The hepcidin circuits act: Balancing iron and inflammation

Bryan D. Maliken, James E. Nelson, Kris V. Kowdley – 22 April 2011 – Hepcidin is a peptide hormone that regulates iron homeostasis and acts as an antimicrobial peptide. It is expressed and secreted by a variety of cell types in response to iron loading and inflammation. Hepcidin mediates iron homeostasis by binding to the iron exporter ferroportin, inducing its internalization and degradation via activation of the protein kinase Jak2 and the subsequent phosphorylation of ferroportin.

Resistance mutations define specific antiviral effects for inhibitors of the hepatitis C virus p7 ion channel

Toshana L. Foster, Mark Verow, Ann L. Wozniak, Matthew J. Bentham, Joseph Thompson, Elizabeth Atkins, Steven A. Weinman, Colin Fishwick, Richard Foster, Mark Harris, Stephen Griffin – 21 April 2011 – The hepatitis C virus (HCV) p7 ion channel plays a critical role during infectious virus production and represents an important new therapeutic target. Its activity is blocked by structurally distinct classes of small molecules, with sensitivity varying between isolate p7 sequences.

Long‐term propagation of serum hepatitis C virus (HCV) with production of enveloped HCV particles in human HepaRG hepatocytes

Ndiémé Ndongo‐Thiam, Pascale Berthillon, Elisabeth Errazuriz, Isabelle Bordes, Sylvie De Sequeira, Christian Trépo, Marie‐Anne Petit – 21 April 2011 – HepaRG human liver progenitor cells exhibit morphology and functionality of adult hepatocytes. We investigated the susceptibility of HepaRG hepatocytes to in vitro infection with serum‐derived hepatitis C virus (HCV) particles (HCVsp) and the potential neutralizing activity of the E1E2‐specific monoclonal antibody (mAb) D32.10. The infection was performed using HCVsp when the cells actively divided at day 3 postplating.

Hepatic stellate cells: Partners in crime for liver metastases?

Ningling Kang, Gregory J. Gores, Vijay H. Shah – 21 April 2011 – Hepatic stellate cells (HSCs) were recently postulated as a component of the prometastatic liver microenvironment, because they can transdifferentiate into highly proliferative and motile myofibroblasts that are implicated in the desmoplastic reaction and metastatic growth. This review focuses on bidirectional interactions between tumor cells and HSCs in the liver microenvironment and discusses mechanisms whereby tumor‐derived factors activate HSCs, and in turn, activated HSCs promote metastatic growth.

A prospective study of the rate of progression in compensated, histologically advanced chronic hepatitis C

Jules L. Dienstag, Marc G. Ghany, Timothy R. Morgan, Adrian M. Di Bisceglie, Herbert L. Bonkovsky, Hae‐Young Kim, Leonard B. Seeff, Gyongyi Szabo, Elizabeth C. Wright, Richard K. Sterling, Gregory T. Everson, Karen L. Lindsay, William M. Lee, Anna S. Lok, Chihiro Morishima, Anne M. Stoddard, James E. Everhart, for the HALT‐C Trial Group – 21 April 2011 – The incidence of liver disease progression among subjects with histologically advanced but compensated chronic hepatitis C is incomplete.

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