Fig. 6
From: MiR-423-5p activated by E2F1 promotes neovascularization in diabetic retinopathy by targeting HIPK2
MiR-423-5p regulated angiogenesis via targeting HIPK2 to modulate HIF1α/VEGF signaling. A miR-423-5p inhibitor suppressed HG-induced increase in miR-423-5p level and reduction in HIPK2 mRNA level. sh-HIPK2 downregulated HIPK2 mRNA level in miR-423-5p inhibitor-transfected cells grown in HG. B CCK-8 assay showed miR-423-5p inhibitor suppressed HG-induced increase in cell viability. sh-HIPK2 increased the viability of cells transfected with miR-423-5p inhibitor after HG. C Transwell assay indicated that miR-423-5p inhibitor inhibited HG-induced increase in migration while sh-HIPK2 enhanced the migration of cells transfected with miR-423-5p inhibitor following HG. D miR-423-5p inhibitor suppressed HG-induced in HIF1α protein level while sh-HIPK2 increased HIF1α again in cells transfected with miR-423-5p inhibitor grown in HG. E miR-423-5p inhibitor suppressed HG-induced VEGF level while sh-HIPK2 increased the level of secreted VEGF again in cells transfected with miR-423-5p inhibitor grown in HG. F Vascular tube formation assay showed that miR-423-5p inhibitor suppressed HG-induced angiogenesis while sh-HIPK2 promoted angiogenesis in miR-423-5p inhibitor-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; HIPK2, homeodomain-interacting protein kinase 2; HIF1α, hypoxia inducible factor 1α; VEGF, vascular endothelial growth factor; NC, negative control