Ammonia mediates cortical hemichannel dysfunction in rodent models of chronic liver disease

Anna Hadjihambi, Francesco Chiara, Patrick S. Hosford, Abeba Habtetion, Anastassios Karagiannis, Nathan Davies, Alexander V. Gourine, Rajiv Jalan – 9 January 2017 – The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and ammonia is thought to play a key role. Astroglial dysfunction is known to be present in HE. Astrocytes are extensively connected by gap junctions formed of connexins, which also exist as functional hemichannels allowing exchange of molecules between the cytoplasm and the extracellular milieu.

Bone marrow stem cell therapy partially ameliorates pathological consequences in livers of mice expressing mutant human α1‐antitrypsin

Prakash Baligar, Veena Kochat, Shailendra K. Arindkar, Zaffar Equbal, Snehashish Mukherjee, Swati Patel, Perumal Nagarajan, Sujata Mohanty, Jeffrey H. Teckman, Asok Mukhopadhyay – 5 January 2017 – Alpha‐1‐antitrypsin (AAT) deficiency (AATD) is a genetic disease, caused by mutation of the AAT gene. Accumulation of mutated AAT protein aggregates in hepatocytes leads to endoplasmic reticulum stress, resulting in impairment of liver functions and, in some cases, hepatocellular carcinoma, whereas decline of AAT levels in sera is responsible for pulmonary emphysema.

Knockout of the primary sclerosing cholangitis‐risk gene Fut2 causes liver disease in mice

Luca Maroni, Simon D. Hohenester, Stan F.J. van de Graaf, Dagmar Tolenaars, Krijn van Lienden, Joanne Verheij, Marco Marzioni, Tom H. Karlsen, Ronald P.J. Oude Elferink, Ulrich Beuers – 5 January 2017 – The etiopathogenesis of primary sclerosing cholangitis is unknown. Genetic variants of fucosyltransferase 2 (FUT2) have been identified in genome‐wide association studies as risk factors for primary sclerosing cholangitis. We investigated the role of Fut2 in murine liver pathophysiology by studying Fut2–/– mice.

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