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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [miRNA-seq]

ABSTRACT: We report the application of small-RNA sequencing for high-throughput profiling in mouse epicardial cell (MCEC).

ORGANISM(S): Mus musculus

PROVIDER: GSE197296 | GEO | 2022/02/26

REPOSITORIES: GEO

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

Project description:The purpose of the study was to compare epicardial transcript abundance between control and Hdac3 knockout (KO) epicardial cells (MEC).

2022-02-26 | GSE197297 | GEO

Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

Project description:Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [miRNA-seq]

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-26 | GSE197298 | GEO

Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

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miRNA content from human and mouse epicardial extracellular vesicles

Project description:The goal of the present study is to determine the miRNA cargo present in epicardial extracellular vesicles. For that, epicardial cells and human primary epicardial cells were cultured. Conditioned media was isolated from mouse epicardial cells and human primary epicardial cells derived from right atrial appendages in two different states: “cobble” (inactive) cells and “spindle” (active) . RNA from EVs was isolated and sequenced to determine the miRNA content profile.

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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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Novel gene-pathway identification during the development of human epicardial fat through early life

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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

Heterogeneity of mouse pro-epicardial cells

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