Transcriptome Data of KLF4 Overexpression in Human Umbilical Vein Endothelial Cells

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)]. Transcriptome data of HUVECs overexpressing KLF4 using adenovirus followed by deep sequencing, in biological duplicate, using Illumina NextSeq 500.