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dc.contributor.authorPattranuch Chusrien_US
dc.contributor.authorKattareeya Kumthipen_US
dc.contributor.authorJian Hongen_US
dc.contributor.authorChuanlong Zhuen_US
dc.contributor.authorXiaoqiong Duanen_US
dc.contributor.authorNikolaus Jilgen_US
dc.contributor.authorDahlene N. Fuscoen_US
dc.contributor.authorCynthia Brisacen_US
dc.contributor.authorEsperance A. Schaeferen_US
dc.contributor.authorDachuan Caien_US
dc.contributor.authorLee F. Pengen_US
dc.contributor.authorNiwat Maneekarnen_US
dc.contributor.authorWenyu Linen_US
dc.contributor.authorRaymond T. Chungen_US
dc.description.abstractHCV replication disrupts normal endoplasmic reticulum (ER) function and activates a signaling network called the unfolded protein response (UPR). UPR is directed by three ER transmembrane proteins including ATF6, IRE1, and PERK. HCV increases TGF-β1 and oxidative stress, which play important roles in liver fibrogenesis. HCV has been shown to induce TGF-β1 through the generation of reactive oxygen species (ROS) and p38 MAPK, JNK, ERK1/2, and NFκB-dependent pathways. However, the relationship between HCV-induced ER stress and UPR activation with TGF-β1 production has not been fully characterized. In this study, we found that ROS and JNK inhibitors block HCV up-regulation of ER stress and UPR activation. ROS, JNK and IRE1 inhibitors blocked HCV-activated NFκB and TGF-β1 expression. ROS, ER stress, NFκB, and TGF-β1 signaling were blocked by JNK specific siRNA. Knockdown IRE1 inhibited JFH1-activated NFκB and TGF-β1 activity. Knockdown of JNK and IRE1 blunted JFH1 HCV up-regulation of NFκB and TGF-β1 activation. We conclude that HCV activates NFκB and TGF-β1 through ROS production and induction of JNK and the IRE1 pathway. HCV infection induces ER stress and the UPR in a JNK-dependent manner. ER stress and UPR activation partially contribute to HCV-induced NF-κB activation and enhancement of TGF-β1.en_US
dc.titleHCV induces transforming growth factor β1 through activation of endoplasmic reticulum stress and the unfolded protein responseen_US
article.title.sourcetitleScientific Reportsen_US
article.volume6en_US General Hospitalen_US Mai Universityen_US of Nanjing Medical Universityen_US Academy of Medical Sciencesen_US Medical Universityen_US
Appears in Collections:CMUL: Journal Articles

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