Fig. 2: FGF6 and FGF9 induce UCP1 expression by promoting prostaglandin E2 biosynthesis.

a FGF6/9-induced Ucp1 expression in the presence or absence of heparin or HS. N = 3 per group. b Ucp1 expression in control (shLacZ) and Fgfr3 knockdown cell lines upon 24 h treatment with vehicle, FGF6, or FGF9. N = 3 per group. c Prostaglandin biosynthesis pathway. Genes encoding the enzymes marked in red are upregulated by FGF6 treatment. d Counts per millions for transcripts encoding PGE2 biosynthesis enzymes from RNA-sequencing of brown preadipocytes treated with FGF6 or vehicle for 24 h. e PGE2 concentration in the culture media of brown preadipocytes upon treatment with vehicle, FGF6, or FGF9. N = 3 per group. f Ucp1 expression in brown preadipocytes treated with PGE2 for 24 h. N = 2 per group. g Ucp1 expression in control (shLacZ) and Ptges knockdown cells treated with vehicle, FGF6, or FGF9 for 24 h. N = 3 per group. h Ucp1 expression in white preadipocytes treated with vehicle, FGF6, or FGF9 in the presence of PTGES-selective inhibitor (CAY10526) or equimolar concentration of DMSO. N = 3 per group. i Ucp1 expression in white preadipocytes treated with vehicle, FGF6, or FGF9 in the presence of both EP2 and EP4 receptor antagonists (AH6809 + AH23848) or equimolar concentration of DMSO. N = 3 per group. FGF6 and FGF9 were used at concentrations of 200 and 100 ng/ml, respectively. Data are presented as means ± SEM. Two-way ANOVA. ****p < 0.0001, ***p < 0.001, **p < 0.01, and *p < 0.05. A representative from a total of two to three independent experiments is shown. Source data are provided as a Source Data file.