Project description:Sterol regulatory element-binding protein 2 (SREBP2) is a transcription factor that has been recently discovered to mediate vascular endothelial cell (EC) dysfunction. We therefore investigated the role of SREBP2 in EC function through comparing the transciptional profiling of human umbilical vein endothelial cells (HUVECs) that were infected with adenovirus overexpressing SREBP2 (Ad-SREBP2) or with empty vector (Ad-null) control. Gene ontology analysis revealed that SREBP2 not only regulates cholesterol biosynthesis, but also mediates the TGF, WNT, and cytoskeleton remodeling pathways. Among the responsive genes, SREBP2 exhibited the induction of mesenchymal transition.
Project description:Sterol regulatory element-binding protein 2 (SREBP2) is a transcription factor that has been recently discovered to mediate vascular endothelial cell (EC) dysfunction. We therefore investigated the role of SREBP2 in the epigenetic function of EC biology through comparing ATAC-seq of human umbilical vein endothelial cells (HUVECs) that were infected with adenovirus overexpressing SREBP2 (Ad-SREBP2) or with empty vector (Ad-null) control. Gene ontology analysis revealed that SREBP2 not only decondenses chromatin for cholesterol biosynthesis, but also mediates the TGF pathway. Among the responsive promoter, SREBP2 exhibited the induction of genes related to mesenchymal transition.
Project description:Atheroprotective flow (e.g., pulsatile shear stress) and statins drastically induce the expression of krüppel-like factor 4 (KLF4) in vascular endothelial cells (ECs). We therefore investigated the role of KLF4 in EC function through comparing the transciptional profiling of human umbilical vein endothelial cells (HUVECs) that were infected with adenovirus overexpression KLF4 (Ad-KLF4) or with empty vector (Ad-null) control. Gene ontology analysis revealed that KLF4 not only regulates EC homeostasis through the upregulation of nitric oxide synthesis and vascular development, but also mediates response to lipid. Among the lipid responsive genes, KLF4 exhibited induction of cholesterol efflux and oxidation [i.e., liver X receptor (LXR) and cholesterol 25-hydroxylase (Ch25h)], while suppressing cholesterol biosynthesis [i.e., sterol regulatory element-binding protein 2 (SREBP2)].
Project description:Oxidoreductase enzymes are critical to redox regulation of intracellular proteins within human cells. We used microarrays to identify which oxidreducatse genes are expressed in unstimulated human umbilical vein endothelial cells. Human umbilical vein endothelial cells were grown under optimal conditions and then RNA extracted and hybridized on Affymetrix microarrays.
Project description:We profiled global gene expression in primary human umbilical vein endothelial cells to determine the gene expression changes associated with knocking down PKM2 and p53. We identified a p53 dependent transcriptional response that remodels metabolism in cells lacking p53, thus limiting cell growth. Human Umbilical Vein Endothelial Cells were transfected with siRNA duplexes targeting PKM2 and / or p53, RNA was extracted and subjected to RNA sequencing
Project description:We quantified differential microRNA (miRNA) expression in Human umbilical vein endothelial cells (HUVECs)response to Angiogenin (ANG) treatment.These data were used to determine which miRNAs are altered on ANG in Human umbilical vein endothelial cells.
Project description:To investigate machanism of miR-210-3p regulating angiogenic ability of human umbilical vein endothelial cells (HUVECs) in hypoxic conditions, we transfected miR-210-3p mimic to overexpress miR-210-3p in human umbilical vein endothelial cells. We than performed RNA sequencing of miR-210-3p mimic-transfected and control HUVECs under hypoxic conditions to evaluate the transcriptional changes in the miR-210-3p-overexpressing HUVECs.