Oxidative stress stimulates proliferation and invasiveness of hepatic stellate cells via a MMP2‐mediated mechanism

Andrea Galli, Gianluca Svegliati‐Baroni, Elisabetta Ceni, Stefano Milani, Francesco Ridolfi, Renata Salzano, Mirko Tarocchi, Cecilia Grappone, Giulia Pellegrini, Antonio Benedetti, Calogero Surrenti, Alessandro Casini – 19 April 2005 – Experimental evidence indicates that reactive oxygen species (ROS) are involved in the development of hepatic fibrosis; they induce hepatic stellate cells (HSC) proliferation and collagen synthesis.

Expression and localization of hepatobiliary transport proteins in progressive familial intrahepatic cholestasis

Verena Keitel, Martin Burdelski, Ulrich Warskulat, Thomas Kühlkamp, Dietrich Keppler, Dieter Häussinger, Ralf Kubitz – 19 April 2005 – Mutations of the bile salt export pump (BSEP) or the multidrug resistance P‐glycoprotein 3 (MDR3) are linked to impaired bile salt homeostasis and lead to progressive familial intrahepatic cholestasis (PFIC)‐2 and ‐3, respectively. The regulation of bile salt transporters in PFIC is not known.

Systemic infusion of angiotensin II exacerbates liver fibrosis in bile duct–ligated rats

Ramón Bataller, Erwin Gäbele, Christopher J. Parsons, Terry Morris, Liu Yang, Robert Schoonhoven, David A. Brenner, Richard A. Rippe – 19 April 2005 – Recent evidence indicates that the renin–angiotensin system (RAS) plays a major role in liver fibrosis. Here, we investigate whether the circulatory RAS, which is frequently activated in patients with chronic liver disease, contributes to fibrosis progression. To test this hypothesis, we increased circulatory angiotensin II (Ang II) levels in rats undergoing biliary fibrosis.

A chimeric GB virus B with 5′ nontranslated RNA sequence from hepatitis C virus causes hepatitis in tamarins

Rene Rijnbrand, Yan Yang, Lucy Beales, Francis Bodola, Kathryn Goettge, Lisette Cohen, Robert E. Lanford, Stanley M. Lemon, Annette Martin – 19 April 2005 – Only humans and chimpanzees are fully permissive for replication of hepatitis C virus (HCV), an important cause of liver cirrhosis and cancer worldwide. The absence of suitable animal models limits opportunities for in vivo evaluation of candidate hepatitis C therapeutics and slows progress in the field.

The downstream financial effect of hepatology

Stanley Martin Cohen, Sushama Gundlapalli, Ami R. Shah, Tricia J. Johnson, John A. Rechner, Donald M. Jensen – 19 April 2005 – As a more consultative but less procedurally oriented specialty, Hepatology has been considered a financial liability in some academic centers. However, no actual data exist on the relative contribution of a Hepatology practice. The purpose of this study was to evaluate the direct and indirect (i.e., downstream effect) charges generated by a Hepatology section in comparison with a Gastroenterology section.

Anandamide induces necrosis in primary hepatic stellate cells

Sören V. Siegmund, Hiroshi Uchinami, Yosuke Osawa, David A. Brenner, Robert F. Schwabe – 19 April 2005 – The endogenous cannabinoid anandamide (AEA) is a lipid mediator that blocks proliferation and induces apoptosis in many cell types. Although AEA levels are elevated in liver fibrosis, its role in fibrogenesis remains unclear. This study investigated effects of AEA in primary hepatic stellate cells (HSCs). Anandamide blocked HSC proliferation at concentrations of 1 to 10 μmol/L but did not affect HSC proliferation or activation at nanomolar concentrations.

Hyperhomocysteinemia and the MTHFR C677T polymorphism promote steatosis and fibrosis in chronic hepatitis C patients

Luigi E. Adinolfi, Diego Ingrosso, Giuseppe Cesaro, Amelia Cimmino, Maria D'Antò, Rosanna Capasso, Vincenzo Zappia, Giuseppe Ruggiero – 19 April 2005 – The factors and mechanisms implicated in the development of hepatitis C virus (HCV)‐related steatosis are unknown. Hyperhomocysteinemia causes steatosis, and the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism induces hyperhomocysteinemia. We investigated the role of these factors in the development of HCV‐related steatosis and in the progression of chronic hepatitis C (CHC).

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