Impaired uptake of conjugated bile acids and hepatitis b virus pres1‐binding in na+‐taurocholate cotransporting polypeptide knockout mice

Davor Slijepcevic, Christina Kaufman, Catharina G.K. Wichers, Eduardo H. Gilglioni, Florian A. Lempp, Suzanne Duijst, Dirk R. de Waart, Ronald P.J. Oude Elferink, Walter Mier, Bruno Stieger, Ulrich Beuers, Stephan Urban, Stan F.J. van de Graaf – 10 January 2015 – The Na+‐taurocholate cotransporting polypeptide (NTCP) mediates uptake of conjugated bile acids (BAs) and is localized at the basolateral membrane of hepatocytes. It has recently been recognized as the receptor mediating hepatocyte‐specific entry of hepatitis B virus and hepatitis delta virus.

How to optimize hepatitis C virus treatment impact on life years saved in resource‐constrained countries

Dorothée Obach, Yazdan Yazdanpanah, Gamal Esmat, Anchalee Avihingsanon, Sahar Dewedar, Nicolas Durier, Alain Attia, Wagida A. Anwar, Anthony Cousien, Pisit Tangkijvanich, Serge Paul Eholié, Wahid Doss, Aya Mostafa, Arnaud Fontanet, Mostafa K. Mohamed, Sylvie Deuffic‐Burban – 10 January 2015 – In resource‐constrained countries where the prevalence of hepatitis C virus (HCV) disease is usually high, it is important to know which population should be treated first in order to increase treatment effectiveness.

Adaptive remodeling of the biliary architecture underlies liver homeostasis

Kota Kaneko, Kenji Kamimoto, Atsushi Miyajima, Tohru Itoh – 8 January 2015 – Serving as the center for metabolism and detoxification, the liver is inherently susceptible to a wide variety of damage imposed by toxins or chemicals. Induction of cell populations with biliary epithelial phenotypes, which include progenitor‐like cells and are referred to as liver progenitor cells, is often observed in histopathological examination of various liver diseases in both human patients and animal models and has been implicated in regeneration.

Adaptive remodeling of the biliary architecture underlies liver homeostasis

Kota Kaneko, Kenji Kamimoto, Atsushi Miyajima, Tohru Itoh – 8 January 2015 – Serving as the center for metabolism and detoxification, the liver is inherently susceptible to a wide variety of damage imposed by toxins or chemicals. Induction of cell populations with biliary epithelial phenotypes, which include progenitor‐like cells and are referred to as liver progenitor cells, is often observed in histopathological examination of various liver diseases in both human patients and animal models and has been implicated in regeneration.

Cannabinoid receptor 1 promotes hepatocellular carcinoma initiation and progression through multiple mechanisms

Bani Mukhopadhyay, Kornel Schuebel, Partha Mukhopadhyay, Resat Cinar, Grzegorz Godlewski, Keming Xiong, Ken Mackie, Martin Lizak, Qiaoping Yuan, David Goldman, George Kunos – 7 January 2015 – Hepatocellular carcinoma (HCC) has high mortality and no adequate treatment. Endocannabinoids interact with hepatic cannabinoid 1 receptors (CB1Rs) to promote hepatocyte proliferation in liver regeneration by inducing cell cycle proteins involved in mitotic progression, including Forkhead Box M1.

IL‐33 facilitates oncogene‐induced cholangiocarcinoma in mice by an interleukin‐6‐sensitive mechanism

Daisaku Yamada, Sumera Rizvi, Nataliya Razumilava, Steven F. Bronk, Jaime I. Davila, Mia D. Champion, Mitesh J. Borad, Jorge A. Bezerra, Xin Chen, Gregory J. Gores – 7 January 2015 – Cholangiocarcinoma (CCA) is a lethal hepatobiliary neoplasm originating from the biliary apparatus. In humans, CCA risk factors include hepatobiliary inflammation and fibrosis. The recently identified interleukin (IL)−1 family member, IL‐33, has been shown to be a biliary mitogen which also promotes liver inflammation and fibrosis. Our aim was to generate a mouse model of CCA mimicking the human disease.

The small GTPase Rab7 as a central regulator of hepatocellular lipophagy

Barbara Schroeder, Ryan J. Schulze, Shaun G. Weller, Arthur C. Sletten, Carol A. Casey, Mark A. McNiven – 6 January 2015 – Autophagy is a central mechanism by which hepatocytes catabolize lipid droplets (LDs). Currently, the regulatory mechanisms that control this important process are poorly defined. The small guanosine triphosphatase (GTPase) Rab7 has been implicated in the late endocytic pathway and is known to associate with LDs, although its role in LD breakdown has not been tested.

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