Expression of apolipoprotein C-IV is regulated by Ku antigen/peroxisome proliferator-activated receptor γ complex and correlates with liver steatosis

Abstract

Background/Aims-We previously reported that hepatitis C virus (HCV) core protein up regulated transcription of apolipoprotein C-IV (ApoC-IV, 10.7-fold increase), a member of the apolipoprotein family implicated in liver steatosis. Here, we identified host transcription factors regulating the ApoC-IV gene expression.

Hepatitis C Virus (HCV)–Apolipoprotein Interactions and Immune Evasion and Their Impact on HCV Vaccine Design

“…In particular, low ApoC-II serum levels were found to be associated with advanced liver fibrosis, which indicate an important role in liver pathogenesis ( 64 ). A similar effect has been observed for the HCV core protein induced upregulation of ApoC-IV that has been also reported to induce hepatic steatosis ( 65 ).…”

Very low-density lipoprotein/lipo-viro particles reverse lipoprotein lipase-mediated inhibition of hepatitis C virus infection via apolipoprotein C-III

“…Previous reports of the effect of apoCs on HCV pathogenesis have shown that: (1) apoC-I associates with HCV virions and enhances HCV infection34 45; (2) apoC-III is a plasmatic biomarker for the resolution of HCV infection46 and (3) the HCV core mediates the overexpression of apoC-IV, which then induces hepatic steatosis 47. This investigation further identifies the VLDL's apoC-III as a positive regulator of HCV infection (tables 3 and 4, figure 6B).…”

Structure of HDL: Particle Subclasses and Molecular Components

“…The protein inhibits lipoprotein lipase (LPL) and hepatic lipase and decreases the uptake of chylomicrons by hepatic cells. ApoC-IV induces hypertriglyceridemia when overexpressed in mice (Allan and Taylor 1996;Kim et al 2008). In normolipidemic plasma, greater than 80 % of the protein resides in VLDL, with most of the remainder in HDL.…”