Vascular cell adhesion molecule 1 expression by biliary epithelium promotes persistence of inflammation by inhibiting effector T‐cell apoptosis

Simon C. Afford, Elizabeth H. Humphreys, Danielle T. Reid, Clare L. Russell, Vanessa M. Banz, Ye Oo, Tina Vo, Craig Jenne, David H. Adams, Bertus Eksteen – 12 December 2013 – Chronic hepatitis occurs when effector lymphocytes are recruited to the liver from blood and retained in tissue to interact with target cells, such as hepatocytes or bile ducts (BDs). Vascular cell adhesion molecule 1 (VCAM‐1; CD106), a member of the immunoglobulin superfamily, supports leukocyte adhesion by binding α4β1 integrins and is critical for the recruitment of monocytes and lymphocytes during inflammation.

SIRT1 controls liver regeneration by regulating bile acid metabolism through farnesoid X receptor and mammalian target of rapamycin signaling

Juan L. García‐Rodríguez, Lucía Barbier‐Torres, Sara Fernández‐Álvarez, Virginia Gutiérrez‐de Juan, María J. Monte, Emina Halilbasic, Daniel Herranz, Luis Álvarez, Patricia Aspichueta, Jose J.G. Marín, Michael Trauner, Jose M. Mato, Manuel Serrano, Naiara Beraza, María Luz Martínez‐Chantar – 12 December 2013 – Sirtuin1 (SIRT1) regulates central metabolic functions such as lipogenesis, protein synthesis, gluconeogenesis, and bile acid (BA) homeostasis through deacetylation. Here we describe that SIRT1 tightly controls the regenerative response of the liver.

Molecular mechanistic explanation for the spectrum of cholestatic disease caused by the S320F variant of ABCB4

Edward J. Andress, Michael Nicolaou, Marta R. Romero, Sandhia Naik, Peter H. Dixon, Catherine Williamson, Kenneth J. Linton – 12 December 2013 – ABCB4 flops phosphatidylcholine into the bile canaliculus to protect the biliary tree from the detergent activity of bile salts. Homozygous‐null ABCB4 mutations cause the childhood liver disease, progressive familial intrahepatic cholestasis, but cause and effect is less clear, with many missense mutations linked to less severe cholestatic diseases.

Hepatocyte‐specific Ptpn6 deletion promotes hepatic lipid accretion, but reduces NAFLD in diet‐induced obesity: Potential role of PPARγ

Elaine Xu, Marie‐Pier Forest, Michael Schwab, Rita Kohen Avramoglu, Emmanuelle St‐Amand, Annabelle Z. Caron, Kerstin Bellmann, Michaël Shum, Gregory Voisin, Marilene Paquet, Alain Montoudis, Emile Lévy, Katherine A. Siminovitch, Benjamin G. Neel, Nicole Beauchemin, André Marette – 11 December 2013 – Hepatocyte‐specific Shp1 knockout mice (Ptpn6H‐KO) are protected from hepatic insulin resistance evoked by high‐fat diet (HFD) feeding for 8 weeks.

Rationale of personalized immunosuppressive medication for hepatocellular carcinoma patients after liver transplantation

Kan Chen, Kwan Man, Herold J. Metselaar, Harry L. A. Janssen, Maikel P. Peppelenbosch, Qiuwei Pan – 10 December 2013 – Liver transplantation is the only potentially curative treatment for hepatocellular carcinoma (HCC) that is not eligible for surgical resection. However, disease recurrence is the main challenge to the success of this treatment. Immunosuppressants that are universally used after transplantation to prevent graft rejection could potentially have a significant impact on HCC recurrence.

T‐cell Ig and ITIM domain regulates natural killer cell activation in murine acute viral hepatitis

Jiacheng Bi, Qing Zhang, Dan Liang, Lei Xiong, Haiming Wei, Rui Sun, Zhigang Tian – 9 December 2013 – Uncontrolled natural killer (NK) cell activation during the early response to acute viral infection can lead to severe immunopathology, and the mechanisms NK cells use to achieve self‐tolerance in such contexts are currently unclear. Here, NK cells up‐regulated a coinhibitory receptor, T‐cell Ig and ITIM domain (TIGIT), during challenge with the viral double‐stranded RNA (dsRNA) analog poly I:C.

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