The PPARγ Agonist Rosiglitazone Is Antifibrotic for Scleroderma Lung Fibroblasts: Mechanisms of Action and Differential Racial Effects
Figure 4
Effect of rosiglitazone on CTGF, α-SMA, and NF-κB in lung fibroblasts isolated from white (W) and black (B) SSc-ILD patients (SSc) and controls (N). (a) Lung fibroblasts were incubated with rosiglitazone (20 μM) for 24 hours and subjected to Western analysis for CTGF and α-SMA expression. Anti-β-actin antibody was used as a loading control. Immunoblots are representative from 5 independent experiments. (b) NF-κB DNA-binding activity. Light gray bars: binding activity assessed by biotinylated NF-κB wild-type (WT) double-stranded DNA (dsDNA); dark gray bars: WT dsDNA plus nonspecific, nonbiotinylated dsDNA with a mutant NF-κB consensus-binding motif; black bars: WT dsDNA plus specific NF-κB competitor dsDNA lacking biotin end labels; Neg: negative control. Each bar represents the mean ± SD of duplicate determinations from 4 independent experiments. *Statistically significant differences between nuclear extract prepared from cells stimulated with rosiglitazone versus nuclear extracts from nonstimulated cells ().
