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

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE198484 | GEO | 2022/12/04

REPOSITORIES: GEO

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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

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

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

FGF-dependent regulation of VEGF signaling via transcriptional control of VEGF receptor 2 expression

Project description:Numerous studies have suggested a link between fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) signaling pathways; however the nature of this link has not been established. To evaluate this relationship we investigated VEGF signaling in endothelial cells with disrupted FGF signaling in vitro and in vivo. We find that endothelial cells lacking FGF signaling become unresponsive to VEGF due to down regulation of VEGFR2 expression caused by reduced Vegfr2 enhancer activation, which is in turn caused by reduced activation of Ets family transcription factors. In vivo this manifests in the loss of vascular integrity and morphogenesis. Thus, basal FGF stimulation of the endothelium is required for maintenance of VEGFR2 expression and the ability to respond to VEGF stimulation and accounts for the hierarchic control of vascular formation by FGFs and VEGF.

2011-06-07 | GSE28483 | GEO

FGF-dependent regulation of VEGF signaling via transcriptional control of VEGF receptor 2 expression

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RNA-Seq Provides Insights into VEGF-Induced Signaling in Human Retinal Microvascular Endothelial Cells: Implications in Retinopathy of Prematurity [RNA-seq_2]

Project description:The pathophysiology of retinopathy of prematurity (ROP) is postulated to first involve delayed intraretinal vascularization, followed by intravitreal neovascularization (IVNV). Although intravitreal agents that reduce the bioactivity of vascular endothelial growth factor (VEGF) are used to treat IVNV, concerns exist regarding their effects on intraretinal vascularization. In an experimental ROP model, VEGF receptor 2 (VEGFR2) knockdown in retinal endothelial cells reduced IVNV and promoted intraretinal vascularization, whereas knockdown of a downstream effector, signal transducer and activator of transcription 3 (STAT3) in retinal endothelial cells only reduced IVNV. In this study, we tested the hypothesis that the different pathways involved in VEGF-triggered VEGFR2 signaling and VEGF-triggered STAT3 signaling in retinal endothelial cells would allow us to delineate signaling pathways involved in IVNV from those involved in intraretinal vascularization in ROP. To address our hypothesis, we used RNA-sequencing and pathway enrichment analysis to determine changes in the transcriptome of cultured human retinal microvascular endothelial cells (HRMECs). Of the enriched pathways, inactivation of oncostatin M signaling was predicted by either KDR or STAT3 knockdown in the presence of VEGF. Activation of kinetochore metaphase signaling was predicted by KDR knockdown, whereas inactivation was predicted by STAT3 knockdown in the presence of VEGF. Inactivation of signaling by the Rho family of GTPases was predicted by KDR knockdown, but activation was predicted by STAT3 knockdown in the presence of VEGF. Taken together, our data identified unique signaling pathway differences between VEGF-triggered VEGFR2 and VEGF-triggered STAT3 in HRMECs that might have implications in ROP.

2022-12-29 | GSE221861 | GEO

RNA-Seq Provides Insights into VEGF-Induced Signaling in Human Retinal Microvascular Endothelial Cells: Implications in Retinopathy of Prematurity [RNA-seq_1]

2022-12-29 | GSE221860 | GEO

Human umbilical vein endothelial cells (HUVECs): VEGF vs. ctrl, oxPAPC vs. ctrl

Project description:MicroRNA profiling of human endothelial cells comparing VEGF and oxPAPC treated cells with their respective control-treated cells

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VEGF-A stimulated gene expression in human liver sinusoidal endothelial cells

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Gene expression of HCT116 cells after stimulation with oncostatin M (OSM)

Project description:To evaluate gene expression profiles in intestinal epithelial cells (IEC) after OSM stimulation, we have employed whole genome microarray expression profiling as a discovery platform to identify relevant genes which are potentially of interest to reveal the role of OSM in intestinal inflammation. The most strongly up-regulated genes were SERPINS, which belong to the family of serin peptidase inhibitors with antiprotease activities, most of them serine and cysteine proteases. SERPINB4, SERPINB3 and SERPINA3 were the genes with the strongest up-regulation, also verified in qPCR. OSM-induced SERPIN up-regulation may contribute to anti-apoptotic and proliferative effects of OSM in IEC. HCT116 cells were starved overnight with medium containing 1% FCS after reaching 70% confluency. On the next day, cells were stimulated in quadruplicates with 100 ng/mL OSM or left unstimulated. RNA was isolated 6 hours after stimulation and RNA concentration and purity was measured.

2014-12-13 | E-GEOD-53295 | biostudies-arrayexpress

VEGF-A stimulated gene expression in human liver sinusoidal endothelial cells

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