Figure 1 — A2E-induced inflammation and angiogenesis in RPE cells in vitro are modulated by PPAR-α, -β/δ, -γ, and RXR antagonists and by norbixin

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

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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).