Transcriptomic profile of ANGPTL3-deficient HepG2 cells
Cardiovascular disease is a leading cause of death worldwide, and inhibition of the hepatically secreted protein ANGPTL3 has emerged as an effective treatment for lowering low-density lipoprotein cholesterol (LDL), the cardinal risk factor for coronary artery disease (CAD). In this study, we examine the effects of complete genetic deficiency of ANGPTL3 on the hepatocyte transcriptome using a HepG2 cell culture model with the ANGPTL3 locus "knocked out" (KO) via CRISPR-Cas9. Overall design: Wild type (WT) and ANGPTL3-knockout (KO) HepG2 cells were exposed to either vehicle control (fatty acid-free BSA) or 200uM oleic acid (conjugated to fatty acid-free BSA) in serum-free media for 12hr before sample collection.