Fig. 3

β-catenin transcriptional activity is involved in AGE-induced angiogenesis via upregulating HDAC9/KDR. A-C HUVECs were treated by AGEs (100 μg/mL) for 24 h in the presence of 20 μM ICG-001, an inhibitor that antagonizes β-catenin/TCF-mediated transcription, and then the CCK8 assay (A), Transwell assay (B), and tube formation assay (C) were perform to evaluate the proliferation, migrated cell number and tube length, branching points, respectively. n = 4 to 5, scale bar indicates 100 or 200 μm. D HUVECs were treated with AGEs (100 μg/mL) for 24 h in the presence of ICG-001 with different doses and then the mRNA levels of PLK2, JAK1, HDAC9, KDR, NRP1 were detected by qPCR. n = 5 to 7. E–G Effects of HDAC9 and KDR on AGE-induced angiogenesis. After transfection with negative control (NC) siRNA or with specific siRNA targeting HDAC9 or KDR for 48 h, HUVECs were treated with AGEs (100 μg/ml) for 24 h followed by the CCK8 assay (E), Transwell assay (F), and tube formation assay (G) to evaluate the OD value, migrated cell number and tube length, branching points respectively. n = 5 to 6, scale bar indicates 100 or 200 μm. Data are shown as Mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001