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CAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential

ABSTRACT: cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential

PROVIDER: PRJNA510253 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8326950.fastq.gz	Fastqsanger.gz
	SRR8326951.fastq.gz	Fastqsanger.gz
	SRR8326952.fastq.gz	Fastqsanger.gz
	SRR8326953.fastq.gz	Fastqsanger.gz
	SRR8326946.fastq.gz	Fastqsanger.gz

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cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [RNA-seq]

Project description:Although the generation of ETV2-induced endothelial cells (iECs) from human fibroblasts serves as a novel therapeutic strategy in regenerative medicine, the process is inefficient, resulting in incomplete iEC angiogenesis. Therefore, we employed ChIP-sequencing and identified molecular mechanisms underlying ETV2-mediated endothelial transdifferentiation to efficiently produce iECs retaining appropriate functionality in long-term culture. We revealed that the majority of ETV2 targets in human fibroblasts are related to vasculature development and signaling transduction pathways including Rap1 signaling. From a screening of signaling pathway modulators, we confirmed that forskolin facilitated efficient and rapid iEC reprogramming via activation of cAMP/EPAC/RAP1 axis. The iECs obtained via cAMP signaling activation showed superior angiogenesis in vivo as well as in vitro. Moreover, these cells could form aligned endothelium along the vascular lumen ex vivo when seeded into decellularized liver scaffold. Overall, our study provided evidence that cAMP/EPAC/RAP1 axis is required for the efficient generation of iECs with angiogenesis potential.

2019-11-09 | GSE123907 | GEO

cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [ChIP-seq]

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cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [ChIP-seq]

Project description:cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [ChIP-seq]

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cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [RNA-seq]

Project description:cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [RNA-seq]

| PRJNA510255 | ENA

cAMP/EPAC Signaling Enables ETV2 to Induce Endothelial Cells with High Angiogenesis Potential.

Project description:Although the generation of ETV2-induced endothelial cells (iECs) from human fibroblasts serves as a novel therapeutic strategy in regenerative medicine, the process is inefficient, resulting in incomplete iEC angiogenesis. Therefore, we employed chromatin immunoprecipitation (ChIP) sequencing and identified molecular mechanisms underlying ETV2-mediated endothelial transdifferentiation to efficiently produce iECs retaining appropriate functionality in long-term culture. We revealed that the majority of ETV2 targets in human fibroblasts are related to vasculature development and signaling transduction pathways, including Rap1 signaling. From a screening of signaling pathway modulators, we confirmed that forskolin facilitated efficient and rapid iEC reprogramming via activation of the cyclic AMP (cAMP)/exchange proteins directly activated by cAMP (EPAC)/RAP1 axis. The iECs obtained via cAMP signaling activation showed superior angiogenesis in vivo as well as in vitro. Moreover, these cells could form aligned endothelium along the vascular lumen ex vivo when seeded into decellularized liver scaffold. Overall, our study provided evidence that the cAMP/EPAC/RAP1 axis is required for the efficient generation of iECs with angiogenesis potential.

| S-EPMC7002895 | biostudies-literature

cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential

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

2019-11-09 | GSE123908 | GEO

HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT) Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment.

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Expression data from BeWo cells treated without or with PKA- or EPAC-selected cAMP analogs

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