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.
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.
Project description:This research aimed to investigate the aberrant expression of circRNA, messenger RNA, and microRNA in orbital venous malformation. A competitive endogenous RNA network was constructed to elucidate their potential roles in orbital venous malformation.
Project description:This research aimed to investigate the aberrant expression of circRNA, messenger RNA, and microRNA in orbital venous malformation. A competitive endogenous RNA network was constructed to elucidate their potential roles in orbital venous malformation.
Project description:Proteomics and high connotation functional gene screening (HCS) were used to screen key functional genes that play important roles in the pathogenesis of venous malformation.
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:Single cell transcriptome sequencing of venous malformation
Project description:Akt is a robust oncogene that plays key roles in the development and progression of many cancers, including glioma. We evaluated the differential propensities of the Akt isoforms toward progression in the well-characterized RCAs/Ntv-a mouse model of PDGFB-driven low grade glioma. A constitutively active myristoylated form of Akt1 did not induce high-grade glioma (HGG). In stark contrast, Akt2 and Akt3 showed strong progression potential with 78% and 97% of tumors diagnosed as HGG, respectively. We further revealed that significant variations in polarity and hydropathy values among the Akt isoforms in both the pleckstrin homology domain (P domain) and regulatory domain (R domain) were critical in mediating glioma progression. Gene expression profiles from representative Akt-derived tumors indicated dominant and distinct roles for Akt3, consisting primarily of DNA repair pathways. TCGA data from human GBM closely reflected the DNA repair function, as Akt3 was significantly correlated with a 76 gene signature DNA repair panel. Consistently, compared to Akt1 and Akt2 overexpression models, Akt3-expressing human GBM cells had enhanced activation of DNA repair proteins, leading to increased DNA repair and subsequent resistance to radiation and temozolomide. Given the wide range of Akt3-amplified cancers, Akt3 may represent a key resistance factor. 5 different experimental conditions were compared (including GFP, PDGFB, PDGFB in conjunciton with Akt1, Akt2, or Akt3) with 3 mice per treatment