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      A role for tissue transglutaminase in hepatic injury and fibrogenesis, and its regulation by NF-kappaB.

      The American journal of physiology
      Animals, Blotting, Northern, Immunohistochemistry, Liver, enzymology, pathology, Liver Cirrhosis, Experimental, etiology, NF-kappa B, physiology, Promoter Regions, Genetic, RNA, Messenger, metabolism, Rats, Rats, Sprague-Dawley, Reference Values, Transglutaminases, genetics

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          Abstract

          This study was undertaken to delineate a possible role for tissue transglutaminase (tTG), an enzyme that catalyzes protein cross-linking, in hepatic fibrogenesis. Rats were treated with CCl4 solution and then killed at different stages of liver injury and fibrogenesis. Liver tTG mRNA levels were markedly increased as early as 6 h after the first injection, peaked at 4 days and 1 wk, and remained increased for 8 wk. The enzymatic activity of tTG was increased in livers of rats treated with CCl4, in a fashion that paralleled the Northern blot results. Cell isolation experiments indicated that all hepatic cell types synthesize tTG mRNA. Increased binding to the nuclear factor-kappaB (NF-kappaB) motif of the tTG promoter was found in the nuclear extracts prepared from CCl4-treated samples. These data demonstrate an increase in tTG gene expression during hepatic injury and fibrosis, suggesting a possible role for this enzyme in stabilizing the fibrotic bands during hepatic fibrogenesis. Moreover, increased NF-kappaB binding to the tTG promoter may represent one of the mechanisms by which cell injury induces tTG transcription and thus potentiates the process of fibrogenesis.

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