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hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3
Circular RNAs (circRNAs) regulate the expression of genes that are critical for various biological and pathological processes. Previous studies have reported that the expression of hsa_circ_0058092 is decreased in patients with diabetes mellitus (DM); however, the specific role of this circRNA in DM...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387092/ https://www.ncbi.nlm.nih.gov/pubmed/32705235 http://dx.doi.org/10.3892/ijmm.2020.4664 |
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author | Cheng, Jie Hu, Weiwei Zheng, Fenghui Wu, Yongfa Li, Maoquan |
author_facet | Cheng, Jie Hu, Weiwei Zheng, Fenghui Wu, Yongfa Li, Maoquan |
author_sort | Cheng, Jie |
collection | PubMed |
description | Circular RNAs (circRNAs) regulate the expression of genes that are critical for various biological and pathological processes. Previous studies have reported that the expression of hsa_circ_0058092 is decreased in patients with diabetes mellitus (DM); however, the specific role of this circRNA in DM is unknown. In the present study, endothelial progenitor cells (EPCs) were isolated and a decreased hsa_circ_0058092 expression was found under conditions of hyperglycemia (HG). The overexpression of hsa_circ_0058092 protected the EPCs against HG-induced damage by preserving cell survival, proliferation, migration and angiogenic differentiation. The overexpression of hsa_circ_0058092 also decreased the HG-induced increase in NADPH-oxidase proteins and inflammatory cytokines. Further investigation revealed that the overexpression of hsa_circ_0058092 enhanced FOXO3 expression, which was mediated through the interaction with miR-217. Furthermore, the upregulation of miR-217 or the downregulation of FOXO3 abolished the protective effects of hsa_circ_0058092 against HG-induced EPC damage. On the whole, these data suggest that hsa_circ_0058092 acts via the miR-217/FOXO3 pathway to protect against EPCs HG-induced damage, and to preserve the migration and angiogenesis of EPCs. |
format | Online Article Text |
id | pubmed-7387092 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73870922020-07-31 hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 Cheng, Jie Hu, Weiwei Zheng, Fenghui Wu, Yongfa Li, Maoquan Int J Mol Med Articles Circular RNAs (circRNAs) regulate the expression of genes that are critical for various biological and pathological processes. Previous studies have reported that the expression of hsa_circ_0058092 is decreased in patients with diabetes mellitus (DM); however, the specific role of this circRNA in DM is unknown. In the present study, endothelial progenitor cells (EPCs) were isolated and a decreased hsa_circ_0058092 expression was found under conditions of hyperglycemia (HG). The overexpression of hsa_circ_0058092 protected the EPCs against HG-induced damage by preserving cell survival, proliferation, migration and angiogenic differentiation. The overexpression of hsa_circ_0058092 also decreased the HG-induced increase in NADPH-oxidase proteins and inflammatory cytokines. Further investigation revealed that the overexpression of hsa_circ_0058092 enhanced FOXO3 expression, which was mediated through the interaction with miR-217. Furthermore, the upregulation of miR-217 or the downregulation of FOXO3 abolished the protective effects of hsa_circ_0058092 against HG-induced EPC damage. On the whole, these data suggest that hsa_circ_0058092 acts via the miR-217/FOXO3 pathway to protect against EPCs HG-induced damage, and to preserve the migration and angiogenesis of EPCs. D.A. Spandidos 2020-09 2020-06-29 /pmc/articles/PMC7387092/ /pubmed/32705235 http://dx.doi.org/10.3892/ijmm.2020.4664 Text en Copyright: © Cheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Cheng, Jie Hu, Weiwei Zheng, Fenghui Wu, Yongfa Li, Maoquan hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title_full | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title_fullStr | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title_full_unstemmed | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title_short | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via miR-217/FOXO3 |
title_sort | hsa_circ_0058092 protects against hyperglycemia-induced endothelial progenitor cell damage via mir-217/foxo3 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387092/ https://www.ncbi.nlm.nih.gov/pubmed/32705235 http://dx.doi.org/10.3892/ijmm.2020.4664 |
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