VLDL Hydrolysis by Hepatic Lipase Regulates PPARδ Transcriptional Responses
Figure 1
Hepatic lipase activates PPARδ selectively in the presence of human VLDL.
(A) HEK293 cells transfected with human PPARα, γ, or δ ligand binding domain-Gal4 fusion constructs along with the pUAS×4TK Gal4 dependent luciferase reporter were stimulated with human VLDL 50 µg/mL, IDL 20 µg/mL, HDL 100 µg/mL or LDL 100 µg/mL for 12 hours. Luciferase values were normalized to β-galactosidase and results expressed as mean fold change of the normalized luciferase RLU. Each experimental condition was performed in triplicate and results are mean +/− SD. *p<.05 vs. empty vector. (B) HEK-293 cells were transfected with the PPARδ-LBD along with the luciferase reporter above. Cells were stimulated with indicated concentrations of human, pooled VLDL for 12 hours, then samples harvested for analysis. * p<.05 vs. empty vector. (C) HEK-293 cells were transfected with a PPRE-Luciferase reporter along with CMV-β-galactosidase and pcDNA or HL. Following transfection cells were stimulated with VLDL 50 µg/mL, HDL 100 µg/mL or LDL 100 µg/mL as before for 12 hours. *p<.05 vs. pcDNA.