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Endothelial Rap1B mediates VEGF immunosuppression

ABSTRACT: Endothelial Rap1B mediates VEGF immunosuppression

PROVIDER: PRJNA772189 | ENA |

REPOSITORIES: ENA

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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

Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

Project description:Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

2010-08-17 | E-TABM-765 | biostudies-arrayexpress

Human dermal lymphatic endothelial cells stimulated with VEGF-A or VEGF-C for 1h, 4h, 8h and 24h

Project description:Lymphatic vessel growth and activation, mediated by vascular endothelial growth factor- (VEGF)-C and/or VEGF-A, play an important role in metastatic cancer spread and in chronic inflammation. We aimed to comprehensively identify downstream molecular targets induced by VEGF-A or VEGF-C in lymphatic endothelium. To this end, we treated human dermal lymphatic endothelial cells (LEC) with VEGF-A or VEGF-C for up to 24 hours, followed by a time-series transcriptional profiling using gene microarray technology. We identified a number of genes - many of them not previously known to be involved in lymphangiogenesis - that clustered either as early response genes, transiently induced genes or progressively induced genes. Endothelial specific molecule-1 (ESM-1) was one of the genes that were most potently induced by both VEGF-A and VEGF-C. Keywords: Time course, growth factor comparison

2008-07-25 | GSE11228 | GEO

Phosphoproteomic analysis of endothelial cells treated with VEGF and Ang-1

Project description:The phosphoproteomes of bovine aortic endothelial cells (BAECs) treated with VEGF or Angiopoietin-1 for 10min were analyzed using LC-MS/MS.

2016-02-09 | PXD002456 | Pride

Analysis of gene expression changes in endothelial cells upon siRNA of VEGF, Foxo1 or both VEGF+Foxo1

Project description:Analysis of transcriptional changes upon silencing of endothelial VEGF. Because transcription factor Foxo1 levels increase under VEGF silencing, we hypothesized that Foxo1 transcriptional activity would be apparent in a whole-genome microarray. Double-silencing of VEGF+Foxo1 was also performed to determine which transcriptional changes are Foxo1-dependent in a VEGF-deficient background.

2015-12-31 | E-MTAB-2515 | biostudies-arrayexpress

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

Project description:Transcriptomic analysis of VEGF-A stimulated liver sinusoidal endothelial cell gene expression. Untreated cells were compared to those treated with VEGF-A. VEGF-A stimulation is critical for normal LSEC phenotype, and the response to liver injury Two conditions: untreated vs. VEGF-A treated. LSEC from 2 donors were pooled. 4 technical repeats.

2013-06-01 | E-GEOD-41110 | biostudies-arrayexpress

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

2013-06-01 | GSE41110 | 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

2017-11-01 | GSE102501 | GEO

Trasncripional regulation by FOXO1 in Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

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

Evaluation and comparison of the glyco-gene expression profile of endothelial cells stimulated with VEGF, bFGF and galectin-3

Project description:Dr. Panjwani's laboratory is focusing on the mechanism by which galectins-3 and 7 mediate corneal epithelial cell migration. Recently published studies, that we have confirmed and expended on in our laboratory, clearly demonstrate that galectin-3 mediates angiogenesis in vitro and in vivo. More interestingly we have found that bFGF- and VEGF-mediated angiogenesis can be inhibited by galectin-3 inhibitors, which suggests an important role of carbohydrate recognition systems in the process of angiogenesis. In an effort to characterize the role of carbohydrate recognition system in angiogenesis, we are interested to evaluate and compare the glyco-gene expression profile of endothelial cells stimulated with VEGF, bFGF and galectin-3 at time and concentration at which, the compounds stimulate angiogenesis in vitro. RNA preparations of Galectin-3, VEGF, bFGF, Media Control biological replicates were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to GLYCO_v3 microarrays.

2011-04-29 | E-GEOD-28943 | biostudies-arrayexpress

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