Trasncripional regulation by Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE220505 | GEO | 2024/03/01
REPOSITORIES: GEO
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Project description:HUVEC cells were treated with human recombinant VEGF-A165 for either 0h or 18h. Whole cells were used for scRNA-seq analysis.
2024-03-01 | GSE235885 | GEO
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
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 and genes which are differently expressed or VEGF-A induced in HUVEC and CEP, HUVEC and CEP 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.
2014-12-06 | GSE22695 | GEO
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
Project description:FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes. Therefore, to identify genes regulated by FOXO1 in long-term VEGF stimulation, we performed RNA-seq analysis of FOXO1-knockdowned human unbilical vein endothelial cells (HUVECs) by siRNA and 18h VEGF treatment.
2024-03-01 | GSE220504 | GEO
Project description:In order to identify new genes potentially involved in angiogenesis process, we performed a deep-sequencing transcriptome analysis of HUVECs stimulated with recombinant VEGF-A, introducing a difference with respect to the several previous studies. Primary ECs are normally cultured in vitro using an endothelial growth medium (EGM) constituted by an endothelial basal medium (EBM) supplemented with 2% fetal bovine serum (FBS) and a mix of growth factors and reagents, typically represented by basic Fibroblast Growth Factor (bFGF), Insulin-like Growth Factor 1 (IGF1), Epidermal Growth Factor (EGF), heparin, hydrocortisone, ascorbic acid and the same VEGF-A. In previous studies, HUVECs or other primary ECs were starved in EBM with low FBS concentration before the stimulation with VEGF-A. Instead of starvation, we grown HUVECs in complete EGM-2 medium except for VEGF-A to maintain the best condition for in vitro survival and propagation of primary ECs. After 24 hours of VEGF-A deprivation, VEGF-A was re-added to the medium and the stimulation was performed for six hours.
2021-04-08 | E-MTAB-9337 | biostudies-arrayexpress
Project description:This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium. Four samples each of E9.5 wildtype or VEGF120 mouse forebrain were analyzed with the Mouse 430 2.0 Affymetrix GeneChip
2011-12-01 | E-GEOD-30767 | biostudies-arrayexpress
Project description:This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium.
2011-12-01 | GSE30767 | GEO
Project description:The goal of this study is to investigate changes in gene expression profile of lymphatic endothelial cells (LECs) following stimulation with VEGF-C. Primary murine LECs from C57Bl/6 mice were expanded ex vivo from five individual mice (taken from digests of axillary, brachial, cervical, inguinal, popliteal lymph nodes), and stimulated with media only or supplemented with 10 or 100 ng/mL of murine VEGF-C (recombinant, expressed in HEK-293E cells) for 72 h (3 d). This timepoint was chosen because we had detected no significant changes in cell number or density in a daily check up to this timepoint, and ELISAs/Luminex assays detected no significant changes in most chemokine/cytokine biomarkers before 72 h. At this time, LECs were lysed and mRNA isolated for RNAseq analysis to determine differences in gene expression as a function of VEGF-C stimulation. Unstimulated, 10 ng/mL VEGFC-stimulated, and 100 ng/mL VEGFC-stimulated LEC transcriptomes (n = 5 per condition) are provided here. Grant ID - AdG-323053 Agency - European Research Council (ERC) Grant Title - LYMPHIMMUNE - Flow in the tumor microenvironment: Linking mechanobiology with immunology
2018-12-31 | GSE102351 | GEO
Project description:To investigate the effect of vascular endothelial growth factor (VEGF) on gene expression profile after focal cerebral ischemia in mouse, we employed Agilent SurePrint G3 Mouse Gene Expression 8M-CM-^W60K Microarray as a platform to identify which genes influenced by VEGF in mouse after focal cerebral ischemia. Mice were randomized to sham group, in which mice underwent sham surgery; MCAO group, in which transient (90 min) middle cerebral artery occlusion (MCAO) model was performed and mice received vehicle (PBS, 0.01M, pH 7.4) intracerebroventricularly in the right lateral ventricle 3hr after reperfusion; VEGF group (n = 36), in which rhVEGF-A165 (10M-NM-<g/ml, dissolved in 0.01M PBS) was injected into the right lateral ventricle 3hr after reperfusion. Mice were sacrificed at 24hr after reperfusion, brains removed and peri-infarct areas were used for microarray. Gene expression microarray was applied to investigate the differentially expressed genes among sham group, MCAO group and VEGF group. Expression of thirty-seven genes was confirmed in the same RNA samples by real-time PCR. Gene expression in sham group, MCAO group and VEGF group was measured at 24 hours after reperfusion. Three independent experiments were performed using different mice for each experiment.
2014-06-23 | E-GEOD-58720 | biostudies-arrayexpress