morphogenesis and coronary vessel formation. Together, our results establish critical functions of the PRMT1-Mdm4-p53 pathway in epicardial EMT, invasion and cell fate transition.

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Comparison of gene expression data between control and tissue specific epicardial PDGF receptor (a and b) knockout embryonic hearts

Project description:Epicardial cells undergo an epithelial-to-mesenchymal transtion (EMT) to generate coronary vascular smooth muscle cells (VSMC) and cardiac fibroblasts. Little is known about the mechanisms regulating EMT or the in vivo signals directing epicardial-derived cell (EPDC) fate. Here, we show that loss of PDGF signaling leads to a disruption in Sox9 expression, and when Sox9 expression was restored in mutant hearts, the EMT defect was rescued. Interestingly, mutants lacking only one of the PDGF genes exhibited a lineage specific requirement for the individual receptors. Loss of PDGFRα resulted in a deficit in cardiac fibroblast formation, while cVSMC development was unperturbed. Conversely, PDGFRβ was required for cVSMC development but not cardiac fibroblast development. Combined, our data demonstrate a novel role for PDGF receptors in epicardial EMT and EPDC development. GSM671723-GSM671724: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout hearts using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA) GSM671877-GSM671882: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout primary epicardial cultures using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA)

2011-02-28 | E-GEOD-27181 | biostudies-arrayexpress

Direct Coculture of hPSC-derived Cardiac Progenitor Cells with Epicardial cells induces Cardiomyocyte proliferation and ventricular specification

Project description:Epicardial cells (EpiCs) form the epicardium, the outer layer of the heart surrounding the myocardium. During development and in response to injury EpiCs undergo an epithelial to mesenchymal transition (EMT) migrating inward to create fibroblasts and smooth muscle cells in the myocardium. EpiCs have been shown to be necessary for proper myocardium formation, yet little is known about crosstalk between EpiCs and cardiomyocyte (CMs) and the potential impact of EpiCs on CM maturation. Here, we differentiated human pluripotent stem cells (hPSCs) to both cardiac progenitor cells (CPCs) and EpiCs, and cocultured EpiCs and CPCs in the presence of A83-01, to inhibit TGFβ signaling and EMT, for two weeks.

2021-10-12 | GSE168956 | GEO

Retinoic acid signaling modulation guides in vitro specification of human heart field-specific progenitor pools

Project description:He we report a systematic analysis of RA impact on human cardiovascular progenitor specification in orchestry with other signaling cues during early mesoderm formation. To approach this, we used a single cell transciptome profiling to dissect heterogeneity within human heart field-like cell populations and their derivatives. Our analysis enable us to identify known as well as a novel population of cells that can in vitro differentaite towards myocytic as well as epicardial lineages.

2023-01-27 | GSE197660 | GEO

Global gene expression of human iPSC directed differentation towards smooth muscle cells using an Acta2eGFP human iPSC reporter line

Project description:Here, we generated and differentiated a human induced pluripotent stem cell line with an ACTA2eGFP reporter towards a smooth muscle-like cell that can be purified and expresses characteristic markers of smooth muscle cells. We performed microarray analysis of day 30 ACTA2eGFP+ and ACTA2eGFP- sorted populations, and the transcriptomic profile of the ACTA2eGFP+ cells is reminiscent of an immature or a synthetic smooth muscle cell phenotype.

2019-07-31 | GSE132454 | GEO

Specification and Diversification of Pericytes and Smooth Muscle Cells from Mesenchymoangioblasts

Project description:Recently, we identified mesenchymoangioblast (MAB), as a clonal mesodermal precursor for mesenchymal and endothelial cells. Here we show, that MABs have the capacity to produce mesenchymal progenitors, which can be differentiated into pericytes or smooth muscles cells under the influence of PDGF-BB or TGFβ plus sphingosylphosphorylcholine (SPC), respectively. Based on these studies we established the hierarchy of vasculogenic progenitors that provides the platform for interrogation of molecular mechanisms regulating vasculogenic cell specification and diversification from primitive posterior mesoderm.

2017-05-30 | GSE75990 | GEO

Heterogeneity of mouse pro-epicardial cells

Project description:Single cell RNA sequencing (scRNA-Seq) is applied to charaterize the pro-epicardial cells (proEpiCs) in mouse pro-epicardial organ (PEO).

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