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Gene expression analyses in murine proepicardial and epicardial cells

ABSTRACT: Gene expression analyses in murine proepicardial and epicardial cells

PROVIDER: PRJNA782618 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17007077.fastq.gz	Fastqsanger.gz
	SRR17007078.fastq.gz	Fastqsanger.gz
	SRR17007079.fastq.gz	Fastqsanger.gz
	SRR17007080.fastq.gz	Fastqsanger.gz
	SRR17007081.fastq.gz	Fastqsanger.gz

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Gene expression analyses in murine proepicardial and epicardial cells

Project description:We provide herein a transcriptomic analyses of mouse embryonic day 9.5 proepicardial cells, isolated from Wt1CreEGFP mice and mouse embryonic day 10.5 FACS-sorted embryonic epicardial cells also from Wt1CreEGFP mice. Distinct libraries were constructed to performed microRNA and mRNA/lncRNAs sequencing, respectively. Data comparison allowed us to identify 1876 differentially expressed mRNAs, 171 lncRNAs and 68 microRNAs.

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Genome-wide analysis of epicardial gene expression in E11.5 mouse hearts

Project description:Identification of epicardium-enriched genes in the embryonic heart. The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in re-activation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration. Total RNA obtained from lacZ-positive epicardial cells isolated from the E11.5 Tcf21lacZ hearts compared to total dissociated heart cells

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Project description:Detailed FACS analyses of enzymatically disaggregated embryonic hearts from Wt1GFPKI mice revealed two distinct types of Wt1GFP-positive cells based on their GFP expression levels: a Wt1GFP bright population (H) and a Wt1GFP dim (M) population. Quantitative RT-PCR analyses for epicardial genes demonstrated an enrichment in epicardial genes in the Wt1GFP bright population (H)

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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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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.

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Heterogeneity of mouse pro-epicardial cells

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Neutrophils facilitate the epicardial regenerative response after zebrafish heart injury

Project description:Despite extensive studies on endogenous heart regeneration within the past 20 years, the players involved in initiating early regeneration events are far from clear. Here, we assessed the function of neutrophils, the first-responder cells to tissue damage, during heart regeneration. We detected rapid neutrophil mobilization to the injury site after ventricular amputation, peaking at 1-day post-amputation (dpa) and resolving by 3 dpa. Further analyses indicated neutrophil mobilization coincides with peak epicardial cell proliferation and recruited neutrophils associated with activated, expanding epicardial cells at 1 dpa. Neutrophil depletion inhibited myocardial regeneration and significantly reduced epicardial cell expansion, proliferation, and activation. To explore the molecular mechanism of neutrophils on the epicardial regenerative response, we performed scRNA-seq analysis of 1 dpa neutrophils and identified enrichment of the FGF and ERK signaling pathways. Pharmacological inhibition of FGF signaling indicated its’ requirement for epicardial cell expansion, while neutrophil depletion blocked ERK signaling activation in epicardial cells. Altogether, our studies revealed that neutrophils quickly induce epicardial cells, which later accumulate at the injury site and contribute to heart regeneration.

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