Figure 3
From: IL-17A exacerbates diabetic retinopathy by impairing Müller cell function via Act1 signaling
IL-17A exacerbates HG-induced Müller cell activation and dysfunction via Act1/IKK signaling. (a) Expression of proteins related to Müller cell activation (GFAP) and function (VEGF, GS and EAAT1) in cultured Müller cells. (b) GFAP content in cultured Müller cell lysates assessed via ELISA. (c) VEGF concentration in cultured Müller cell supernatants assessed via ELISA. (d) Glutamate content in Müller cell lysates measured by HPLC. The treatment time periods of IL-17A, Ad-Act1-shRNA and the IKK inhibitor Wedel were the same as described in Figure 2. The cutline at the lower left of this figure is shared by (a–d). **P<0.01 vs control; +P<0.05, ++P<0.01 vs HG; &&P<0.01 vs HG+IL-17A+Ad-GFP or HG+IL-17A; NS (no significance) vs HG+IL-17A. Ad-Act1-shRNA, adenoviral vector that expressed short hairpin RNA targeting Act1; Ad-GFP, adenoviral vector that expressed green fluorescent protein; ELISA, enzyme-linked immunosorbent assay; EAAT1, excitatory amino acid transporter-1; GFAP, glial fibrillary acidic protein; GS, glutamine synthetase; HG, high glucose; HPLC, high-performance liquid chromatography; IL, interleukin; VEGF, vascular endothelial growth factor.
