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World J Gastroenterol. May 28, 2011; 17(20): 2482-2499
Published online May 28, 2011. doi: 10.3748/wjg.v17.i20.2482
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 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.

Keywords: Fibronectin; Liver disease; Alcoholic liver disease; Endocytosis; Cellular fibronectin