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. 2017 Dec 28;59(2):184–194. doi: 10.1194/jlr.M077321

Fig. 5.

Fig. 5.

The PPARδ agonist GW1516 enhanced LPAAT3 expression during satellite cell differentiation. mRNA expressions were measured by RT-PCR; culture media were not supplemented with fatty acids. A–C: Effects of GW1516 (0.2, 1, or 5 μM) on gene expression at day 2 of differentiation. A: LPAAT3 expression was enhanced by GW1516 at each concentration; LPAAT2 was also slightly upregulated at the highest concentration. GW1516 upregulated PPAR-target genes UCP3 and PDK4 (B), but did not affect levels of myogenic marker genes Pax7, MyoD, and myogenin (C). D: GW1516-treatment time course. Satellite cells were incubated with vehicle or 1 μM GW1516 during 4 days of differentiation. GW1516 enhanced LPAAT3 expression more at later time points. E, F: GW1516-induced LPAAT3 expression is PPARδ dependent. PPARδ-targeting (siPPARδ #1 or siPPARδ #2) or nontargeting (siCONTROL) siRNAs were applied for 16 h, and then cells were differentiated for 2 days. E: siRNA efficiency. PPARδ-targeting siRNAs reduced PPARδ levels relative to nontargeting siRNA. F: PPARδ knockdown blocked GW1516-induced LPAAT3 expression; 1 μM GW1516 or vehicle was applied during 2 days differentiation. All data represent the mean ± SEM of three or four independent experiments; one-way ANOVA (A–C, E) or t-tests (D, F) were performed. #P < 0.05, GW1516 versus vehicle; *P < 0.05, siCONTROL versus PPARδ siRNA.