Fig. 4
From: MiR-423-5p activated by E2F1 promotes neovascularization in diabetic retinopathy by targeting HIPK2
Knockdown of E2F1 inhibited angiogenesis via repressing miR-423-5p expression. A sh-E2F1 suppressed HG-induced increases in E2F1 mRNA and miR-423-5p levels. miR-423-5p mimics upregulated miR-423-5p level again in sh-E2F1-transfected cells following HG. B CCK-8 assay showed sh-E2F1 suppressed HG-induced increase in cell viability. miR-423-5p mimics increased the viability of cells transfected with sh-E2F1 after HG. C Transwell assay indicated that sh-E2F1 inhibited HG-induced increase in migration while miR-423-5p mimics enhanced the migration of cells transfected with sh-E2F1 following HG. D sh-E2F1 suppressed HG-induced in HIF1α protein level while miR-423-5p mimics increased HIF1α again in cells transfected with sh-E2F1 grown in HG. E sh-E2F1 suppressed HG-induced VEGF level while miR-423-5p mimics increased the level of secreted VEGF again in cells transfected with sh-E2F1 grown in HG. F Vascular tube formation assay showed that sh-E2F1 suppressed HG-induced angiogenesis while miR-423-5p mimics promoted angiogenesis in sh-E2F1-transfected cells grown in HG. All results were presented as the mean ± SD (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001. HG, high glucose; NG, normal glucose; E2F1, E2F transcription factor 1; HIF1α, hypoxia inducible factor 1α; VEGF, vascular endothelial growth factor; NC, negative control