Project description: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.
Project description:Purpose: The goal of this study was to evaluate the effect of ANGPTL3 inhibition on liver transcriptomes in LDLR KO mice. Methods: Mice were treated once weekly for 3 weeks with 25mg/kg control mAb or ANGPTL3 mAb. Livers were harvested 6 days after the last mAb treatment. Results: ANGPTL3 inhibition had no major impact on hepatic gene expression.
Project description:Even though the functions of ANGPTL3 in the circulation are relatively well characterized, many mechanistic questions regarding the molecular consequences of ANGPTL3 loss-of-function and protection against cardiovascular disease remain unanswered. To help understant the molecular mechanisms exerted by ANGPTL3 deficiency, we studied the alterations of ANGPTL3 loss-of-function in hepatocytes and plasma lipid molecular species profiles.
Project description:This SuperSeries is composed of the following subset Series: GSE36242: Transcriptomic response to benzo[a]pyrene treatment in HepG2 cells (RNA-Seq) GSE36243: Transcriptomic response to benzo[a]pyrene treatment in HepG2 cells (Affymetrix) Refer to individual Series