Altered hepatic gene expression in nonalcoholic fatty liver disease is associated with lower hepatic n‐3 and n‐6 polyunsaturated fatty acids

Bianca M. Arendt, Elena M. Comelli, David W.L. Ma, Wendy Lou, Anastasia Teterina, TaeHyung Kim, Scott K. Fung, David K.H. Wong, Ian McGilvray, Sandra E. Fischer, Johane P. Allard – 10 January 2015 – In nonalcoholic fatty liver disease, hepatic gene expression and fatty acid (FA) composition have been reported independently, but a comprehensive gene expression profiling in relation to FA composition is lacking. The aim was to assess this relationship.

Experimental transmission of equine hepacivirus in horses as a model for hepatitis C virus

Joshua D. Ramsay, Ryan Evanoff, Tom E. Wilkinson, Thomas J. Divers, Donald P. Knowles, Robert H. Mealey – 10 January 2015 – Equine hepacivirus (EHCV; nonprimate hepacivirus) is a hepatotropic member of the Flaviviridae family that infects horses. Although EHCV is the closest known relative to hepatitis C virus (HCV), its complete replication kinetics in vivo have not been described, and direct evidence that it causes hepatitis has been lacking. In this study, we detected EHCV in 2 horses that developed post‐transfusion hepatitis.

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.

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.

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.

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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