Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway
Patients with diabetes mellitus frequently have chronic wounds or diabetic ulcers as a result of impaired wound healing, which may lead to limb amputation. Human umbilical vein endothelial cell (HUVEC) dysfunction also delays wound healing. Here, we investigated the mechanism of miR-200b in HUVECs under high glucose conditions and the potential of miR-200b as a therapeutic target.
Materials and Methods
In this experimental study, HUVECs were cultured with 5 or 30 mM glucose for 48 hours.
Cell proliferation was evaluated by CCK-8 assays. Cell mobility was tested by wound healing and Transwell assays.
Angiogenesis was analyzed
miR-200b expression was induced by high glucose treatment of HUVECs (P<0.01), and it significantly repressed cell proliferation, migration, and tube formation (P<0.05). Notch1 was directly targeted and repressed by miR-200b at both the mRNA and protein levels. Inhibition of miR-200b restored Notch1 expression (P<0.05) and reactivated the Notch pathway. The effects of miR-200b inhibition in HUVECs could be reversed by treatment with a Notch pathway inhibitor (P<0.05), indicating that the miR-200b/Notch axis modulates the proliferation, migration, and tube formation ability of HUVECs.
Inhibition of miR-200b activated the angiogenic ability of endothelial cells and promoted wound healing
through reactivation of the Notch pathway