Mitochondria‐targeted ubiquinone (MitoQ) decreases ethanol‐dependent micro and macro hepatosteatosis

Balu K. Chacko, Anup Srivastava, Michelle S. Johnson, Gloria A. Benavides, Mi Jung Chang, Yaozu Ye, Nirag Jhala, Michael P. Murphy, Balaraman Kalyanaraman, Victor M. Darley‐Usmar – 21 April 2011 – Chronic alcohol‐induced liver disease results in inflammation, steatosis, and increased oxidative and nitrosative damage to the mitochondrion. We hypothesized that targeting an antioxidant to the mitochondria would prevent oxidative damage and attenuate the steatosis associated with alcoholic liver disease.

Ubiquitination is associated with lysosomal degradation of cell surface‐resident ATP‐binding cassette transporter A1 (ABCA1) through the endosomal sorting complex required for transport (ESCRT) pathway

Tadahaya Mizuno, Hisamitsu Hayashi, Sotaro Naoi, Yuichi Sugiyama – 21 April 2011 – ATP‐binding cassette transporter A1 (ABCA1) plays an essential role in the biogenesis of high‐density lipoprotein in liver and in the prevention of foam cell formation in macrophages by mediating the efflux of cellular cholesterol and phospholipids to apolipoprotein A‐I (apoA‐I). Our current study investigated the mechanism of degradation of cell surface‐resident ABCA1, focusing on ubiquitination.

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.

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.

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.

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.

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