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Papers In Press, published online ahead of print May 4, 2000
Department of Internal Medicine and Transplant Research Program, University of California, Davis, Sacramento, CA 95817
Corresponding Author: mazern{at}ucdavis.edu
The mechanisms by which ethanol inhibits hepatocyte proliferation have been a source of some considerable investigation. Our studies have suggested a possible role for tissue transglutaminase (tTG) in this process. Others have shown that tTG has two distinctly different functions: it catalyzes protein cross-linking which can lead to apoptosis and enhancement of extracellular matrix stability and it can function as a G protein (Gh). Under that circumstance, we speculated that the cross-linking activity would be decreased, and that it would function to enhance hepatocyte proliferation in response to adrenergic stimulation. Ethanol treatment inhibited hepatocyte proliferation and led to enhanced tTG cross-linking activity, whereas treatment of hepatocytes with an 1 adrenergic agonist, phenylephrine, enhanced hepatocyte proliferation while decreasing tTG crosslinking. However, phenylephrine treatment of several hepatoma cell lines had no effect on cellular proliferation or tTG crosslinking activity, and of note, Northern blot analysis demonstrated that whereas primary hepatocytes had high levels of the 1adrenergic receptor (1AR) mRNA, the hepatoma cell lines did not have this mRNA. When the Hep G2 cell line was stably transduced with an expression vector containing the 1R cDNA, the cell line responded to phenylephrine treatment with enhanced proliferation and with decreased tTG crosslinking activity. Ethanol treatment of the 1BAR-transfected cells suppressed the phospholipase C-mediated signaling pathways as detected in the phenylephrine-induced Ca2+ response. These results suggest that phenylephrine stimulation of hepatocyte proliferation appears to be occurring through the 1BAR which is known to be coupled with the tTG G protein moiety, Gh and that tTG appears to play a significant role in either enhancing or inhibiting hepatocyte proliferation depending on its cellular location and whether it functions as a cross-linking enzyme or a G protein.
J. Biol. Chem, 10.1074/jbc.M000091200
Submitted on January 5, 2000
Revised on April 18, 2000
Accepted on May 4, 2000
Roles of tissue transglutaminase in ethanol-induced inhibition of hepatocyte proliferation and alpha1-adrenergic signal transduction
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