The pathogen receptor liver and lymph node sinusoidal endotelial cell C‐type lectin is expressed in human Kupffer cells and regulated by PU.1

Ángeles Domínguez‐Soto, Laura Aragoneses‐Fenoll, Fernando Gómez‐Aguado, María Teresa Corcuera, Joan Clária, Carmelo García‐Monzón, Matilde Bustos, Angel L. Corbí – 28 December 2008 – Human LSECtin (liver and lymph node sinusoidal endothelial cell C‐type lectin, CLEC4G) is a C‐type lectin encoded within the L‐SIGN/DC‐SIGN/CD23 gene cluster. LSECtin acts as a pathogen attachment factor for Ebolavirus and the SARS coronavirus, and its expression can be induced by interleukin‐4 on monocytes and macrophages.

Bile acids activate fibroblast growth factor 19 signaling in human hepatocytes to inhibit cholesterol 7α‐hydroxylase gene expression

Kwang‐Hoon Song, Tiangang Li, Erika Owsley, Stephen Strom, John Y. L. Chiang – 28 December 2008 – Mouse fibroblast growth factor 15 (FGF15) and human ortholog FGF19 have been identified as the bile acid–induced intestinal factors that mediate bile acid feedback inhibition of cholesterol 7α‐hydroxylase gene (C YP7A1) transcription in mouse liver. The mechanism underlying FGF15/FGF19 inhibition of bile acid synthesis in hepatocytes remains unclear.

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.

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.

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.

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.

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.

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.

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