Research Paper Volume 13, Issue 18 pp 22040—22058

A2E-induced inflammation and angiogenesis in RPE cells in vitro are modulated by PPAR-α, -β/δ, -γ, and RXR antagonists and by norbixin

A2E induces the transactivation of all PPAR isoforms. Effect of increasing concentration of A2E on endogenous PPAR transactivation (A). Effect of A2E (20 μM) on the transactivation of over-expressed PPAR-α (B), PPAR β/δ (C) and PPAR-γ (D). Effect of selective PPAR agonists GW9578 (GW95, 20 μM), GW0742 (GW07, 30 μM) and troglitazone (TGZ, 20 μM) on the respective transactivation of over-expressed PPAR-α (E), PPAR β/δ (F) and PPAR-γ (G). Bars represent mean ± s.e.m. with n = 3–4. *p **p ***p ****p

Figure 1. A2E induces the transactivation of all PPAR isoforms. Effect of increasing concentration of A2E on endogenous PPAR transactivation (A). Effect of A2E (20 μM) on the transactivation of over-expressed PPAR-α (B), PPAR β/δ (C) and PPAR-γ (D). Effect of selective PPAR agonists GW9578 (GW95, 20 μM), GW0742 (GW07, 30 μM) and troglitazone (TGZ, 20 μM) on the respective transactivation of over-expressed PPAR-α (E), PPAR β/δ (F) and PPAR-γ (G). Bars represent mean ± s.e.m. with n = 3–4. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 compared to control (CONT) corresponding to DMSO alone added to the medium. (One-way ANOVA, Dunnett’s post-test).