Induction of murine hepatocyte death by membrane‐bound CD95 (Fas/APO‐1)‐ligand: Characterization of an in Vitro system

Stephan F. Schlosser, Francesco Azzaroli, Tao Dao, Ravi Hingorani, I. Nicholas Crispe, James L. Boyer – 30 December 2003 – Hepatocytes constitutively express CD95 (also called Fas/APO‐1) and are therefore potential targets for CD95‐ligand (CD95L)‐mediated injury. To study this mechanism of cell death in hepatocytes we developed an in vitro model of liver cell apoptosis using membrane‐bound CD95L as the inducing agent. Primary mouse hepatocytes were cocultured with NIH 3T3 fibroblasts, stably transfected with mouse CD95L (FCD95L+).

Nitric oxide prevents tumor necrosis factor α–induced rat hepatocyte apoptosis by the interruption of mitochondrial apoptotic signaling through S‐nitrosylation of caspase‐8

Young‐Myeong Kim, Tae‐Hyoung Kim, Hun‐Taeg Chung, Robert V. Talanian, Xiao‐Ming Yin, Timothy R. Billiar – 30 December 2003 – Mitochondrial cytochrome c release plays a critical role in apoptotic signal cascade after the activation of cell surface death receptors. We investigated the role played by nitric oxide (NO) in mitochondrial apoptotic signaling in tumor necrosis factor α (TNF‐α) plus actinomycin D (TNF‐α/ActD)‐induced apoptosis.

Hyperstimulation With Interleukin 6 Inhibits Cell Cycle Progression After Hepatectomy in Mice

Torsten Wüstefeld, Tim Rakemann, Stefan Kubicka, Michael P. Manns, Christian Trautwein – 30 December 2003 – Interleukin 6 (IL‐6) is an important mediator of hepatocyte proliferation after hepatectomy. However, elevated IL‐6 levels are found in patients with chronic liver disease. Therefore, it is unclear if hyperstimulation with IL‐6 may have an influence on liver regeneration. We investigated whether a strong activation of IL‐6–dependent pathways may change the course of hepatocyte proliferation after hepatectomy.

Recent Portal or Mesenteric Venous Thrombosis: Increased Recognition and Frequent Recanalization on Anticoagulant Therapy

Bertrand Condat, Fabienne Pessione, Marie Helene Denninger, Sophie Hillaire, Dominique Valla – 30 December 2003 – Characteristics and outcomes of recent portal or mesenteric venous thrombosis are ill‐known. We intended to compare these features with those of patients with portal cavernoma, and also to assess the incidence of recanalization of recent thrombosis on anticoagulation therapy.

Induction by interleukin 6 of Gs‐coupled prostaglandin E2 receptors in rat hepatocytes mediating a prostaglandin E2–dependent inhibition of the hepatocyte's acute phase response

Alexandra Fennekohl, Maria Lucas, Gerhard P. Püschel – 30 December 2003 – Prostanoids, that are released from nonparenchymal liver cells in response to proinflammatory stimuli, are involved in the regulation of hepatic functions during inflammation. They exert their effects on their target cells via heptahelical receptors in the plasma membrane. For the 5 prostanoids prostaglandin E2 (PGE2), prostaglandin F2α, prostaglandin D2(PGD2), prostacyclin, and thromboxane A2 there exist 8 receptors that are coupled to different heterotrimeric G proteins.

production and release of endothelin‐1 from the gut and spleen in portal hypertension due to cirrhosis

Naofumi Nagasue, Dipok Kumar Dhar, Akira Yamanoi, Yamaguchi Emi, Jun Udagawa, Akitaka Yamamoto, Mitsuo Tachibana, Hirofumi Kubota, Hitoshi Kohno, Takayuki Harada – 30 December 2003 – This study was aimed to evaluate the source of endothelin‐1 (ET‐1) in cirrhotic patients. ET‐1 is implicated in the pathogenesis of portal hypertension. However, the mechanism and source for increased plasma ET‐1 in cirrhotic patients are still obscure.

Host genetic factors influence disease progression in chronic hepatitis C

Elizabeth E. Powell, Catherine J. Edwards‐Smith, John L. Hay, Andrew D. Clouston, Darrell H. Crawford, Claudia Shorthouse, David M. Purdie, Julie R. Jonsson – 30 December 2003 – Progressive hepatic fibrosis and cirrhosis develops in 20% to 30% of patients with chronic hepatitis C virus (HCV). We propose that host genetic factors influencing fibrogenesis may account for some of the variability in progression of this disease.

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