ApoC-III ASO promotes tissue LPL activity in the absence of apoE-mediated TRL clearance.

ABSTRACT: Hypertriglyceridemia results from accumulation of triglyceride (TG)-rich lipoproteins (TRLs) in the circulation and is associated with increased CVD risk. ApoC-III is an apolipoprotein on TRLs and a prominent negative regulator of TG catabolism. We recently established that in vivo apoC-III predominantly inhibits LDL receptor-mediated and LDL receptor-related protein 1-mediated hepatic TRL clearance and that apoC-III-enriched TRLs are preferentially cleared by syndecan-1 (SDC1). In this study, we determined the impact of apoE, a common ligand for all three receptors, on apoC-III metabolism using apoC-III antisense oligonucleotide (ASO) treatment in mice lacking apoE and functional SDC1 (Apoe ^-/- Ndst1 ^f/f Alb-Cre ⁺). ApoC-III ASO treatm

SUBMITTER: Ramms B 

PROVIDER: S-EPMC6672034 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature