20 - World Journal of Gastroenterology

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69: 562-573 91 Murphy FR, Issa R, Zhou X, Ratnarajah S, Nagase H, Arthur MJ, Benyon C, Iredale JP. Inhibition of apoptosis of activated hepatic stellate cells by tissue inhibitor of metalloproteinase-1 is mediated via effects on matrix metalloproteinase inhibition: implications for reversibility of liver fibrosis. J Biol Chem 2002; 277: 11069-11076 92 Mohammed FF, Pennington CJ, Kassiri Z, Rubin JS, Soloway PD, Ruther U, Edwards DR, Khokha R. Metalloproteinase inhibitor TIMP-1 affects hepatocyte cell cycle via HGF activation in murine liver regeneration. Hepatology 2005; 41: 857-867 93 Iimuro Y, Nishio T, Morimoto T, Nitta T, Stefanovic B, Choi SK, Brenner DA, Yamaoka Y. Delivery of matrix metalloproteinase-1 attenuates established liver fibrosis in the rat. Gastroenterology 2003; 124: 445-458 WJG|www.wjgnet.com Thompson KJ et al . Targeting collagen expression in alcoholic liver disease 94 Siller-López F, Sandoval A, Salgado S, Salazar A, Bueno M, Garcia J, Vera J, Gálvez J, Hernández I, Ramos M, Aguilar- Cordova E, Armendariz-Borunda J. Treatment with human metalloproteinase-8 gene delivery ameliorates experimental rat liver cirrhosis. Gastroenterology 2004; 126: 1122-1133; discussion 949 95 Surosky RT, Urabe M, Godwin SG, McQuiston SA, Kurtzman GJ, Ozawa K, Natsoulis G. Adeno-associated virus Rep proteins target DNA sequences to a unique locus in the human genome. J Virol 1997; 71: 7951-7959 96 Cong M, Liu T, Wang P, Xu Y, Tang S, Wang B, Jia J, Liu Y, Hermonat PL, You H. Suppression of tissue inhibitor of metalloproteinase-1 by recombinant adeno-associated viruses carrying siRNAs in hepatic stellate cells. Int J Mol Med 2009; 24: 685-692 S- Editor Tian L L- Editor Stewart GJ E- Editor Ma WH 2481 May 28, 2011|Volume 17|Issue 20|
Online Submissions: http://www.wjgnet.com/1007-9327office wjg@wjgnet.com doi:10.3748/wjg.v17.i20.2482 Natalia A Osna, MD, PhD, Series Editor Fibronectin: Functional character and role in alcoholic liver disease Razia S Aziz-Seible, Carol A Casey Razia S Aziz-Seible, Department of Biomedical Sciences, Creighton University, 2500 California Plaza, Omaha, NE 68178, United States Carol A Casey, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, 985870 Nebraska Medical Center, Omaha, NE 68198-5870, United States Carol A Casey, Department of Internal Medicine, University of Nebraska Medical Center, 986350 Nebraska Medical Center, Omaha, NE 68198-6350, United States Carol A Casey, The Liver Study Unit, Omaha Veterans Affairs Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, United States Author contributions: Aziz-Seible RS and Casey CA both contributed to the preparation of this manuscript. Supported by The National Institute on Alcohol Abuse and Alcoholism and the US Department of Veterans Affairs Correspondence to: Carol A Casey, PhD, The Liver Study Unit, Omaha Veterans Affairs Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, United States. ccasey@unmc.edu Telephone: +1-402-9953737 Fax: +1-402-4490604 Received: January 21,2011 Revised: April 7, 2011 Accepted: April 14, 2011 Published online: May 28, 2011 Abstract Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest a role for these proteins beyond the structural considerations of the extracellular matrix. These interactions implicate fibronectin in the regulation of mechanisms that also determine cell behavior and activity. The two major forms, plasma fibronectin (pFn) and cellular fibronectin (cFn), exist as balanced amounts under normal physiological conditions. However, during injury and/or disease, tissue and circulating levels of cFn become disproportionately elevated. The accumulating cFn, in addition to being a consequence of prolonged tissue damage, may in fact WJG|www.wjgnet.com 2482 World J Gastroenterol 2011 May 28; 17(20): 2482-2499 ISSN 1007-9327 (print) ISSN 2219-2840 (online) © 2011 Baishideng. All rights reserved. stimulate cellular events that promote further damage. In this review, we summarize what is known regarding such interactions between fibronectin and cells that may influence the biological response to injury. We elaborate on the effects of cFn in the liver, specifically under a condition of chronic alcohol-induced injury. Studies have revealed that chronic alcohol consumption stimulates excess production of cFn by sinusoidal endothelial cells and hepatic stellate cells while impairing its clearance by other cell types resulting in the build up of this glycoprotein throughout the liver and its consequent increased availability to influence cellular activity that could promote the development of alcoholic liver disease. We describe recent findings by our laboratory that support a plausible role for cFn in the promotion of liver injury under a condition of chronic alcohol abuse and the implications of cFn stimulation on the pathogenesis of alcoholic liver disease. These findings suggest an effect of cFn in regulating cell behavior in the alcohol-injured liver that is worth further characterizing not only to gain a more comprehensive understanding of the role this reactive glycoprotein plays in the progression of injury but also for the insight further studies could provide towards the development of novel therapies for alcoholic liver disease. © 2011 Baishideng. All rights reserved. TOPIC HIGHLIGHT Key words: Fibronectin; Liver disease; Alcoholic liver disease; Endocytosis; Cellular fibronectin Peer reviewer: Fernando J Corrales, Associate Professor of Biochemistry, Division of Hepatology and Gene Therapy, Proteomics Laboratory, CIMA, University of Navarra, Avd. Pío XII, 55, Pamplona, 31008, Spain Aziz-Seible RS, Casey CA. Fibronectin: Functional character and role in alcoholic liver disease. World J Gastroenterol 2011; 17(20): 2482-2499 Available from: URL: http://www.wjgnet. com/1007-9327/full/v17/i20/2482.htm DOI: http://dx.doi. org/10.3748/wjg.v17.i20.2482 May 28, 2011|Volume 17|Issue 20|
Page 1 and 2: World Journal of Gastroenterology W
Page 3 and 4: Robert JL Fraser, Daw Park Jacob Ge
Page 5 and 6: Italy Donato F Altomare, Bari Piero
Page 7 and 8: Fernando Azpiroz, Barcelona Ramon B
Page 9 and 10: S Contents EDITORIAL TOPIC HIGHLIGH
Page 11 and 12: Contents APPENDIX FLYLEAF EDITORS F
Page 13: Online Submissions: http://www.wjgn
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20 - World Journal of Gastroenterology

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