Publication | Closed Access
A role for tissue transglutaminase in hepatic injury and fibrogenesis, and its regulation by NF-kappaB
156
Citations
0
References
1997
Year
Liver FibrosisImmunologyPathologyCell DeathFatty Liver DiseaseCholangiopathiesCirrhosisInflammationCcl4 SolutionHepatotoxicityHepatology FibrosisCell SignalingFibrosisLiver PhysiologyHepatology InflammationGene ExpressionCell BiologyTissue TransglutaminaseDrug-induced Liver InjuryHepatologyTtg MrnaNatural SciencesHepatitisLiver DiseaseLiverMedicineHepatocellular CarcinomaHepatic Injury
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.