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Expression profiling of mouse liver after treatment with Vascular Endothelial Growth Factor (VEGF) inhibitor aflibercept

ABSTRACT: Transcriptional profiling of mouse liver was compared between VEGF inhibitor aflibercept and control treatment after 9 weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE50519 | GEO | 2013/09/01

SECONDARY ACCESSION(S): PRJNA217822

REPOSITORIES: GEO

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Expression profiling of mouse liver after treatment with Vascular Endothelial Growth Factor (VEGF) inhibitor aflibercept

Project description:Transcriptional profiling of mouse liver was compared between VEGF inhibitor aflibercept and control treatment after 9 weeks. 8-10 week-old SCID mice received VEGF Trap protein (aflibercept) subcutaneously twice per week at 25mg per kg body weight for 9 weeks. For control groups, mice were treated with humanized Fc (Regeneron). 5 biological replicates were performed for the control group and 4 biological replicates were performed for the treatment group

2013-09-01 | E-GEOD-50519 | biostudies-arrayexpress

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

Project description:HUVEC cells were treated with human recombinant VEGF-A165 for either 0h or 18h. A total RNA sample was used for RNA-seq analysis.

2024-03-01 | GSE220505 | 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.

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Single-cell trasncripional regulation by Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

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

Vascular endothelial growth factor (VEGF) isoform regulation of early forebrain development

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

Vascular endothelial growth factor (VEGF) isoform regulation of early forebrain development

2011-12-01 | GSE30767 | GEO

PAVES: Pegfilgrastim Anti-vascular Endothelial Growth Factor (VEGF) Evaluation Study

Project description:This is a phase 3, randomized, double-blind, placebo-controlled multi-center study evaluating the efficacy of pegfilgrastim to reduce the incidence of febrile neutropenia (FN) in patients with newly diagnosed, locally-advanced or metastatic colorectal cancer receiving first-line treatment with bevacizumab and either 5-fluorouracil, Oxaliplatin, Leucovorin (FOLFOX) or 5-fluorouracil, Irinotecan, Leucovorin (FOLFIRI). This study will also investigate the effect of adding pegfilgrastim to bevacizumab and either FOLFOX or FOLFIRI by evaluating overall survival, progression-free survival, and overall response rate in each arm at regular intervals over a maximum of 60 months follow-up.

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

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

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The Effect of Monoclonal Vascular Endothelial Growth Factor (VEGF) Antibody (Bevacizumab) on Pituitary Function

Project description:The purpose of this research is to determine whether the drug, Bevacizumab (a monoclonal anti VEGF-A antibody), which is approved to treat patients with metastatic colon cancer induces hyperprolactinemia (increased prolactin secretion) in humans with intact pituitary function. Past studies have shown Bevacizumab to shrink tumor size and also increase prolactin levels. The mechanism of the hyperprolactinemia might be inhibition of pituitary portal vein transport, suggesting that Bevacizumab induces prolactin secretion from normal lactotrophs in the pituitary gland. Patients who have been treated with Bevacizumab for at least one month will be recruited to participate. The subjects who are being treated with Bevacizumab by Dr. Stephen Wolin (a sub-investigator) will be screened by him for study eligibility. Dr. Wolin will approach eligible patients with all the information and background of the study and see if they have an interest in being consented. If consented, there will be 2 blood draws for the research that is not part of their standard care in which 10 ml of blood is collected and prolactin, growth hormone, IGF-I, TSH, thyroxine, ACTH, and cortisol will be measured. One 5ml blood draw will occur before the administration of Bevacizumab and the second 5 ml blood draw will occur after the administration of the Bevacizumab. The investigators will then review the laboratory results. The blood tests are of the hormones of the pituitary gland to test pituitary function and see if there are any abnormalities with the secretions of the gland. Pituitary function abnormalities and hyperprolactinemia are diagnosed by looking at hormone levels in the blood and comparing them to the normal reference ranges. This study will only involve 10 subjects and will be conducted entirely at Cedars-Sinai Medical Center.

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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

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