Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE100095 | GEO | 2017/09/30

SECONDARY ACCESSION(S): PRJNA390666

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in undifferentiated or cyclic adenosine monophosphate-exposed BeWo trophoblast cells

Project description:BeWo trophoblast cells differentiate in response to expsure to cyclic adenosine monophosphate (cAMP) analogs. Differentiation includes syncytialization (fusion) and hormonogenesis. The goal of this study was to globally determine transcripts differentially expressed in BeWo trophoblast cells following a 24-h exposure to 250 uM 8-bromo-cAMP. 3 replicates undifferentiated BeWo trophoblast cells; and 3 replicates BeWo trophoblast cells treated with 250 uM 8-Br-cAMP for 24 h.

2015-08-01 | E-GEOD-66840 | biostudies-arrayexpress

Gene expression in undifferentiated or cyclic adenosine monophosphate-exposed BeWo trophoblast cells

2015-08-01 | GSE66840 | 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.

2009-08-25 | GSE17777 | GEO

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

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]

2019-11-09 | GSE123906 | GEO

JEG3 vs BeWo

Project description:In this experiment we compared total RNA from two commonly used choriocarcinoma cell lines, JEG3 and BeWo, to identify differentially expressed transcripts. Keywords: other

2005-05-30 | GSE2531 | GEO

Analyses of PDE-regulated phosphoproteomes reveal unique and specific cAMP signaling modules in T cells

Project description:Specific functions for different cyclic nucleotide phosphodiesterases (PDEs) have not yet been identified in most cell types. Conventional approaches to study PDE function typically rely on global cAMP measurements, general increases in cAMP- dependent protein kinase (PKA) activity, or activity of exchange protein activated by cAMP (EPAC). Although newer approaches utilizing subcellularly-targeted FRET reporter sensors have helped to define more compartmentalized regulation of cAMP, PKA, and EPAC, they have limited ability to link this regulation to downstream effector molecules and biological functions. To address this problem, we have begun to use an unbiased, mass spectrometry-based approach coupled with treatment using PDE isozyme-selective inhibitors to characterize the phosphoproteome of the "functional pools" of cAMP/PKA/EPAC that are regulated by specific cAMP-PDEs (the PDE-regulated phosphoproteomes).

2017-05-27 | MSV000081115 | MassIVE

Transcriptomic Profiling of Trophoblast Fusion Using BeWo and JEG-3 Cell Lines

Project description:Introduction: In human placenta, alteration in trophoblast differentiation has a major impact on placental maintenance and integrity. Moreover, abnormal syncytial fusion seems to be implicated in the development of many complications including pre-eclampsia and intra-uterine growth restriction (IUGR). However, little is known about the mechanisms that control cytotrophoblast fusion into syncytiotrophoblast. BeWo cell line is commonly used to study placental function since it can be induced to form syncytium and secretes hormones. This fusion is triggered by cAMP or forskolin treatments. In contrast, JEG-3 cell line fails to undergo substantial fusion. Therefore, we will use BeWo and JEG-3 cells to identify a set of genes responsible of trophoblast fusion. Methods: BeWo and JEG-3 cells were treated with forskolin for 48 to induce fusion. RNA was extracted, hybridized to Affymetrix HuGene ST1.0 arrays and analyzed using system biology. Trophoblast differentiation was evaluated by real time PCR and immunocytochemistry analysis. Moreover, some of the identified genes were validated by real time PCR. Results: Our results identified a list of 32 altered genes in fused BeWo cells compared to JEG-3 cells after forskolin treatment. Among these genes, 4 were validated by real-time PCR including salt inducible Kinase 1 (SIK1) gene which is specifically upregulated in BeWo cells upon fusion. Moreover, using system biology analysis, SIK1 showed to be at the center of many biological and functional processes which suggest that it might play a major role in trophoblast differentiation. Conclusion: This study identified new target genes implicated in trophoblast fusion; a process implicated in the etiology of many pregnancy-related diseases such as preeclampsia, IUGR, and gestational diabetes.

2019-02-26 | GSE127170 | GEO

Genome-wide analysis of ARNT/HIF binding sites in BeWo cells cultured under low oxygen

Project description:In this study, we provide new insight into the role of the hypoxia-inducible factor (HIF) complex in the inhibition of syncytiotrophoblast formation under low oxygen. Through a genome-wide analysis of binding sites for the aryl hydrocarbon nuclear receptor translocator (ARNT; a key component of HIF), we identified the downstream targets of ARNT/HIF that potentially mediate its repressive effect on syncytialization.

2023-03-20 | GSE209936 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data