20 - World Journal of Gastroenterology

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30 Walters KA, Joyce MA, Thompson JC, Smith MW, Yeh MM, Proll S, Zhu LF, Gao TJ, Kneteman NM, Tyrrell DL, Katze MG. Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response. PLoS Pathog 2006; 2: e59 31 Nishimura M, Yoshitsugu H, Yokoi T, Tateno C, Kataoka M, Horie T, Yoshizato K, Naito S. Evaluation of mRNA expression of human drug-metabolizing enzymes and transporters in chimeric mouse with humanized liver. Xenobiotica 2005; 35: 877-890 32 Katoh M, Matsui T, Okumura H, Nakajima M, Nishimura M, Naito S, Tateno C, Yoshizato K, Yokoi T. Expression of human phase II enzymes in chimeric mice with humanized liver. Drug Metab Dispos 2005; 33: 1333-1340 33 Katoh M, Watanabe M, Tabata T, Sato Y, Nakajima M, Nishimura M, Naito S, Tateno C, Iwasaki K, Yoshizato K, Yokoi T. In vivo induction of human cytochrome P450 3A4 by rifabutin in chimeric mice with humanized liver. Xenobiotica 2005; 35: 863-875 34 Katoh M, Sawada T, Soeno Y, Nakajima M, Tateno C, WJG|www.wjgnet.com Mercer DF. Hepatitis and alcohol effects on liver Yoshizato K, Yokoi T. In vivo drug metabolism model for human cytochrome P450 enzyme using chimeric mice with humanized liver. J Pharm Sci 2007; 96: 428-437 35 Grompe M, al-Dhalimy M, Finegold M, Ou CN, Burlingame T, Kennaway NG, Soriano P. Loss of fumarylacetoacetate hydrolase is responsible for the neonatal hepatic dysfunction phenotype of lethal albino mice. Genes Dev 1993; 7: 2298-2307 36 Azuma H, Paulk N, Ranade A, Dorrell C, Al-Dhalimy M, Ellis E, Strom S, Kay MA, Finegold M, Grompe M. Robust expansion of human hepatocytes in Fah-/-/Rag2-/-/Il2rg-/- mice. Nat Biotechnol 2007; 25: 903-910 37 Lieber A, Vrancken Peeters MJ, Meuse L, Fausto N, Perkins J, Kay MA. Adenovirus-mediated urokinase gene transfer induces liver regeneration and allows for efficient retrovirus transduction of hepatocytes in vivo. Proc Natl Acad Sci USA 1995; 92: 6210-6214 38 Bissig KD, Wieland SF, Tran P, Isogawa M, Le TT, Chisari FV, Verma IM. Human liver chimeric mice provide a model for hepatitis B and C virus infection and treatment. J Clin Invest 2010; 120: 924-930 S- Editor Tian L L- Editor Kerr C E- Editor Ma WH 2519 May 28, 2011|Volume 17|Issue 20|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i20.2520 Natalia A Osna, MD, PhD, Series Editor Role of lipid rafts in liver health and disease Angela Dolganiuc Angela Dolganiuc, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, United States Author contributions: Dolganiuc A solely contributed to this paper. Supported by Grant AA016571 from NIAAA Correspondence to: Angela Dolganiuc, MD, PhD, Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, LRB-270-H, Worcester, MA 01605, United States. angela.dolganiuc@umassmed.edu Telephone: +1-508-8565955 Fax: +1-508-8565303 Received: January 6, 2011 Revised: February 24, 2011 Accepted: March 3, 2011 Published online: May 28, 2011 Abstract Liver diseases are an increasingly common cause of morbidity and mortality; new approaches for investigation of mechanisms of liver diseases and identification of therapeutic targets are emergent. Lipid rafts (LRs) are specialized domains of cellular membranes that are enriched in saturated lipids; they are small, mobile, and are key components of cellular architecture, protein partition to cellular membranes, and signaling events. LRs have been identified in the membranes of all liver cells, parenchymal and non-parenchymal; more importantly, LRs are active participants in multiple physiological and pathological conditions in individual types of liver cells. This article aims to review experimental-based evidence with regard to LRs in the liver, from the perspective of the liver as a whole organ composed of a multitude of cell types. We have gathered up-to-date information related to the role of LRs in individual types of liver cells, in liver health and diseases, and identified the possibilities of LR-dependent therapeutic targets in liver diseases. © 2011 Baishideng. All rights reserved. Key words: Hepatocytes; Stellate cells; Kupffer cells; Endothelial cells; Signaling; Therapeutic; Viral; Hepatitis C virus; Metabolism WJG|www.wjgnet.com World J Gastroenterol 2011 May 28; 17(20): 2520-2535 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. Peer reviewer: Munechika Enjoji, MD, PhD, Department of Clinical Pharmacology, Fukuoka University, 8-17-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan Dolganiuc A. Role of lipid rafts in liver health and disease. World J Gastroenterol 2011; 17(20): 2520-2535 Available from: URL: http://www.wjgnet.com/1007-9327/full/v17/i20/2520.htm DOI: http://dx.doi.org/10.3748/wjg.v17.i20.2520 INTRODUCTION TOPIC HIGHLIGHT The liver is the largest parenchymal organ of the body and has a multitude of important and complex functions; among the most notable are the metabolism of fat, proteins, and carbohydrates, synthesis and secretion of bile, microelement recycling and detoxification of products resulting from body metabolism (bilirubin, ammonia, etc.) and from exogenous toxins (drugs, alcohol and environment) [1] . The liver is also an immune [2] and an endocrine [3,4] organ and functions as a blood capacitance reservoir [5,6] . To accomplish these many assignments, the liver accommodates a wide variety of cell types, including those that call liver “home”, namely liver progenitor cells, hepatocytes, Kupffer cells (KCs), stellate cells (SCs) and the cellular components of vasculature, and those that use the liver as a temporary and/or terminal station, such as blood cells [1,7] . Liver diseases are the 10th leading cause of death and account for significant morbidity across the entire age and gender spectrum of the US population [8,9] . The mechanisms of liver diseases are extensively researched but not fully understood. More recently, research data have emerged proposing that some pathogenic mechanisms, such as inflammation, tissue death and regeneration, and organ remodeling, are shared across a large spectrum of liver diseases of distinct etiologies [10-14] , with the suggestion that common denominators of cell structure or function may be involved. Here we have focused on a common denominator of the cellular structure, the lipid rafts (LRs), as players in liver physiology and pathology. 2520 May 28, 2011|Volume 17|Issue 20|
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World Journal of Gastroenterology W
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Robert JL Fraser, Daw Park Jacob Ge
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Italy Donato F Altomare, Bari Piero
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Fernando Azpiroz, Barcelona Ramon B
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S Contents EDITORIAL TOPIC HIGHLIGH
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Contents APPENDIX FLYLEAF EDITORS F
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Online Submissions: http://www.wjgn
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Mandrekar P. Epigenetics and alcoho
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Moghe A et al . Altered nutrients,
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Page 52 and 53: to autocrine TNF-a signaling after
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Page 56 and 57: stress in alcohol toxicity. Free Ra
Page 58 and 59: HIV, VIRAL HEPATITIS AND ALCOHOL US
Page 60 and 61: Table 1 Common mechanisms of liver/
Page 62 and 63: perpermeability and endotoxemia pri
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Page 70 and 71: metabolism. Nature 2009; 458: 1131-
Page 72: Online Submissions: http://www.wjgn
Page 75: Mercer DF. Hepatitis and alcohol ef
Page 79 and 80: Dolganiuc A. Role of lipid rafts in
Page 93 and 94: Online Submissions: http://www.wjgn
Page 95: Lakner AM et al . microRNAs and liv
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Page 119 and 120: Bardag-Gorce F. Proteasome inhibito
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Page 123 and 124: A Livin expression (%) 120 100 80 6
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M, Coggi G, Bosari S. Inhibitors of
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Institute, UPMC Montefiore, 7 South
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A B C D E Figure 1 Change in coloni
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Jiang HP et al . Differential prote
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A B C Vespasiani Gentilucci U et al
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Vespasiani Gentilucci U et al . Non
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Instructions to authors ISSN and EI
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Instructions to authors used rather
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Instructions to authors Chaoyang Di
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