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. 2013 Mar;54(3):592–601. doi: 10.1194/jlr.M028472

Fig. 4.

Fig. 4.

Fsp27/CIDEC is not a PPARα target gene. A: HepG2 cells transfected for 48 h with mouse Fsp27 promoter constructs cloned in pGL3-basic and cotransfected with pcDNA3, PPARγ, or PPARα expression vectors, represented by fold activation to pcDNA3. Twenty-four hours before harvesting, cells were treated with 10 µM of PPARγ and PPARα ligands, rosiglitazone, and Wy14643, respectively (closed bars). Human HMGCS2 promoter cotransfected with PPARα and treated or not with its ligand was used as a positive control. The mean of two independent experiments performed in duplicate are shown. B: CIDEC and HMGCS2 mRNA levels in HepG2 cells treated with the PPARα synthetic ligand Wy14643 (10 µM) for 24 h. C: CIDEC and PEPCK mRNA levels in HepG2 cells treated with etomoxir and a PPARγ antagonist (GW9662) (10 µM each) for 6 h. Results are means of ± SEM (n = 3–4 independent experiments). **P < 0.01, ***P < 0.001 relative to control (DMSO-treated cells); ##P < 0.01 relative to etomoxir-treated cells.