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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of HUVEC cells following treatment with angiogenesis trigger, VEGF or a more general mitogenic growth factor, EGF

ABSTRACT: 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. Experiment Overall Design: HUVEC, quiescent by maintaining dense cultures in complete medium for four days without change of medium were stimulted with 100ng of VEGF or 50ng of EGF for 30, 60, 150 and 360 minutes and total RNA was isolated using Trizol.

ORGANISM(S): Homo sapiens

SUBMITTER: Bernhard Schweighofer

PROVIDER: E-GEOD-10778 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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

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siRNA-mediated Egr-3 knockdown in VEGF-treated HUVEC

2009-11-30 | GSE18913 | GEO

RNA-seq of human umbilical vein endothelial cells (HUVECs) stimulated with recombinant Vascular Endothelial Growth Factor A (VEGF-A) against untreated control

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2021-04-08 | E-MTAB-9337 | biostudies-arrayexpress

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Project description:RNAi-mediated knockdown of DICER1 and DROSHA, enzymes critically involved in miRNA biogenesis, has been postulated to affect the homeostasis and the angiogenic capacity of human endothelial cells. To re-evaluate this issue, we reduced the expression of DICER1 or DROSHA by RNAi-mediated knockdown and subsequently investigated the effect of these interventions on the angiogenic capacity of human umbilical vein endothelial cells (HUVEC) in vitro (proliferation, migration, tube formation, endothelial cell spheroid sprouting) and in a HUVEC xenograft assay in immune incompetent NSGTM mice in vivo. In contrast to previous reports, neither knockdown of DICER1 nor knockdown of DROSHA profoundly affected migration or tube formation of HUVEC or the angiogenic capacity of HUVEC in vivo. Furthermore, knockdown of DICER1 and the combined knockdown of DICER1 and DROSHA tended to increase VEGF-induced BrdU incorporation and induced angiogenic sprouting from HUVEC spheroids. Consistent with these observations, global proteomic analyses showed that knockdown of DICER1 or DROSHA only moderately altered HUVEC protein expression profiles but additively reduced, for example, expression of the angiogenesis inhibitor thrombospondin-1. In conclusion, global reduction of miRNA biogenesis by knockdown of DICER1 or DROSHA does not inhibit the angiogenic capacity of HUVEC. Further studies are therefore needed to elucidate the influence of these enzymes in the context of human endothelial cell-related angiogenesis.

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Project description:The angio-suppressive effect of 20(R)-ginsenoside Rg3 (Rg3-R) has been previously demonstrated, and microRNAs (miRNAs) are a vital group of small non-coding RNAs that function as post-transcriptional modulator of gene expression. Thus, using human umbilical vein endothelial cells (HUVEC) as model, we compared the microRNA (miRNA) expression profile of vascular endothelial growth factor (VEGF)-induced cells with the profile of the cell co-treated with VEGF and Rg3-R. Among the screened 553 human miRNAs, 6 up-regulated (miR-520h, miR-487b, miR-197, miR-524*, miR-342 and miR-219) and 3 down-regulated (miR-23a, miR-489 and miR-377) miRNAs were detected in Rg3-R treated vascular endothelial growth factor (VEGF)-induced HUVECs compared to VEGF alone. Real time RT-PCR was subsequently performed to verify the miRNA microarray result. Two condition experiment: VEGF-induced HUVEC and VEGF-induced HUVEC treated with Rg3-R. Three independent microarray experiments, with triplicate per microarray.

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