Hepatitis C virus protein expression causes calcium‐mediated mitochondrial bioenergetic dysfunction and nitro‐oxidative stress

Claudia Piccoli, Rosella Scrima, Giovanni Quarato, Annamaria D'Aprile, Maria Ripoli, Lucia Lecce, Domenico Boffoli, Darius Moradpour, Nazzareno Capitanio – 13 June 2007 – Hepatitis C virus (HCV) infection induces a state of oxidative stress that is more pronounced than that in many other inflammatory diseases. In this study we used well‐characterized cell lines inducibly expressing the entire HCV open‐reading frame to investigate the impact of viral protein expression on cell bioenergetics.

Tissue‐type plasminogen activator deficiency exacerbates cholestatic liver injury in mice

Hongtao Wang, Yan Zhang, Robert O. Heuckeroth – 30 May 2007 – Recent studies demonstrating a role for plasminogen activator inhibitor (PAI)‐1 in cholestatic liver disease in mice suggested that tissue‐type plasminogen activator (tPA) or urokinase plasminogen activator (uPA) might be important after biliary tract obstruction. We now demonstrate that blocking tPA exacerbates liver injury after bile duct ligation (BDL).

4‐phenylbutyrate enhances the cell surface expression and the transport capacity of wild‐type and mutated bile salt export pumps

Hisamitsu Hayashi, Yuichi Sugiyama – 30 May 2007 – Progressive familial intrahepatic cholestasis type 2 (PFIC2) is caused by a mutation in the bile salt export pump (BSEP/ABCB11) gene. We previously reported that E297G and D482G BSEP, which are frequently found mutations in European patients, result in impaired membrane trafficking, whereas both mutants retain their transport function. The dysfunctional localization is probably attributable to the retention of BSEP in endoplasmic reticulum (ER) followed by proteasomal degradation.

Subscribe to