Figure 1.

siRNA-mediated silencing of HDAC2 inhibits TGF-β1-induced extracellular matrix protein production in fibroblasts derived from human PD plaque. (a) Expression of mRNA for HDAC2 in PD fibroblasts after specific knockdown using siRNA or control siRNA (scramble siRNA). Data are presented as the ratio of the product of HDAC2 gene transcript to that of GAPDH mRNA. 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<0.01 compared with the no treatment and scramble siRNA groups by ANOVA. (b) Effect of TGF-β1 on HDAC2 protein expression. Fibroblasts were transfected with scramble siRNA or siRNA specific to HDAC2 by using Lipofectamine reagent for 48 h and were then treated with TGF-β1 (10 ng ml⁻¹) for 24 h. Whole-cell extracts were fractionated in a sodium dodecylsulfate-polyacrylamide gel. Data are presented as the relative density of HDAC2 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 compared with no treatment group, ^†P<0.05 compared with TGF-β1+the scramble siRNA group by ANOVA. (c) Representative Western blot for PAI-1, fibronectin, collagen I, and collagen IV in fibroblasts. Data are presented as the relative density of each protein compared with that of β-actin. Each bar depicts the mean values (±s.e.) from four experiments per group. *P<0.01, ^†P<0.05 compared with other groups, ^‡P<0.05 compared with no treatment group by Kruskal–Wallis tests. HDAC2, histone deacetylase 2; PAI-1, plasminogen activator inhibitor-1; PD, Peyronie's disease; siRNA, small interfering RNA; TGF-β1, transforming growth factor-β1.