Hepatitis C virus NS5A and core proteins induce oxidative stress-mediated calcium signalling alterations in hepatocytes

J Hepatol. 2009 May;50(5):872-82. doi: 10.1016/j.jhep.2008.12.026. Epub 2009 Feb 26.

Abstract

Background/aims: The hepatitis C virus (HCV) structural core and non-structural NS5A proteins induce in liver cells a series of intracellular events, including elevation of reactive oxygen and nitrogen species (ROS/RNS). Since oxidative stress is associated to altered intracellular Ca(2+) homeostasis, we aimed to investigate the effect of these proteins on Ca(2+) mobilization in human hepatocyte-derived transfected cells, and the protective effect of quercetin treatment.

Methods: Ca(2+) mobilization and actin reorganization were determined by spectrofluorimetry. Production of ROS/RNS was determined by flow cytometry.

Results: Cells transfected with NS5A and core proteins showed enhanced ROS/RNS production and resting cytosolic Ca(2+) concentration, and reduced Ca(2+) concentration into the stores. Phenylephrine-evoked Ca(2+) release, Ca(2+) entry and extrusion by the plasma membrane Ca(2+)-ATPase were significantly reduced in transfected cells. Similar effects were observed in cytokine-activated cells. Phenylephrine-evoked actin reorganization was reduced in the presence of core and NS5A proteins. These effects were significantly prevented by quercetin. Altered Ca(2+) mobilization and increased calpain activation were observed in replicon-containing cells.

Conclusions: NS5A and core proteins induce oxidative stress-mediated Ca(2+) homeostasis alterations in human hepatocyte-derived cells, which might underlie the effects of both proteins in the pathogenesis of liver disorders associated to HCV infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Antioxidants / pharmacology
  • Calcium / metabolism*
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology*
  • Calcium-Binding Proteins / pharmacology
  • Cell Line
  • Cell Survival / physiology
  • Cysteine Proteinase Inhibitors / pharmacology
  • Cytokines / metabolism
  • Hepacivirus / physiology
  • Hepatitis C / drug therapy
  • Hepatitis C / metabolism
  • Hepatocytes / cytology
  • Hepatocytes / drug effects
  • Hepatocytes / physiology*
  • Homeostasis / drug effects
  • Homeostasis / physiology
  • Humans
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*
  • Quercetin / pharmacology
  • Reactive Nitrogen Species / metabolism
  • Reactive Oxygen Species / metabolism
  • Viral Core Proteins / physiology*
  • Viral Nonstructural Proteins / physiology*
  • Virus Replication / drug effects
  • Virus Replication / physiology

Substances

  • Actins
  • Antioxidants
  • Calcium-Binding Proteins
  • Cysteine Proteinase Inhibitors
  • Cytokines
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Viral Core Proteins
  • Viral Nonstructural Proteins
  • nucleocapsid protein, Hepatitis C virus
  • calpastatin
  • Quercetin
  • NS-5 protein, hepatitis C virus
  • Calcium