Cyclin E1 controls proliferation of hepatic stellate cells and is essential for liver fibrogenesis in mice

Yulia A. Nevzorova, Jörg‐Martin Bangen, Wei Hu, Ute Haas, Ralf Weiskirchen, Nikolaus Gassler, Sebastian Huss, Frank Tacke, Piotr Sicinski, Christian Trautwein, Christian Liedtke – 27 March 2012 – Liver fibrogenesis is associated with the transition of quiescent hepatocytes and hepatic stellate cells (HSCs) into the cell cycle. Exit from quiescence is controlled by E‐type cyclins (cyclin E1 [CcnE1] and cyclin E2 [CcnE2]). Thus, the aim of the current study was to investigate the contribution of E‐type cyclins for liver fibrosis in man and mice.

Impaired intrahepatic natural killer cell cytotoxic function in chronic hepatitis C virus infection

Stefania Varchetta, Dalila Mele, Stefania Mantovani, Barbara Oliviero, Eleonora Cremonesi, Serena Ludovisi, Giuseppe Michelone, Mario Alessiani, Riccardo Rosati, Marco Montorsi, Mario U. Mondelli – 20 March 2012 – Hepatitis C virus (HCV) persistence in the host results from inefficiencies of innate and adaptive immune responses. Most studies addressing the role of innate immunity concentrated on peripheral blood (PB) natural killer (NK) cells, whereas only limited information is available on intrahepatic (IH) NK cells.

Transcriptomic analysis of the woodchuck model of chronic hepatitis B

Simon P. Fletcher, Daniel J. Chin, Yongmei Ji, A. Leonardo Iniguez, Bruce Taillon, David C. Swinney, Palanikumar Ravindran, Donavan T. Cheng, Hans Bitter, Uri Lopatin, Han Ma, Klaus Klumpp, Stephan Menne – 20 March 2012 – The Eastern woodchuck (Marmota monax) is naturally infected with woodchuck hepatitis virus (WHV), a hepadnavirus closely related to the human hepatitis B virus (HBV).

Hepatitis C virus infection enhances TNFα‐induced cell death via suppression of NF‐κB

Junseong Park, Wonseok Kang, Seung‐Wook Ryu, Woo‐Il Kim, Dong‐Yeop Chang, Dong Ho Lee, Do Youn Park, Youn‐Hee Choi, Kyungsun Choi, Eui‐Cheol Shin, Chulhee Choi – 20 March 2012 – Hepatitis C virus (HCV) infection results in liver injury and long‐term complications, such as liver cirrhosis and hepatocellular carcinoma. Liver injury in HCV infection is believed to be caused by host immune responses, not by viral cytopathic effects. Tumor necrosis factor‐alpha (TNF‐α) plays a pivotal role in the inflammatory processes of hepatitis C.

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