Expression of paramyxovirus V proteins promotes replication and spread of hepatitis C virus in cultures of primary human fetal liver cells

Linda Andrus, Svetlana Marukian, Christopher T. Jones, Maria Teresa Catanese, Timothy P. Sheahan, John W. Schoggins, Walter T. Barry, Lynn B. Dustin, Kartik Trehan, Alexander Ploss, Sangeeta N. Bhatia, Charles M. Rice – 2 December 2011 – Here we demonstrate that primary cultures of human fetal liver cells (HFLC) reliably support infection with laboratory strains of hepatitis C virus (HCV), although levels of virus replication vary significantly between different donor cell preparations and frequently decline in a manner suggestive of active viral clearance.

Tenascin‐C: A novel mediator of hepatic ischemia and reperfusion injury

Naohisa Kuriyama, Sergio Duarte, Takashi Hamada, Ronald W. Busuttil, Ana J. Coito – 2 December 2011 – Hepatic ischemia/reperfusion (IRI) injury remains a major challenge in clinical orthotopic liver transplantation (OLT). Tenascin‐C (Tnc) is an extracellular matrix protein (ECM) involved in various aspects of immunity and tissue injury. Using a Tnc‐deficient mouse model, we present data that suggest an active role for Tnc in liver IRI. We show that Tnc‐deficient mice have a reduction in liver damage and a significant improvement in liver regeneration after IRI.

Hypoxia‐inducible MicroRNA‐210 augments the metastatic potential of tumor cells by targeting vacuole membrane protein 1 in hepatocellular carcinoma

Qiao Ying, Linhui Liang, Weijie Guo, Ruopeng Zha, Qi Tian, Shenglin Huang, Jian Yao, Jie Ding, Meiyan Bao, Chao Ge, Ming Yao, Jinjun Li, Xianghuo He – 2 December 2011 – As the “master” microRNA that is induced by hypoxia, miR‐210 is involved in multiple processes in the hypoxia pathway. However, whether miR‐210 mediates hypoxia‐induced tumor cell metastasis still remains unclear. Here, we demonstrate that miR‐210 is frequently up‐regulated in hepatocellular carcinoma (HCC) samples and promotes the migration and invasion of HCC cells.

Seasonal variation in the patient diagnosis of primary biliary cirrhosis: Further evidence for an environmental component to etiology

Richard J.Q. McNally, Peter W. James, Samantha Ducker, Oliver F.W. James – 2 December 2011 – The etiology of primary biliary cirrhosis (PBC) is far from clear. Both genetic and environmental factors are likely to be involved. We have previously reported evidence of space‐time clustering, suggesting that a transient environmental agent may be involved in etiology.

Primate‐specific microRNA‐637 inhibits tumorigenesis in hepatocellular carcinoma by disrupting signal transducer and activator of transcription 3 signaling

Jin‐fang Zhang, Ming‐liang He, Wei‐ming Fu, Hua Wang, Lian‐zhou Chen, Xiao Zhu, Ying Chen, Dan Xie, Paul Lai, Gong Chen, Gang Lu, Marie C.M. Lin, Hsiang‐fu Kung – 2 December 2011 – MiR‐637 (microRNA‐637) is a primate‐specific miRNA belonging to the small noncoding RNA family, which represses gene regulation at the post‐transcriptional expression level. Although it was discovered approximately 5 years ago, its biomedical significance and regulatory mechanism remain obscure.

The cyclophilin inhibitor alisporivir prevents hepatitis C virus–mediated mitochondrial dysfunction

Giovanni Quarato, Annamaria D'Aprile, Bruno Gavillet, Grégoire Vuagniaux, Darius Moradpour, Nazzareno Capitanio, Claudia Piccoli – 2 December 2011 – Alisporivir (Debio‐025) is an analogue of cyclosporine A and represents the prototype of a new class of non‐immunosuppressive cyclophilin inhibitors. In vitro and in vivo studies have shown that alisporivir inhibits hepatitis C virus (HCV) replication, and ongoing clinical trials are exploring its therapeutic potential in patients with chronic hepatitis C.

Infiltrating monocytes versus resident kupffer cells: Do alternatively activated macrophages need to be targeted alternatively?

Frank Tacke, Christian Kurts – 2 December 2011 – A defining feature of inflammation is the accumulation of innate immune cells in the tissue that are thought to be recruited from the blood. We reveal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density.

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