FIG. 4.

The differential responses of WT PPARγ versus EF-PPARγ to selected PPARγ ligands and antagonists. (A) Swiss-PPARγ (WT and EF) cells were cultured until they were confluent; after 2 days, they were exposed to DEX, MIX, and insulin, with or without the following PPARγ ligands: FMOC-leu (15 μM), 15δ-PGD2 (7 μM), troglitazone (5 μM), rosiglitazone (10 μM), and GW1929 (10 μM). GAPDH, glyceraldehyde-3-phosphate dehydrogenase. (B) WT PPARγ cells were differentiated as in panel A by exposure to DEX, MIX, and insulin in the presence or absence of troglitazone with or without either T0070907 (10 μM) or GW9662 (10 μM) (PPARγ antagonists). (C) WT PPARγ and EF-PPARγ cells were induced to differentiate with DEX, MIX, insulin, and the indicated doses of troglitazone (Trog). In panels A, B, and C, total RNA of the cells was isolated at day 5 using Trizol reagent (Invitrogen) and subjected to RT-PCR analysis of the indicated group 1 and group 2 genes as described in Materials and Methods.