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Title: Liver fibrosis secondary to bile duct injury: Correlation of Smad7 with TGF-β and extracellular matrix proteins
Author: Del Pilar Alatorre-Carranza, M.
Miranda-Diaz, A.
Yanez-Sanchez, I.
Pizano-Martinez, O.
Hermosillo-Sandoval, J.M.
Vazquez-Del Mercado, M.
Hernandez-Hoyos, S.
Martinez-Abundis, R.
Fafutis-Morris, M.
Segura-Ortega, J.
Delgado-Rizo, V.
Issue Date: 2009
Abstract: Background: Liver fibrosis is the result of continuous liver injury stemming from different etiological factors. Bile duct injury induces an altered expression of TGF-β, which has an important role in liver fibrosis because this cytokine induces the expression of target genes such as collagens, PAI-1, TIMPs, and others that lead to extracellular matrix deposition. Smad7 is the principal inhibitor that regulates the target gene transcription of the TGF-β signaling. The aim of the study was to determine whether Smad7 mRNA expression correlates with the gene expression of TGF-β, Col I, Col III, Col IV, or PAI-1 in liver fibrosis secondary to bile duct injury (BDI). Results: Serum TGF-β concentration was higher in BDI patients (39 296 pg/ml) than in liver donors (9008 pg/ml). Morphometric analysis of liver sections showed 41.85% of tissue contained fibrotic deposits in BDI patients. mRNA expression of Smad7, Col I, and PAI-1 was also significantly higher (P < 0.05) in patients with BDI than in controls. Smad7 mRNA expression correlated significantly with TGF-β concentration, Col I and Col III expression, and the amount of fibrosis. Conclusion: We found augmented serum concentration of TGF-β and an increase in the percentage of fibrotic tissue in the liver of BDI patients. Contrary to expected results, the 6-fold increase in Smad7 expression did not inhibit the expression of TGF-β, collagens, and PAI-1. We also observed greater expression of Col I and Col III mRNA in BDI patients and significant correlations between their expression and TGF-β concentration and Smad7 mRNA expression. © 2009 del Pilar Alatorre-Carranza et al; licensee BioMed Central Ltd.
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