FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells

V. S. Shavva, A. M. Bogomolova, A. A. Nikitin, E. B. Dizhe, G. N. Oleinikova, I. A. Lapikov, D. A. Tanyanskiy, A. P. Perevozchikov, S. V. Orlov

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Reactive oxygen species damage various cell components including DNA, proteins, lipids and these impairments could be a reason for severe human diseases including atherosclerosis. Forkhead box O1 (FOXO1), an important metabolic transcription factor, upregulates antioxidant and proapoptotic genes during oxidative stress. Apolipoprotein A-I (ApoA-I) forms High Density Lipoprotein (HDL) particles that are responsible for cholesterol transfer from peripheral tissues to liver for removal in bile in vertebrates. The main sources for plasma ApoA-I in mammals are liver and jejunum. Hepatic apoA-I transcription depends on a multitude of metabolic transcription factors. We demonstrate that ApoA-I synthesis and secretion are decreased during H2O2-induced oxidative stress in human hepatoma cell line HepG2. Here we first show that FOXO1 binds to site B of apoA-I hepatic enhancer and downregulates apoA-I gene activity in HepG2 cells. Moreover, FOXO1 and LXRα transcription factors participate in H2O2-triggered downregulatio
Original languageEnglish
JournalCell Stress and Chaperones
DOIs
StatePublished - 2016
Externally publishedYes

Keywords

  • apolipoprotein A-I
  • oxidative stress
  • hydrogen peroxide
  • FOXO1
  • LXRα

Fingerprint

Dive into the research topics of 'FOXO1 and LXRα downregulate the apolipoprotein A-I gene expression during hydrogen peroxide-induced oxidative stress in HepG2 cells'. Together they form a unique fingerprint.

Cite this