Platelets and Platelet‐Derived Extracellular Vesicles in Liver Physiology and Disease

Alexandre Balaphas, Jeremy Meyer, Karin Sadoul, Pierre Fontana, Philippe Morel, Carmen Gonelle‐Gispert, Leo H. Bühler – 22 April 2019 – Beyond their role in hemostasis, platelets are proposed as key mediators of several physiological and pathophysiological processes of the liver, such as liver regeneration, toxic or viral acute liver injury, liver fibrosis, and carcinogenesis. The effects of platelets on the liver involve interactions with sinusoidal endothelial cells and the release of platelet‐contained molecules following platelet activation.

Liver Macrophages: Old Dogmas and New Insights

Adrien Guillot, Frank Tacke – 22 April 2019 – Inflammation is a hallmark of virtually all liver diseases, such as liver cancer, fibrosis, nonalcoholic steatohepatitis, alcoholic liver disease, and cholangiopathies. Liver macrophages have been thoroughly studied in human disease and mouse models, unravelling that the hepatic mononuclear phagocyte system is more versatile and complex than previously believed. Liver macrophages mainly consist of liver‐resident phagocytes, or Kupffer cells (KCs), and bone marrow‐derived recruited monocytes.

Emricasan Ameliorates Portal Hypertension and Liver Fibrosis in Cirrhotic Rats Through a Hepatocyte‐Mediated Paracrine Mechanism

Jordi Gracia‐Sancho, Nicolò Manicardi, Martí Ortega‐Ribera, Raquel Maeso‐Díaz, Sergi Guixé‐Muntet, Anabel Fernández‐Iglesias, Diana Hide, Héctor García‐Calderó, Zoe Boyer‐Díaz, Patricia C. Contreras, Alfred Spada, Jaime Bosch – 22 April 2019 – In cirrhosis, liver microvascular dysfunction is a key factor increasing hepatic vascular resistance to portal blood flow, which leads to portal hypertension. De‐regulated inflammatory and pro‐apoptotic processes due to chronic injury play important roles in the dysfunction of liver sinusoidal cells.

Immune Determinants in the Acquisition and Maintenance of Antibody to Hepatitis B Surface Antigen in Adults After First‐Time Hepatitis B Vaccination

Hiroyoshi Doi, Sachiyo Yoshio, Keiichiro Yoneyama, Hironari Kawai, Yuzuru Sakamoto, Tomonari Shimagaki, Yoshihiko Aoki, Yosuke Osawa, Hitoshi Yoshida, Tatsuya Kanto – 22 April 2019 – Global implementation of a birth‐dose hepatitis B (HB) vaccine has significantly reduced the prevalence of hepatitis B virus (HBV) carriers. Durable and sufficient titers of antibodies to hepatitis B surface antigen (anti‐HBs) are desirable for vaccinees to gain resistance to HBV exposure.

Circular RNA MAT2B Promotes Glycolysis and Malignancy of Hepatocellular Carcinoma Through the miR‐338‐3p/PKM2 Axis Under Hypoxic Stress

Qing Li, Xiongxiong Pan, Deming Zhu, Zhengming Deng, Runqiu Jiang, Xuehao Wang – 20 April 2019 – Glucose metabolism reprogramming, which is a well‐established characteristic of multiple cancers, demands a higher rate of glycolysis to meet the increasing demands for macromolecular synthesis and to maintain rapid proliferation in a hypoxic environment. However, the mechanism underlying this switch remains to be elucidated. In this study, we investigated the function of circular RNA MAT2B (circMAT2B) in hepatocellular carcinoma (HCC) glucose metabolism reprogramming and malignancy.

Impaired Chylomicron Assembly Modifies Hepatic Metabolism Through Bile Acid–Dependent and Transmissible Microbial Adaptations

Yan Xie, Hitoshi Matsumoto, Susan Kennedy, Elizabeth P. Newberry, William Moritz, Brian J. DeBosch, Kelle H. Moley, Deborah C. Rubin, Brad W. Warner, Andrew L. Kau, Phillip I. Tarr, Todd N. Wylie, Kristine M. Wylie, Nicholas O. Davidson – 20 April 2019 – The mechanisms by which alterations in intestinal bile acid (BA) metabolism improve systemic glucose tolerance and hepatic metabolic homeostasis are incompletely understood.

p300 Acetyltransferase Is a Cytoplasm‐to‐Nucleus Shuttle for SMAD2/3 and TAZ Nuclear Transport in Transforming Growth Factor β–Stimulated Hepatic Stellate Cells

Yuanguo Wang, Kangsheng Tu, Donglian Liu, Luyang Guo, Yunru Chen, Qing Li, Jessica L. Maiers, Zhikui Liu, Vijay H. Shah, Changwei Dou, Daniel Tschumperlin, Luke Voneschen, Rendong Yang, Ningling Kang – 20 April 2019 – Nuclear translocation of mothers against decapentaplegic homolog 2/3 (SMAD2/3), core transcription factors of transforming growth factor β (TGF‐β) signaling, is critical for hepatic stellate cell (HSC) differentiation into metastasis‐promoting myofibroblasts.

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