Fig. 2.

MiR-25-3p induces vascular leakiness and angiogenesis. a Permeability of the HUVEC monolayers to rhodamine–dextran (70 kDa) after exposure to exosomes derived from SW480/mock, SW480/miR-25-3p, HCT116 NC, and HCT116/zip-miR-25-3p for 72 h. Mean ± SEM are provided (n = 3). b Effect of exosomes derived from SW480/mock, SW480/miR-25-3p, HCT116 NC, and HCT116/zip-miR-25-3p on tube formation ability of HUVECs by tube formation assay. Mean ± SEM are provided (n = 3). Scale bar represents 100 µm. c Effect of exosomes derived from SW480/mock, SW480/miR-25-3p, HCT116 NC, and HCT116/zip-miR-25-3p on vascular outgrowth of rat aortic rings. Vascular outgrowth was quantified by counting all sprouts from one ring. Mean ± SEM are provided (n = 3). Scale bar represents 200 µm. d Effect of SW480/mock exosomes loading with miR-25-3p mimics and SW480/miR-25-3p exosomes loading with miR-25-3p inhibitor on permeability of HUVEC monolayers. Mean ± SEM are provided (n = 3). e Effect of SW480/mock exosomes loading with miR-25-3p mimics and SW480/miR-25-3p exosomes loading with miR-25-3p inhibitor on tube formation ability of HUVECs. Scale bar represents 100 µm. Mean ± SEM are provided (n = 3). f Effect of SW480/mock exosomes loading with miR-25-3p mimics and SW480/miR-25-3p exosomes loading with miR-25-3p inhibitor on vascular outgrowth of rat aortic rings. Scale bar represents 200 µm. Mean ± SEM are provided (n = 3). **P < 0.01, ***P < 0.001 according to two-tailed Student’s t test