RNA-sequencing of Endothelial Cell Lines Expressing TIE2 WT or Mutant TIE2-L914F
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE307395 | GEO | 2025/09/26
REPOSITORIES: GEO
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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
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.
2013-06-04 | GSE46684 | GEO
Project description:Venous Malformation: from causative TIE2 mutations to murine model and targeted therapy
| PRJEB9698 | ENA
Project description:To identify the miRNA expressing profiles of TIE2 expressing Monocytes (TEMs), we have employed the Agilent Human miRNA 8×60K (Design ID:046064) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.
2017-05-19 | GSE68322 | GEO
Project description:To identify the gene expressing profiles of TIE2 expressing Monocytes(TEMs), we have employed the Agilent lncRNA Gene Expression 4Ã180K(Design ID:042818) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.Expressions of sixteen genes (CDKN1A, FDXR, SESN1, BBC3 and PHPT1) from this signature was quantified in the same RNA samples by real-time PCR, confirming low variability between donors as well as the predicted radiation response pattern. The gene expressions of three independent paried TEMs and TIE2- Monocytes samples from different donors were measured.
2017-05-17 | E-GEOD-57783 | biostudies-arrayexpress
Project description:To identify the gene expressing profiles of TIE2 expressing Monocytes(TEMs), we have employed the Agilent lncRNA Gene Expression 4×180K(Design ID:042818) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.Expressions of sixteen genes (CDKN1A, FDXR, SESN1, BBC3 and PHPT1) from this signature was quantified in the same RNA samples by real-time PCR, confirming low variability between donors as well as the predicted radiation response pattern.
2017-05-17 | GSE57783 | GEO
Project description:RNA-sequencing of Endothelial Cell Lines Expressing TIE2 WT or Mutant TIE2-L914F
| PRJNA1320648 | ENA
Project description:Stroke is a leading cause of death and long-term disability. In up to 30% of cases the underlying etiology is cerebral small vessel disease (SVD), the mechanisms of which are insufficiently understood. Genome-wide association studies have identified FOXF2 as a major risk gene for SVD and stroke. Foxf2 encodes a transcription factor that in the brain is primarily expressed in endothelial cells (ECs) and pericytes but the mechanisms linking Foxf2 to cerebrovascular disease are unknown. Here we show that Foxf2 maintains EC function via Tie2 signaling and limits infarct size in mice after middle cerebral artery occlusion. EC-specific inactivation of Foxf2 in adult mice resulted in blood-brain barrier leakage, which was exacerbated after experimental stroke compared to controls. Proteomic analyses of brain ECs from Foxf2 deficient mice as well as human pluripotent stem cell (iPSC) derived ECs lacking FOXF2 revealed a downregulation of multiple proteins involved in Tie2 signaling. We further found that endothelial Foxf2 deficiency compromises functional hyperemia, reduces endothelial NO production, and increases the size of experimentally induced infarcts via Tie2 signaling. Pharmacological treatment with the Tie2 activator AKB-9778 rescued the effects of Foxf2 deficiency on key outcomes. Moreover, RNA sequencing in combination with chromatin immunoprecipitation sequencing (ChIP-seq) in ECs revealed that FOXF2 functions as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. Collectively, our results highlight the role of endothelial dysfunction and of reduced Tie2 signaling in SVD and stroke, thus offering new perspectives for therapeutic interventions.
2025-04-26 | GSE265959 | GEO
Project description:Stroke is a leading cause of death and long-term disability. In up to 30% of cases the underlying etiology is cerebral small vessel disease (SVD), the mechanisms of which are insufficiently understood. Genome-wide association studies have identified FOXF2 as a major risk gene for SVD and stroke. Foxf2 encodes a transcription factor that in the brain is primarily expressed in endothelial cells (ECs) and pericytes but the mechanisms linking Foxf2 to cerebrovascular disease are unknown. Here we show that Foxf2 maintains EC function via Tie2 signaling and limits infarct size in mice after middle cerebral artery occlusion. EC-specific inactivation of Foxf2 in adult mice resulted in blood-brain barrier leakage, which was exacerbated after experimental stroke compared to controls. Proteomic analyses of brain ECs from Foxf2 deficient mice as well as human pluripotent stem cell (iPSC) derived ECs lacking FOXF2 revealed a downregulation of multiple proteins involved in Tie2 signaling. We further found that endothelial Foxf2 deficiency compromises functional hyperemia, reduces endothelial NO production, and increases the size of experimentally induced infarcts via Tie2 signaling. Pharmacological treatment with the Tie2 activator AKB-9778 rescued the effects of Foxf2 deficiency on key outcomes. Moreover, RNA sequencing in combination with chromatin immunoprecipitation and sequencing in ECs revealed that FOXF2 functions as a transcriptional activator of Tie2 and other endothelial lineage-specific genes. Collectively, our results highlight the role of endothelial dysfunction and of reduced Tie2 signaling in SVD and stroke, thus offering new perspectives for therapeutic interventions.
2025-09-10 | GSE265820 | GEO
Project description:Expression data: Venous malformation-causative TIE2-mutations mediate an AKT-dependent decrease in PDGFB
| PRJNA201508 | ENA