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Iron increases HMOX1 and decreases hepatitis C viral expression in HCV-expressing cells

World Journal of Gastroenterology 2009年第36期15卷 4499-4510页

作者： Wei-Hong Hou Lisa Rossi Ying Shan Jian-Yu Zheng Richard W Lambrecht Herbert L Bonkovsky The Cannon Research Center and the Liver Digestive Disease and Metabolism Laboratory Carolinas Medical Center Charlotte NC 28203 United States The University of North Carolina Charlotte NC 28223 United States Richard W Lambrecht Department of Medicin e University of Connecticut Health Center Farmington CT 06030 United States Department of Molecular Microbial & Structural Biology University of Connecticut Health Center Farmington CT 06030 United States The Cannon Research Center and the Liver Digestive Disease and Metabolism Laboratory Carolinas Medical Center Charlotte NC 28203 United States The University of North Carolina Charlotte 28223 United States The University of North Carolina Chapel Hill NC 27514 United States Departments of Medicine and Molecular Microbial & Structural Biology University of Connecticut Health Center Farmington CT 06030 United States Department of Medicine of the University of Massachusetts Medical School Worcester MA 01655 United States

AIM： To investigate effects of iron on oxidative stress, heme oxygenase-1 （HMOX1） and hepatitis C viral （HCV） expression in human hepatoma ceils stably expressing HCV proteins. METHODS： Effects of iron on oxidative stress, HMOX1, and HCV expression were assessed in CON1 cells. Measurements included mRNA by quantitative reverse transcription-polymerase chain reaction, and protein levels by Western blots. RESULTS： Iron, in the form of ferric nitrilotriacetate,increased oxidative stress and upegulated HMOX1 gene expression. Iron did not affect mRNA or protein levels of Bach1, a repressor of HMOXl. Silencing the up-regulation of HMOXl nuclear factor-erythroid 2-related factor 2 （Nrf2） by Nrf2-siRNA decreased FeNTA-mediated up-regulation of HMOXl mRNA levels. These iron effects were completely blocked by deferoxamine （DFO）. Iron also significantly decreased levels of HCV core mRNA and protein by 80%-90%, nonstructural 5A mRNA by 90% and protein by about 50% in the Con1 full length HCV replicon cells, whereas DFO increased them. CONCLUSION： Excess iron up-regulates HMOXl and down-regulates HCV gene expression in hepatoma cells. This probably mitigates liver injury caused by combined iron overload and HCV infection.

关键词： Deferoxamine Core protein of hepatitis Cvirus Hepatitis C Iron Heme oxygenase-1 nuclearfactor-erythroid 2-related factor 2 Bachl Oxidativestress Nonstructural 5A protein of hepatitis C virus

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