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This article includes Supplementary Material available from the authors upon request or via the Internet at http://www.interscience.wiley.com/jpages/0021-9541/suppmat .

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jws-jcp.20772.fig1.tif1173KSupplementary figure 1. TGF-β1 production of MIM-1-4 hepatocytes (white bar), M1-4HSC cells (grey bar) and myofibroblastoid M-HT cells (black bar). The amount of latent TGF-β1 secretion into the medium was determined by ELISA.
jws-jcp.20772.fig2.tif1338KSupplementary figure 2. Repression of Smad-dependent transactivation by exogenous expression of Smad7. A: Smad7 expression as detected by Immunoblotting. B: Hepatocytes were transiently transfected with a luciferase reporter construct responsive to Smad3-mediated transcriptional activation and treated with TGF-β1 at the indicated concentrations. White bars, MIM-1-4; light gray bars, MIM-1-4-S7; MIM-R (dark gray bars); MIM-RS7 (black bars).
jws-jcp.20772.fig3.tif1263KSupplementary figure 3. Proliferation kinetics of epithelial MIM hepatocytes in the presence and absence of TGF-β1. A starting population of 1 x 105 cells was cultured on collagen-coated tissue plates to monitor cumulative cell numbers. A: MIM-1-4 and MIM-R hepatocytes and those expressing exogenous Smad7 (MIM-1-4-S7 and MIM-RS7) in the absence of TGF-β1. B: MIM-1-4, MIM-R, MIM-1-4-S7 and MIM-RS7 treated with TGF-β1 (1 ng/ml).

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