Complex dynamics of hepatitis B virus resistance to adefovir

Coralie Pallier, Christophe Rodriguez, Rozenn Brillet, Patrice Nordmann, Christophe Hézode, Jean‐Michel Pawlotsky – 28 December 2008 – In patients with hepatitis B e antigen‐negative chronic hepatitis B, adefovir dipivoxil administration selects variants bearing reverse transcriptase rtN236T and/or rtA181V/T substitutions in 29% of cases after 5 years.

Ex vivo effects of high‐density lipoprotein exposure on the lipopolysaccharide‐induced inflammatory response in patients with severe cirrhosis

Arnaud Galbois, Dominique Thabut, Khalid A. Tazi, Marika Rudler, Morvarid Shir Mohammadi, Dominique Bonnefont‐Rousselot, Hind Bennani, Annie Bezeaud, Zera Tellier, Cécile Guichard, Nicolas Coant, Eric Ogier‐Denis, Richard Moreau, Didier Lebrec – 28 December 2008 – High‐density lipoproteins (HDL) are known to neutralize lipopolysaccharide (LPS). Because patients with cirrhosis have lower HDL levels, this may contribute to LPS‐induced ex vivo monocyte overproduction of proinflammatory cytokines.

Adenosine induces loss of actin stress fibers and inhibits contraction in hepatic stellate cells via Rho inhibition

Muhammad A. Sohail, Ardeshir Z. Hashmi, Wyel Hakim, Azuma Watanabe, Alexander Zipprich, Roberto J. Groszmann, Jonathan A. Dranoff, Natalie J. Torok, Wajahat Z. Mehal – 28 December 2008 – The Rho/ROCK pathway is activated in differentiated hepatic stellate cells (HSCs) and is necessary for assembly of actin stress fibers, contractility, and chemotaxis. Despite the importance of this pathway in HSC biology, physiological inhibitors of the Rho/ROCK pathway in HSCs are not known.

Cystathionine β‐synthase as a carbon monoxide–sensitive regulator of bile excretion

Tsunehiro Shintani, Takuya Iwabuchi, Tomoyoshi Soga, Yuichiro Kato, Takehiro Yamamoto, Naoharu Takano, Takako Hishiki, Yuki Ueno, Satsuki Ikeda, Tadayuki Sakuragawa, Kazuo Ishikawa, Nobuhito Goda, Yuko Kitagawa, Mayumi Kajimura, Kenji Matsumoto, Makoto Suematsu – 28 December 2008 – Carbon monoxide (CO) is a stress‐inducible gas generated by heme oxygenase (HO) eliciting adaptive responses against toxicants; however, mechanisms for its reception remain unknown.

Liver stem cells and hepatocellular carcinoma

Lopa Mishra, Tanuj Banker, Joseph Murray, Stephen Byers, Arun Thenappan, Aiwu Ruth He, Kirti Shetty, Lynt Johnson, E. P. Reddy – 28 December 2008 – Although the existence of cancer stem cells (CSCs) was first proposed over 40 years ago, only in the past decade have these cells been identified in hematological malignancies, and more recently in solid tumors that include liver, breast, prostate, brain, and colon. Constant proliferation of stem cells is a vital component in liver tissues.

Disruption of the transcription factor recombination signal‐binding protein‐Jκ (RBP‐J) leads to veno‐occlusive disease and interfered liver regeneration in mice

Lin Wang, Chun‐Mei Wang, Li‐Hong Hou, Guo‐Rui Dou, Yao‐Chun Wang, Xing‐Bin Hu, Fei He, Fan Feng, Hong‐Wei Zhang, Ying‐Min Liang, Ke‐Feng Dou, Hua Han – 28 December 2008 – Liver sinusoid (LS) endothelial cells (LSECs) support hepatocytes in resting livers and proliferate during liver regeneration to revascularize regenerated liver parenchyma. We report that recombination signal‐binding protein‐Jκ (RBP‐J), the critical transcription factor mediating Notch signaling, regulates both resting and regenerating LSECs.

Low retinol levels differentially modulate bile salt–induced expression of human and mouse hepatic bile salt transporters

Martijn O. Hoeke, Jacqueline R.M. Plass, Janette Heegsma, Mariska Geuken, Duncan van Rijsbergen, Julius F.W. Baller, Folkert Kuipers, Han Moshage, Peter L.M. Jansen, Klaas Nico Faber – 28 December 2008 – The farnesoid X receptor/retinoid X receptor‐alpha (FXR/RXRα) complex regulates bile salt homeostasis, in part by modulating transcription of the bile salt export pump (BSEP/ABCB11) and small heterodimer partner (SHP/NR0B2). FXR is activated by bile salts, RXRα by the vitamin A derivative 9‐cis retinoic acid (9cRA). Cholestasis is associated with vitamin A malabsorption.

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