Figure 3.

SMAD7 overexpression inhibits TGF-β1-induced myofibroblastic differentiation in fibroblasts derived from human Peyronie's disease plaque. Fibroblasts were transfected with an empty PEI25k/pCMV5 vector or a PEI25k/pCMV5-Smad7 polyplex (pSmad7) for 48 h and were then treated with TGF-β1 (10 ng ml⁻¹) for 24 h. (a) A representative Western blot for smooth muscle α-actin in fibroblasts. Whole-cell extracts were fractionated in a sodium dodecylsulfate-polyacrylamide gel. (b) Data are presented as the relative density of smooth muscle α-actin protein compared with that of β-actin. Each bar depicts the mean values (± s.e.) from four experiments per group. The relative ratio measured in the no treatment group was arbitrary presented as 1. *P< 0.05 by ANOVA. (c) Representative fluorescent immunocytochemistry of fibroblasts with antibody against smooth muscle α-actin. Nuclei were labeled with the DNA dye DAPI. Schale bar = 25 μm. Results were similar from four independent experiments. PEI: poly (ethyleneimine); TGF-β1: transforming growth factor-β1; SMAD7: decapentaplegic homolog 7; DAPI: 4,6-diamidino-2-phenylindole; s.e.: standard error.