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Inhibition of miR-200b Promotes Angiogenesis in Endothelial Cells by Activating The Notch Pathway
OBJECTIVE: 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...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Royan Institute
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7944128/ https://www.ncbi.nlm.nih.gov/pubmed/33650820 http://dx.doi.org/10.22074/cellj.2021.7080 |
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author | Qiu, Tie-Ying Huang, Jin Wang, Li-Ping Zhu, Bi-Song |
author_facet | Qiu, Tie-Ying Huang, Jin Wang, Li-Ping Zhu, Bi-Song |
author_sort | Qiu, Tie-Ying |
collection | PubMed |
description | OBJECTIVE: 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 in vitro Matrigel tube formation assays. Luciferase reporter assays were used to test the binding of miR-200b with Notch1. RESULTS: 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. CONCLUSION: Inhibition 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. |
format | Online Article Text |
id | pubmed-7944128 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Royan Institute |
record_format | MEDLINE/PubMed |
spelling | pubmed-79441282021-04-01 Inhibition of miR-200b Promotes Angiogenesis in Endothelial Cells by Activating The Notch Pathway Qiu, Tie-Ying Huang, Jin Wang, Li-Ping Zhu, Bi-Song Cell J Original Article OBJECTIVE: 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 in vitro Matrigel tube formation assays. Luciferase reporter assays were used to test the binding of miR-200b with Notch1. RESULTS: 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. CONCLUSION: Inhibition 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. Royan Institute 2021 2021-03-01 /pmc/articles/PMC7944128/ /pubmed/33650820 http://dx.doi.org/10.22074/cellj.2021.7080 Text en The Cell Journal (Yakhteh) is an open access journal which means the articles are freely available online for any individual author to download and use the providing address. The journal is licensed under a Creative Commons Attribution-Non Commercial 3.0 Unported License which allows the author(s) to hold the copyright without restrictions that is permitting unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited. http://creativecommons.org/licenses/by/3/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Qiu, Tie-Ying Huang, Jin Wang, Li-Ping Zhu, Bi-Song Inhibition of miR-200b Promotes Angiogenesis in Endothelial Cells by Activating The Notch Pathway |
title | Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway |
title_full | Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway |
title_fullStr | Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway |
title_full_unstemmed | Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway |
title_short | Inhibition of miR-200b Promotes Angiogenesis in Endothelial
Cells by Activating The Notch Pathway |
title_sort | inhibition of mir-200b promotes angiogenesis in endothelial
cells by activating the notch pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7944128/ https://www.ncbi.nlm.nih.gov/pubmed/33650820 http://dx.doi.org/10.22074/cellj.2021.7080 |
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