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. 2016 Sep 8;8(9):1952–1971. doi: 10.18632/aging.101031

Figure 1. PPARβ/δ signaling pathway is functional in AMD vulnerable cells.

Figure 1

(A) Agarose gel image of PCR amplification products of PPARβ/δ and its obligate binding partners RXRα and RXRβ in primary human RPE cells [R], freshly isolated human RPE cells [hR], ARPE19 cells [A], human choroid [hC], and RF/6A cells [C], 36B4 was used as loading control. PPARβ/δ activity in primary RPE (1°RPE) cells (B) and RF/6A cells (C) transfected with the DR1 luciferase reporter and siC or siPPARβ/δ; cells were treated with PPARβ/δ agonist, GW0742 (10μM) or antagonist, GSK0660 (10μM) or DMSO as vehicle control (n = 3): a: p < 0.05 relative to DMSO treated cells; b: p < 0.05 relative to drug+siC treated cells (p <  0.05; two way ANOVA, Sidak's multiple comparisons test). Expression of ANGPTL4 and PDK4 mRNA in primary RPE (1°RPE) cells (D and E) and RF/6A (F and G) in siC and siPPARβ/δ (100 pmoles/250,000 cells) treated cells in response to GW0742, GSK0660, or DMSO as a control (n = 3); a: p < 0.05 relative to DMSO treated cells; b: p < 0.05 relative to drug+siC treated cells (Two way ANOVA, Sidak's multiple comparisons test).