Epigenetic silencing of DACH1 induces loss of transforming growth factor‐β1 antiproliferative response in human hepatocellular carcinoma

Hongbin Zhu, Kongming Wu, Wenji Yan, Ling Hu, Jing Yuan, Yan Dong, Yazhuo Li, Kunyu Jing, Yunsheng Yang, Mingzhou Guo – 20 June 2013 – Human dachshund homolog 1 (DACH1) is a major component of the Retinal Determination Gene Network (RDGN) and functions as a tumor suppressor. However, the regulation of DACH1 expression and its function in hepatocellular carcinoma (HCC) remain unclear. In this study, epigenetic changes of DACH1 were analyzed in HCC cell lines and primary cancers.

Hepatic myofibroblasts promote the progression of human cholangiocarcinoma through activation of epidermal growth factor receptor

Audrey Clapéron, Martine Mergey, Lynda Aoudjehane, Thanh Huong Nguyen Ho‐Bouldoires, Dominique Wendum, Aurélie Prignon, Fatiha Merabtene, Delphine Firrincieli, Christèle Desbois‐Mouthon, Olivier Scatton, Filomena Conti, Chantal Housset, Laura Fouassier – 20 June 2013 – Intrahepatic cholangiocarcinoma (CCA) is characterized by an abundant desmoplastic environment.

Hepatic‐specific lipin‐1 deficiency exacerbates experimental alcohol‐induced steatohepatitis in mice

Ming Hu, Huquan Yin, Mayurranjan S. Mitra, Xiaomei Liang, Joanne M. Ajmo, Karim Nadra, Roman Chrast, Brian N. Finck, Min You – 20 June 2013 – Lipin‐1 regulates lipid metabolism by way of its function as an enzyme in the triglyceride synthesis pathway and as a transcriptional coregulatory protein and is highly up‐regulated in alcoholic fatty liver disease. In the present study, using a liver‐specific lipin‐1‐deficient (lipin‐1LKO) mouse model, we aimed to investigate the functional role of lipin‐1 in the development of alcoholic steatohepatitis and explore the underlying mechanisms.

Dysfunctional CD39POS regulatory T cells and aberrant control of T‐helper type 17 cells in autoimmune hepatitis

Charlotte R. Grant, Rodrigo Liberal, Beth S. Holder, John Cardone, Yun Ma, Simon C. Robson, Giorgina Mieli‐Vergani, Diego Vergani, Maria Serena Longhi – 20 June 2013 – Autoimmune hepatitis (AIH) is an important cause of severe liver disease and is associated with both quantitative and qualitative regulatory T‐cell (Treg) impairments. Tregs express CD39, an ectonucleotidase responsible for extracellular nucleotide hydrolysis, culminating in the production of immunosuppressive adenosine.

Adaptation of iron transport and metabolism to acute high‐altitude hypoxia in mountaineers

Oliver Goetze, Johannes Schmitt, Kerstin Spliethoff, Igor Theurl, Günter Weiss, Dorine W. Swinkels, Harold Tjalsma, Marco Maggiorini, Pierre Krayenbühl, Monika Rau, Heiko Fruehauf, Kacper A. Wojtal, Beat Müllhaupt, Michael Fried, Max Gassmann, Thomas Lutz, Andreas Geier – 20 June 2013 – Human iron homeostasis is regulated by intestinal iron transport, hepatic hepcidin release, and signals from pathways that consume or supply iron.

Concurrent deletion of cyclin E1 and cyclin‐dependent kinase 2 in hepatocytes inhibits DNA replication and liver regeneration in mice

Wei Hu, Yulia A. Nevzorova, Ute Haas, Nives Moro, Piotr Sicinski, Yan Geng, Mariano Barbacid, Christian Trautwein, Christian Liedtke – 20 June 2013 – The liver has a strong regenerative capacity. After injury, quiescent hepatocytes can reenter the mitotic cell cycle to restore tissue homeostasis. This G0/G1‐S cell‐cycle transition of primed hepatocytes is regulated by complexes of cyclin‐dependent kinase 2 (Cdk2) with E‐type cyclins (CcnE1 or CcnE2). However, single genetic ablation of either E‐cyclin or Cdk2 does not affect overall liver regeneration.

Impact of the center on graft failure after liver transplantation

Sumeet K. Asrani, W. Ray Kim, Erick B. Edwards, Joseph J. Larson, Gabriel Thabut, Walter K. Kremers, Terry M. Therneau, Julie Heimbach – 19 June 2013 – The hospital at which liver transplantation (LT) is performed has a substantial impact on post‐LT outcomes. Center‐specific outcome data are closely monitored not only by the centers themselves but also by patients and government regulatory agencies.

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