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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Robert Doebele

PROVIDER: E-GEOD-17777 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Anthrax edema toxin inhibits endothelial cell chemotaxis via Epac and Rap1.

Hong Jia J Doebele Robert C RC Lingen Mark W MW Quilliam Lawrence A LA Tang Wei-Jen WJ Rosner Marsha Rich MR

The Journal of biological chemistry 20070509 27

Angiogenesis involves the assembly of endothelial cells into capillaries from a pre-existing vasculature. Because abnormal angiogenesis is a hallmark of many cancers, it is critical to find factors that control this process. Endothelial cells are enriched in the anthrax receptor; we therefore determined the effect of anthrax edema toxin (ET), an adenylyl cyclase, on chemotaxis. cAMP generated by ET does not block proliferation or survival but causes cytoskeletal changes and inhibits chemotaxis b ...[more]

PMID: 17491018

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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

MicroRNA expression in HMVECs: control vs. VEGF-treated vs. PEDF/VEGF-treated

Project description:MicroRNA expression profiling of human microvascular endothelial cells (HMVECs) treated with either vascular endothelial growth factor (VEGF) only or in combination with the natural angiogenesis inhibitor pigment epithelial-derived factor (PEDF). Originally we were interested in the microRNA-mediated regulation of angiogenesis by the endogenous anti-angiogenic PEDF. To identify the microRNAs involved in PEDF signaling in activated endothelial cells, we compared the levels of microRNAs in non-treated microvascular endothelial cells, cells treated with VEGF, and cells treated with a combination of VEGF and PEDF. After treatment, total RNA content was isolated and sent for analysis to LC Sciences, LLC. They performed expression profiling and completed statistical analysis, based on which we confirmed the regulation of one of the microRNAs, mir-27b. In the following experiments, we identified the targets of mir-27b relevant for angiogenesis and confirmed our findings in zebrafish and mouse models. The manuscript describes the key role of mir-27b in determination of the endothelial tip cell fate and venous differentiation by regulating Notch ligand Delta-like ligand 4 (Dll4) and Sprouty homologue 2 (Spry2). Three-condition experiment: untreated (control) HMVECs vs. VEGF-treated HMVECs vs. PEDF/VEGF-treated HMVECs.

2011-12-31 | E-GEOD-34735 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow derived macrophages (BMDM) treated with anthrax edema toxin (ET)

Project description:Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Experiment Overall Design: BMDM were treated with 1 mg/ml of ET and the RNAs were purified at 0, 2, and 4h after toxin treatment.

2008-06-16 | E-GEOD-9184 | biostudies-arrayexpress

Transcriptome analysis for human lung microvascular endothelial cells

Project description:RNA-seq was performed for the human lung microvascular endothelial cells (HMVEC-L)

2020-07-01 | GSE101201 | GEO

Expression profile from anthrax edema toxin (ET) treated murine bone marrow derived macrophages (BMDM)

2007-09-28 | GSE9184 | GEO

Gene expression in microvascular endothelial cells co-cultured with dorsal root ganglion cells

Project description:Analysis of gene expressions in human microvascular endothelial cells (HMVEC)s following co-cultured with mouse dorsal root ganglion cells. Results provide insight into a role for responses of neurovascular interaction in endothelial cell in angiogenesis and vascular remodeling.

2017-01-31 | GSE93696 | GEO

Homo sapiens

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

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Phospho- and total- proteomic analysis of FAK knockout in primary mouse lung endothelial cells

Project description:We assessed the impact of Endothelial Focal Adhesion kinase (ECFAK) knockout, using primary lung endothelial cells isolated (at P10-P14) from a FAK flox/flox mice crossed with mice expressing a tamoxifen-inducible Cre(iCreERT2) that is driven by endothelial cell (EC)-selective platelet-derived growth factor subunit B (Pdgfb) promoter (Pdgfb-iCreERT2) (Tavora et al., 2010). To induce EC restricted FAK deletion, we injected 4-hydroxytamoxifen (4-OHT) from postnatal day 1 (P1) to P2. Molecular signaling events modulated by ECFAK loss, with or without ex vivo VEGF stimulation, were then examined by phospho and total quantitative proteomics analysis using 6plex isobaric tandem mass tagging multiplexing (TMT). In total, three experiments were performed (a an initial pilot experiment not included in this study, followed by two main biological replicates included - i.e. experiments 2, and 3). The following 4 TMT channels were utilised in each experiment: TMT-126: WT-mock(PBS) stimulated TMT-127: WT-Vegf stimulated TMT128: FAK KO-mock (PBS)stimulated TMT 129:FAK KO-Vegf stimulated

2022-04-13 | PXD030824 | Pride

Global gene expression profiling of endothelial cells from different vascular bed and caliber

Project description:Endothelial cells (EC) were obtained from commercial source (Lonza), expanded and culture until passage 3. HMVEC-LBI correspond to lung microvascular endothelial cells, HPAEC to lung macrovascular endothelial cells, HAEC to cardiac macrovascular endothelial cells and HMVEC-C to cardia microvascular endothelial cells. These cells presented different capacity to generate endothelial microvesicles. The objective of the study was to identify differentially genes between these cells to understand this difference. Total RNA was extracted using the mirVana miRNA Isolation Kit (Ambion), according to the manufacturer’s recommendations. Cy3-CTP labeled RNA was prepared according to standard Agilent protocol from 400ng total RNA. The hybridization was performed for 17 hrs at 65°C. cRNA labeling and hybridization performance were performed and all parameters checked were found within the manufacturers specifications. Arrays were scanned as described in the manufacturers’ protocol. Signal intensities on 20 bit tiff images were calculated by Feature Extraction software (FE, Version 8.5; Agilent Technologies). Data analyses were conducted with GeneSpring GX software (Vers.12.6; Agilent Technologies)

2023-01-30 | E-MTAB-4886 | biostudies-arrayexpress

Transcription profiling of human umbilical vein endothelial cells (HUVEC) treated with VEGF-A

Project description:Angiogenesis, the formation of new capillaries by sprouting from preexisting vessels, is mainly induced by VEGF-A. To identify genes which are induced by VEGF-A in endothelial cells, HUVEC were starved and induced by VEGF-A165 for 30, 60 and 150min. RNA of induced and uninduced cells was isolated and subjected to microarray analysis using Affymetrix microarray. Experiment Overall Design: Human umbilical vein endothelial cells were grown in complete EGM-2 medium in dense culture for four days without change of medium and before the stimulation in EGM-2 medium without growth factors over night. The cells were stimulated with 100ng/ml VEGF-A165 for 30, 60 and 150 min. RNA was isolated with Trizol according to the manufacturer's instructions.

2009-10-20 | E-GEOD-15464 | biostudies-arrayexpress

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