Fig. 7

Gain and loss function of exosomal miR-133a-3p on pro-angiogenisis, proliferation, and apoptosis in HUVECs and H9c2 cells in vitro. Proangiogenic effects of HUVECs were diminished with incubation of MIF-Exo and miR-133a-3p inhibitor (a), and quantification analysis (c). Scale bar: 100 μm. (n = 3 biological replicates for each group). Proliferation effects of HUVECs were attenuated with incubation of MIF-Exo and miR-133a-3p inhibitor (b), and quantification analysis (d). Scale bar: 100 μm. (n = 3 biological replicates for each group; 5 random fields for each biological replicate). Proangiogenic activity of HUVECs restored with incubation of siMIF-Exo and miR-133a-3p mimics (e), and quantification analysis (g). Scale bar: 100 μm. (n = 3 biological replicates for each group). Proliferation of HUVECs rescued with incubation of siMIF-Exo and miR-133a-3p mimics (f), and quantification analysis (h). Scale bar: 100 μm. (n = 3 biological replicates; 5 random fields for each biological replicate). Anti-apoptotic ability of H9c2 cells reduced with incubation of MIF-Exo and miR-133a-3p inhibitor (i), and quantification analysis (k). Scale bar: 100 μm C. (n = 3 biological replicates for each group). Anti-apoptotic ability of H9c2 cells rescued with incubation of siMIF-Exo and miR-133a-3p mimics (j), and quantification analysis (l). (n = 3 biological replicates for each group). Continuous variables and categorical variables were described by means ± SEM and percentages. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001