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

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

PROVIDER: PRJNA510256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8326946.fastq.gz	Fastqsanger.gz
	SRR8326947.fastq.gz	Fastqsanger.gz
	SRR8326948.fastq.gz	Fastqsanger.gz
	SRR8326949.fastq.gz	Fastqsanger.gz

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cAMP/EPAC signaling enables ETV2 to induce endothelial cells with high angiogenesis potential [ChIP-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 | GSE123906 | GEO

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

2019-11-09 | GSE123907 | GEO

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

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

| PRJNA510253 | ENA

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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Transcription profiling of human 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. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.

2009-09-13 | E-GEOD-17777 | biostudies-arrayexpress

Proteomic analysis of cAMP-mediated signaling during differentiation of 3T3-L1 preadipocytes

Project description:Initiation of adipocyte differentiation is promoted by the synergistic action of insulin/insulin-like growth factor, glucocorticoids, and agents activating cAMP-dependent signaling. The action of cAMP is mediated via PKA and Epac, where at least part of the PKA function relates to strong repression of Rho kinase activity, whereas Epac counteracts the reduction in insulin/insulin-like growth factor signaling associated with complete repression of Rho kinase activity. However, detailed knowledge of the Epac-dependent branch and the interplay with PKA is still limited. In the present study, we present a comprehensive evaluation of Epac-mediated processes and their interplay with PKA during the initiation of 3T3-L1 preadipocyte differentiation using a combination of proteomics, molecular approaches and bioinformatics. Proteomic analyses revealed 7 proteins specifically regulated in response to Epac activation, 4 in response to PKA activation, and 11 in response to the combined activation by Epac and PKA during the initial phase of differentiation. Network analyses indicated that the identified proteins are involved in pathways of importance for glucose metabolism, inositol metabolism and calcium-dependent signaling thereby adding a novel facet to our understanding of cAMP-mediated potentiation of adipocyte differentiation.

2014-09-22 | PXD001063 | Pride

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

Project description:Cyclic AMP activates two downstream factors, protein kinase A (PKA) and exchange protein directly activated by cAMP (EPAC) and both downstream signalings induce syncytialization, cell fusion and the production of hCG and progesterone. We used microarray to identify novel transcription factors related to syncytialization in two cAMP signaling-stimulated BeWo cells.

2017-09-30 | GSE100095 | GEO

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