The Peroxisomal 3-keto-acyl-CoA thiolase B Gene Expression Is under the Dual Control of PPARα and HNF4α in the Liver
Figure 4
PPARα transactivation from TB PPRE3 is markedly enhanced by HNF4α. (a) Transactivation assays were performed in COS-7 and HeLa cells (b) or in Hepa 1.6 and H4IIEC3 cells with a Luc reporter vector containing isolated rTB PPRE3. These constructs were transfected together with expression vectors for both mouse PPARα (pSG5-mPPARα) and RXRα (pSG5-mRXRα) in absence (white bars) or presence (black bars) of Wy (10 μM). Cotransfection with pcDNA3.1 WT hHNF4α was performed as indicated. Note that the minimal promoter of the thiolase B gene was used instead of the globin gene promoter which was inactive in H4IIEC3 cells. (c) Transactivation assays were performed in COS-7 or Hepa 1.6 cells with a Luc reporter vector containing isolated ACOX-I PPRE. Normalized luciferase activity of each construct in the absence of PPARα and ligand was set at 1. Values are mean of four independent experiments ±SEM. DMSO was used as vehicle. Significantly different compared to control (transfection with a combination of empty pcDNA3.1 and pSG5 vectors) with ** and *** by one-way ANOVA test. Significantly different between PPARα/RXRα and PPARα/RXRα + HNF4α with $$ and $$$ by one-way ANOVA test.
