Research Paper Volume 13, Issue 1 pp 1186—1211

MicroRNA-139-5p upregulation is associated with diabetic endothelial cell dysfunction by targeting c-jun

MiR-139-5p inhibits the function of ECFCs. (A, B) Migration and proliferation of normal ECFCs transfected with miR-139-5p mimics and DM ECFCs transfected with miR-139-5p inhibitors were assessed. The photos were captured by a 40X microscope and the statistics performed by Image J. (N=3) *P C) Tube formation of normal ECFCs transfected with miR-139-5p mimics and DM ECFCs transfected with miR-139-5p inhibitors were assessed. The photos were captured by a 40X microscope and the statistics performed by Image J. (N=3) *P D) The cloning ability of normal ECFCs transfected with miR-139-5p mimics and diabetic ECFCs transfected with miR-139-5p inhibitors were detected using single cell clone experiments. (N=3) *P

Figure 3. MiR-139-5p inhibits the function of ECFCs. (A, B) Migration and proliferation of normal ECFCs transfected with miR-139-5p mimics and DM ECFCs transfected with miR-139-5p inhibitors were assessed. The photos were captured by a 40X microscope and the statistics performed by Image J. (N=3) *P < .05 versus normal or diabetic ECFCs. (C) Tube formation of normal ECFCs transfected with miR-139-5p mimics and DM ECFCs transfected with miR-139-5p inhibitors were assessed. The photos were captured by a 40X microscope and the statistics performed by Image J. (N=3) *P < .05 versus normal or diabetic ECFCs. (D) The cloning ability of normal ECFCs transfected with miR-139-5p mimics and diabetic ECFCs transfected with miR-139-5p inhibitors were detected using single cell clone experiments. (N=3) *P < .05 versus normal or diabetic ECFCs. Data shown in the graphs represent mean ± standard deviation.