Fig. 2
From: MiR-423-5p activated by E2F1 promotes neovascularization in diabetic retinopathy by targeting HIPK2
Knockdown of miR-423-5p suppressed angiogenesis in hRMEC and hREC cells with HG condition. A HG increased miR-423-5p level and transfection with miR-423-5p inhibitor suppressed that increase in miR-423-5p expression. B CCK-8 results showed HG treatment increased cell viability of hRMEC and hREC cells while miR-423-5p inhibitor suppressed the HG-induced increase in cell viability. C Transwell assay results indicated that HG enhanced migration of cells while transfection with miR-423-5p inhibitor blocked the enhancement caused by HG. D HG increased HIF1α protein level compared to NG while transfection of miR-423-5p inhibitor suppressed that increase in HIF1α protein. E HG increased secreted VEGF level compared to NG while transfection of miR-423-5p inhibitor suppressed that increase in secreted VEGF. F Vascular tube formation assay showed HG facilitated angiogenesis compared to NG while transfection of miR-423-5p inhibitor suppressed the facilitation caused by 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; HIF1α, hypoxia inducible factor 1α; VEGF, vascular endothelial growth factor; NC, negative control