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miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway

PURPOSE: A majority of diabetes mellitus patients with disturbances of glucose metabolism present with vascular complications. This study aimed to explore regulatory mechanisms of miR145 and its potential target gene ANGPT2 on diabetic vasculopathy under hyperglycemia. METHODS: Based on the fact tha...

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Autores principales: Zhang, Wen, Tang, Xin-Hua, Zhang, Jin-Juan, He, Quan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680677/
https://www.ncbi.nlm.nih.gov/pubmed/33239896
http://dx.doi.org/10.2147/DMSO.S273451
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author Zhang, Wen
Tang, Xin-Hua
Zhang, Jin-Juan
He, Quan
author_facet Zhang, Wen
Tang, Xin-Hua
Zhang, Jin-Juan
He, Quan
author_sort Zhang, Wen
collection PubMed
description PURPOSE: A majority of diabetes mellitus patients with disturbances of glucose metabolism present with vascular complications. This study aimed to explore regulatory mechanisms of miR145 and its potential target gene ANGPT2 on diabetic vasculopathy under hyperglycemia. METHODS: Based on the fact that miR145 is detected in rat aortic endothelial cells (RAECs) under hyperglycemia, RAECs were transfected with miR145 mimics/inhibitor for further confirmation. RAEC proliferation was detected with CCK8 assays, and cell apoptosis and CD34(+)-cell population with annexinV–PI staining and anti-CD34FITC on flow cytometry, respectively. Then, qPCR and Western blot were applied to detect mRNA and protein expression of ANGPT2 and involved pathway factor NFκB p65. Subsequently, dual luciferase–reporter gene analysis was utilized to verify whether miR145 acted directly upon the 3ʹUTR of ANGPT2 mRNA. RESULTS: The ANGPT2 gene was confirmed to be a direct target of miR145. miR145 mimics markedly downregulated the expression of ANGPT2 and NFκB p65, boosted the percentage of the CD34(+) phenotype, and promoted proliferation and suppressed apoptosis of RAECs under hyperglycemia. CONCLUSION: miR145 might regulate the viability of RAECs via targeting ANGPT2 and involving NFκB signaling to exert a protective effect on diabetic vasculature.
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spelling pubmed-76806772020-11-24 miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway Zhang, Wen Tang, Xin-Hua Zhang, Jin-Juan He, Quan Diabetes Metab Syndr Obes Original Research PURPOSE: A majority of diabetes mellitus patients with disturbances of glucose metabolism present with vascular complications. This study aimed to explore regulatory mechanisms of miR145 and its potential target gene ANGPT2 on diabetic vasculopathy under hyperglycemia. METHODS: Based on the fact that miR145 is detected in rat aortic endothelial cells (RAECs) under hyperglycemia, RAECs were transfected with miR145 mimics/inhibitor for further confirmation. RAEC proliferation was detected with CCK8 assays, and cell apoptosis and CD34(+)-cell population with annexinV–PI staining and anti-CD34FITC on flow cytometry, respectively. Then, qPCR and Western blot were applied to detect mRNA and protein expression of ANGPT2 and involved pathway factor NFκB p65. Subsequently, dual luciferase–reporter gene analysis was utilized to verify whether miR145 acted directly upon the 3ʹUTR of ANGPT2 mRNA. RESULTS: The ANGPT2 gene was confirmed to be a direct target of miR145. miR145 mimics markedly downregulated the expression of ANGPT2 and NFκB p65, boosted the percentage of the CD34(+) phenotype, and promoted proliferation and suppressed apoptosis of RAECs under hyperglycemia. CONCLUSION: miR145 might regulate the viability of RAECs via targeting ANGPT2 and involving NFκB signaling to exert a protective effect on diabetic vasculature. Dove 2020-11-18 /pmc/articles/PMC7680677/ /pubmed/33239896 http://dx.doi.org/10.2147/DMSO.S273451 Text en © 2020 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Zhang, Wen
Tang, Xin-Hua
Zhang, Jin-Juan
He, Quan
miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title_full miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title_fullStr miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title_full_unstemmed miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title_short miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the ANGPT2 Gene and Involving the NFκB Signaling Pathway
title_sort mir145 regulates the proliferation and apoptosis of rat vascular endothelial cells under hyperglycemia by targeting the angpt2 gene and involving the nfκb signaling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680677/
https://www.ncbi.nlm.nih.gov/pubmed/33239896
http://dx.doi.org/10.2147/DMSO.S273451
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