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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Dauren Biyashev

PROVIDER: E-GEOD-34735 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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).

2011-12-31 | GSE34735 | 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

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

Project description:We asked whether combining Notch and VEGF blockade would enhance suppression of tumor angiogenesis and growth, using the NGP neuroblastoma model. NGP tumors were engineered to express a Notch1 decoy construct (N1D), which restricts Notch signaling, and then treated with either the anti-VEGF antibody bevacizumab or vehicle. Combining Notch and VEGF blockade led to blood vessel regression, increasing endothelial cell apoptosis and disrupting pericyte coverage of endothelial cells. Combined Notch and VEGF blockade did not affect tumor weight, but did additively reduce tumor viability. Our results indicate that Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis, and show that concurrent blockade disrupts primary tumor vasculature and viability further than inhibition of either pathway alone. 6 neuroblastoma tumors were transfected with Notch1 decoy, 6 with Notch1 decoy and treated with bevacizumab, 6 tumors treated with bevacizumab, and 6 control tumors were profiled by human 133A 2.0 arrays

2013-12-01 | E-GEOD-48880 | biostudies-arrayexpress

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

2013-12-01 | GSE48880 | GEO

RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF with or without STAT3 knock-down

Project description:The role of STAT3 signaling induced by stimulation of IL-6 cytokine family members such as OSM and CNTF on the angiogenic response of endothelial cells is still not fully understood. To assess the impact of this pathway on angiogenesis, this study compares human umbilical vein endothelial cells (HUVECs) with or without STAT3 knock-down introduced by siRNA and stimulation with VEGF, OSM+VEGF and CNTF+VEGF in the presence of the CNTF receptor (CNTFR).

2022-12-04 | GSE198484 | GEO

VEGF induction of HUVEC

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.

2009-09-30 | GSE15464 | GEO

RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF

Project description:IL-6 family cytokines as OSM and CNTF modify angiogenesis to different degree. This study investigates to which extend treatment of endothelial cells with those cytokines can modify VEGF induced angiogenic reactions. Human umbilical vein endothelial cells (HUVECs) were stimulated for 24h by cytokines followed by RNA harvesting and processed for RNA sequencing.

2022-12-04 | GSE196776 | GEO

Comparison of VEGF versus EGF gene expression in HUVEC

Project description:Angiogenesis is defined as the formation of new capillaries by sprouting from preexisting vessels. It is mainly triggered by vascular endothelial growth factor (VEGF) and occurs in the adult primarily in wound healing processes or in pathologic tumor vessel growth. To identify genes specifically triggered by VEGF and involved in the process of angiogenesis, we utilized Affymetrix microarrays hybridized with cRNA of human umbilical vein endothelial cells (HUVEC) stimulated with either the main trigger of angiogenesis, VEGF or a more general mitogenic growth factor, EGF. This was done under the assumption that, in comparison to EGF, VEGF would induce an additional set of genes not solely required for cell division but necessary for angiogenesis. The obtained data revealed that in HUVEC VEGF induces a large repertoire of genes, the majority of which are not or significantly less induced by EGF. Keywords: time course

2009-06-30 | GSE10778 | GEO

Endothelial Rap1B mediates VEGF immunosuppression

Project description:Overcoming vascular immunosuppression: lack of endothelial cell (EC) responsiveness to inflammatory stimuli in the proangiogenic environment of tumors, is essential for successful cancer immunotherapy. The mechanisms through which Vascular Endothelial Growth Factor (VEGF) modulates tumor EC response to exclude T cells are not well understood. The goal was to determine the role of EC Rap1B, a small GTPase that positively regulates VEGF-angiogenesis during development, in tumor growth in vivo. Using mouse models of Rap1B deficiency, Rap1B+/- and endothelial-specific Rap1B KO (Rap1BiΔEC) we demonstrate Rap1B restricts tumor growth and angiogenesis. More importantly, EC-specific Rap1B deletion leads to an altered tumor microenvironment with increased recruitment of leukocytes and increased activity of tumor CD8+ T cells. We find that tumor growth, albeit not angiogenesis, is restored in Rap1BiΔEC mice by depleting CD8+ T cells. Mechanistically, global transcriptome analysis indicated upregulation of the TNF-α signaling and cytokine-induced NFκB transcriptional activity in Rap1B-deficient ECs. In particular, endothelial Rap1B deletion led to upregulation of Cell Adhesion Molecules (CAMs) expression in response to proinflammatory cytokines, and increased interaction with leukocytes in vitro. Importantly, deletion of Rap1 abrogated VEGF-mediated inhibition of CAM expression, demonstrating that Rap1B is essential for mediating VEGF-suppressive signaling. Thus, our studies identify a novel endothelial-endogenous mechanism underlying VEGF-dependent desensitization of EC to pro-inflammatory stimuli. Significantly, they identify EC Rap1 as a potential novel vascular target in cancer immunotherapy.

2022-11-21 | GSE186046 | GEO

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