Oxidative stress has been identified as a key mechanism of hepatitis C virus (HCV)-induced pathogenesis. Studies have suggested that HCV increases the generation of hydroxyl radical and peroxynitrite close to the cell nucleus, inflicting DNA damage, but the source of reactive oxygen species (ROS) remains incompletely characterized. We… (More)
Fig. 6. Hepatocyte Nox1 and Nox4 in genotype 1b HCV-replicating cells and the human liver. (A,B) Telomerase-reconstituted primary human hepatocytes, stably transfected with pEF-CG1bRbz/Neo, pEF-CG1bRbz GND/Neo, or control vector alone, were analyzed for (A) Nox4 and (B) Nox1 proteins by confocal microscopy. Lamin A/C was also analyzed as a nuclear marker. (C-E) HCV-infected (HCVþ) and uninfected (HCV ) human liver samples were analyzed for (C) Nox4, (D) Nox1, and (E) Duox1 proteins by immunofluorescence with confocal microscopy. The nuclear membrane was stained with lamin A/C. Nox/Duox proteins are shown in green, and lamin A/C is shown in red.