@article { author = {Qiu, Tie-Ying and Huang, Jin and Wang, Li-Ping and Zhu, Bi-Song}, title = {Inhibition of miR-200b Promotes Angiogenesis in Endothelial Cells by Activating The Notch Pathway}, journal = {Cell Journal (Yakhteh)}, volume = {23}, number = {1}, pages = {51-60}, year = {2021}, publisher = {Royan Institute, Iranian Academic Center for Education Culture and Research (ACECR)}, issn = {2228-5806}, eissn = {2228-5814}, doi = {10.22074/cellj.2021.7080}, abstract = {ObjectivePatients 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 MethodsIn 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 in vitro Matrigel tube formation assays. Luciferase reporter assays were used to test the binding of miR-200b with Notch1. ResultsmiR-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. ConclusionInhibition of miR-200b activated the angiogenic ability of endothelial cells and promoted wound healing through reactivation of the Notch pathway in vitro. miR-200b could be a promising therapeutic target for treating HUVEC dysfunction.}, keywords = {Angiogenesis,HUVEC Dysfunction,MiR,200b,Notch Pathway}, url = {https://www.celljournal.org/article_250689.html}, eprint = {https://www.celljournal.org/article_250689_ad95bf4afd08b841f961d74b2d527aae.pdf} }