Research Article Volume 8, Issue 9 pp 1952—1978

Figure 2. PPARβ/δ regulates both dry- and wet-AMD related pathogenic pathways. Effect of siRNA mediated knockdown of PPARβ/δ on mRNA expression of extracellular matrix genes COL1A1, COL4A4, FN1 and VTN; angiogenesis and fibrosis genes, VEGFA, PDGFB, TGFB1 and SERPINF1; inflammation-related genes, PTGS2, IL1B, CXCL8, CCL2, SPP1, and TNFA; and lipid processing genes APOE, ABCA1, APOA1, LCAT and LDLR in 1°RPE cells (A, C, E, and G) and RF/6A (B, D, F and H) cells. (mean and S.E.M.; n = 3; *p < 0.05, ns: not significant, two way ANOVA, Sidak’s multiple comparisons test); siC, control siRNA; siPPARβ/δ, PPARβ/δ siRNA. Quantification of intracellular lipid accumulation after lipid loading followed by incubation with PPARβ/δ agonist, GW0742 or antagonist, GSK0660 in (I) 1°RPE. (*, p<0.05, compared to DMSO Control; ** p<0.05, compared to DMSO; ns: not significant, n=3, two way ANOVA, Sidak’s multiple comparisons test); Control: DMSO vehicle, αLA: α-linolenic acid, DHA: docosahexaenoic acid, AA: arachidonic acid, and PA: palmitic acid.