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Expression data: Venous malformation-causative TIE2-mutations mediate an AKT-dependent decrease in PDGFB

ABSTRACT: Comparison of transcriptional profiles of human umbilical vein endothelial cells (HUVECs) expressing wild-type vs. VM-causative mutant forms of TIE2/TEK. The effects of the most common Venous Malformation-causative mutations in the endothelial cell tyrosine kinase receptor: R849W and L914F, were tested. 743 genes were differentially expressed across the four groups. The 80 genes distinguishing between L914F and wild-type TIE2-expressing HUVECs were analyzed in greater detail.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46684 | GEO | 2013/06/04

SECONDARY ACCESSION(S): PRJNA201508

REPOSITORIES: GEO

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Expression data: Venous malformation-causative TIE2-mutations mediate an AKT-dependent decrease in PDGFB

Project description:Comparison of transcriptional profiles of human umbilical vein endothelial cells (HUVECs) expressing wild-type vs. VM-causative mutant forms of TIE2/TEK. The effects of the most common Venous Malformation-causative mutations in the endothelial cell tyrosine kinase receptor: R849W and L914F, were tested. 743 genes were differentially expressed across the four groups. The 80 genes distinguishing between L914F and wild-type TIE2-expressing HUVECs were analyzed in greater detail. 3 batches each of: non-transfected, and wild-type TIE2, R849W-TIE2, and L914F-TIE2 overexpressing HUVECs were compared by exon-array profiling.

2013-06-04 | E-GEOD-46684 | biostudies-arrayexpress

Venous malformation-causative TIE2 mutations mediate an AKT-dependent decrease in PDGFB.

Project description: Not available

| S-EPMC3736867 | biostudies-literature

Tek+ cells from the E10 AGM region of Rictorf/f; Tie2-cre and control

Project description:we performed RNAseq analysis on Rictorf/f; Tie2-cre and control tek+ cells, to determine which hematopoietic genes are activated in the endothelium in the AGM by Rictor.

2017-07-30 | GSE59929 | GEO

RNA-Sequencing of HUVEC treated with Tie2 activating antibody

Project description:We analyzed genome-wide transcriptional changes induced by ABTAA+Ang2, using RNA-seq analysis of HUVECs Examination of 3 different antibodies treated to HUVEC to analyze the effect of Tie2 activation

2016-02-15 | E-GEOD-77597 | biostudies-arrayexpress

ROSA26Foxf1; Tie2-cre lung gene expression analysis.

Project description:Analysis of genes deregulated due to heterozygous overexpression of Foxf1 in endothelial and hematopoietic cells using Tie2-cre in embryonic day 18.5 mouse lungs. Total RNA obtained from three ROSA26Foxf1; Tie2-cre mouse lungs compared to three control ROSA26-lox-stop-lox (LSL) -Foxf1 mouse lungs.

2016-09-01 | E-GEOD-77881 | biostudies-arrayexpress

TIE2 mutations in VM

Project description:Venous Malformation: from causative TIE2 mutations to murine model and targeted therapy

| PRJEB9698 | ENA

Gene expression profile in HUVECs before and after Angiopoietin stimulation

Project description:Angiopoietin-Tie2 sytem has been inplicated in both vascular quiescence and angiogenesis. It is unclear how these two opposing signals are regulated from the same receptor-mediated intracellular signal transduction. We have noticed that Tie2 localization upon Angiopoietin stimulation depends upon the presence or absence of cell-cell contacts. Therefore, to identify the downstream signaling of Tie2 upon Angiopoietin stimulation, we performed DNA microarray analyais using RNAs obtained from confluent human umbirical vein endothelial cells (HUVECs) or sparse HUVECs stimulated with after Angiopoietin-1. There is striking difference on gene expression profile between confluent and sparse HUVECs. Keywords: endothelial cell, angiopoietin

2008-04-01 | GSE9677 | GEO

ROSA26Foxf1; Tie2-cre lung gene expression analysis.

Project description:Analysis of genes deregulated due to heterozygous overexpression of Foxf1 in endothelial and hematopoietic cells using Tie2-cre in embryonic day 18.5 mouse lungs.

2016-09-01 | GSE77881 | GEO

Single cell analysis in the adult aorta after Tie2 deletion

Project description:To analyze the Angiopoietin receptor Tie2 on the arterial endothelial cells during atheroclerosis

2023-01-23 | GSE161979 | GEO

Lung endothelial cells (MLECs) from knock-in mouse model with or without the causative HGPS LmnaG609G mutation

Project description:Vascular dysfunction is one of the typical characteristics of aging, but its contributing roles to systemic aging and the therapeutic potential is lacking experimental evidence. Accumulating data suggest that the mechanisms underlying aging are similar to those governing Hutchinson-Gilford progeria syndrome (HGPS), a premature aging disease, in which affected patients succumb to cardiovascular diseases (CVDs). Here, we generated a knock-in mouse model with the causative HGPS LmnaG609G mutation, called progerin. We crossed Lmnaf/f mice with a Tie2-Cre line to get Lmnaf/f;TC mice, which exhibit defective microvasculature and neovascularization, accelerated aging and shortened lifespan. Single-cell transcriptomic analysis of murine lung endothelial cells (MLECs) revealed a significant upregulation of inflammatory response. These data support endothelial dysfunction as a primary trigger of systemic aging and highlight gene therapy as a potential strategy for the clinical treatment of HGPS and age-related vascular dysfunction.

2019-10-17 | GSE138975 | GEO

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