Figure 7.

The interaction of $\text{PPAR}\mathrm{\gamma }2$ with the transcriptional coactivators $\text{PGC}\text{-}1\mathrm{\alpha }$ and ASC-2 in the presence of $\text{PPAR}\mathrm{\gamma }$ agonist rosiglitazone, phytoestrogens, or the $\text{PPAR}\mathrm{\gamma }$ antagonist GW9662. HeLa cells were transiently transfected with $\text{VP}16\text{-PPAR}\mathrm{\gamma }2$ and (A) $\text{Gal}4\text{DBD}\text{-PGC}\text{-}1\mathrm{\alpha }$ or (B) Gal4DBD-ASC-2 expression plasmid or empty controls (VP16, Gal4DBD) together with a 5xGAL4 luciferase reporter and a luciferase normalization control. Following transfection, cells were treated with vehicle (Veh) or $1\mathrm{\mu }\mathrm{M}$ of Rosiglitazone (Rosi), Genistein (Gen), Daidzein (Daid), Resveratrol (Resv), or $\text{PPAR}\mathrm{\gamma }$ antagonist GW9662. After 36 h, cells were harvested and Dual-Luciferase assays were performed. Each value was normalized to the internal luciferase control. Each data point is the average of four independent experiments; individual experiments included three technical replicates used for each treatment. Bars represent $\text{means}\pm \text{SEs}$. The dotted line on each graph indicates the basal level of coactivator interaction with $\text{PPAR}\mathrm{\gamma }2$ for comparison with ligand-mediated interactions. *$p<0.05$ for comparison between Veh and each treatment.