Nuclear factor κB up‐regulation of CCAAT/enhancer‐binding protein β mediates hepatocyte resistance to tumor necrosis factor α toxicity

Yongjun Wang, Rajat Singh, Youqing Xiang, Linda E. Greenbaum, Mark J. Czaja – 20 August 2010 – The sensitization of hepatocytes to cell death from tumor necrosis factor α (TNFα) underlies many forms of hepatic injury, including that from toxins. Critical for hepatocyte resistance to TNFα toxicity is activation of nuclear factor κB (NF‐κB) signaling, which prevents TNFα‐induced death by the up‐regulation of protective proteins.

miR‐194 is a marker of hepatic epithelial cells and suppresses metastasis of liver cancer cells in mice

Zhipeng Meng, Xianghui Fu, Xiaosong Chen, Samuel Zeng, Yan Tian, Richard Jove, Rongzhen Xu, Wendong Huang – 20 August 2010 – MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression by interacting with the 3′ untranslated region (3′‐UTR) of multiple mRNAs. Recent studies have linked miRNAs to the development of cancer metastasis. In this study, we show that miR‐194 is specifically expressed in the human gastrointestinal tract and kidney.

Liver regeneration is impaired in lipodystrophic fatty liver dystrophy mice

Vered Gazit, Alexander Weymann, Eric Hartman, Brian N. Finck, Paul W. Hruz, Anatoly Tzekov, David A. Rudnick – 20 August 2010 – We previously reported that mice subjected to partial hepatectomy exhibit rapid development of hypoglycemia followed by transient accumulation of fat in the early regenerating liver. We also showed that disrupting these metabolic alterations results in impaired liver regeneration. The studies reported here were undertaken to further characterize and investigate the functional importance of changes in systemic adipose metabolism during normal liver regeneration.

The role of intestinal endotoxin in liver injury: A long and evolving history

James P. Nolan – 20 August 2010 – From the mid‐1950s, it was observed that liver injury by a variety of toxins greatly sensitized the host to the effects of administered lipopolysaccharide. In the nutritional cirrhosis of choline deficiency, and in acute toxic injury as well, the need for the presence of enteric endotoxin was demonstrated. The universality of this association was striking for almost all agents associated with liver injury.

E‐cadherin antagonizes transforming growth factor β1 gene induction in hepatic stellate cells by inhibiting RhoA–dependent Smad3 phosphorylation

Il Je Cho, Young Woo Kim, Chang Yeob Han, Eun Hyun Kim, Richard A. Anderson, Young Sok Lee, Chang Ho Lee, Se Jin Hwang, Sang Geon Kim – 20 August 2010 – Cadherins mediate cell‐cell adhesion and catenin (ctn)‐related signaling pathways. Liver fibrosis is accompanied by the loss of E‐cadherin (ECAD), which promotes the process of epithelial‐mesenchymal transition. Currently, no information is available about the inhibitory role of ECAD in hepatic stellate cell activation.

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