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Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis

Diabetic retinopathy (DR) has become the leading cause of blindness among adults at working age. Previous studies have implicated circ_0001897 in the development of DR. In this study, we investigated the functional roles and mechanisms of circ_0001897 in high glucose-induced angiogenesis and inflamm...

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Autores principales: Gong, Yudan, Li, Xinze, Xie, Liuyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275961/
https://www.ncbi.nlm.nih.gov/pubmed/35510503
http://dx.doi.org/10.1080/21655979.2022.2070997
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author Gong, Yudan
Li, Xinze
Xie, Liuyi
author_facet Gong, Yudan
Li, Xinze
Xie, Liuyi
author_sort Gong, Yudan
collection PubMed
description Diabetic retinopathy (DR) has become the leading cause of blindness among adults at working age. Previous studies have implicated circ_0001897 in the development of DR. In this study, we investigated the functional roles and mechanisms of circ_0001897 in high glucose-induced angiogenesis and inflammation. Peripheral blood samples from DR patients and healthy controls were collected to examine circ_0001897 expression, which demonstrated a significant upregulation of circ_0001897 in DR patients. To investigate the functional role and mechanisms of circ_0001897, human retinal microvascular endothelial cells (HRECs) were treated with high glucose (HG) to establish an in vitro DR model of endothelial cells. HG treatment induced the upregulation of circ_0001897 in HRECs, and enhanced cell proliferation, inflammatory responses, as well as in vitro angiogenesis. Circ_0001897 knockdown significantly attenuated the cell proliferation, inflammatory responses, and angiogenesis induced by HG treatment. Mechanistically, circ_0001897 sponged and inhibited the activity of mir-29c-3p, which in turn regulates the downstream target transforming growth factor beta 2 (TGFB2). The effects of circ_0001897 knockdown could be rescued by mir-29c-3p inhibitor or TGFB2 overexpression. Collectively, our data demonstrated the novel role of circ_0001897/mir-29c-3p/TGFB2 axis in regulating HG-induced inflammation and angiogenesis of HRECs. These findings suggest that targeting circ_0001897 could serve as an intervention strategy to ameliorate DR.
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spelling pubmed-92759612022-07-13 Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis Gong, Yudan Li, Xinze Xie, Liuyi Bioengineered Research Paper Diabetic retinopathy (DR) has become the leading cause of blindness among adults at working age. Previous studies have implicated circ_0001897 in the development of DR. In this study, we investigated the functional roles and mechanisms of circ_0001897 in high glucose-induced angiogenesis and inflammation. Peripheral blood samples from DR patients and healthy controls were collected to examine circ_0001897 expression, which demonstrated a significant upregulation of circ_0001897 in DR patients. To investigate the functional role and mechanisms of circ_0001897, human retinal microvascular endothelial cells (HRECs) were treated with high glucose (HG) to establish an in vitro DR model of endothelial cells. HG treatment induced the upregulation of circ_0001897 in HRECs, and enhanced cell proliferation, inflammatory responses, as well as in vitro angiogenesis. Circ_0001897 knockdown significantly attenuated the cell proliferation, inflammatory responses, and angiogenesis induced by HG treatment. Mechanistically, circ_0001897 sponged and inhibited the activity of mir-29c-3p, which in turn regulates the downstream target transforming growth factor beta 2 (TGFB2). The effects of circ_0001897 knockdown could be rescued by mir-29c-3p inhibitor or TGFB2 overexpression. Collectively, our data demonstrated the novel role of circ_0001897/mir-29c-3p/TGFB2 axis in regulating HG-induced inflammation and angiogenesis of HRECs. These findings suggest that targeting circ_0001897 could serve as an intervention strategy to ameliorate DR. Taylor & Francis 2022-05-05 /pmc/articles/PMC9275961/ /pubmed/35510503 http://dx.doi.org/10.1080/21655979.2022.2070997 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Gong, Yudan
Li, Xinze
Xie, Liuyi
Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title_full Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title_fullStr Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title_full_unstemmed Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title_short Circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through miR-29c-3p/transforming growth factor beta 2 axis
title_sort circ_0001897 regulates high glucose-induced angiogenesis and inflammation in retinal microvascular endothelial cells through mir-29c-3p/transforming growth factor beta 2 axis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275961/
https://www.ncbi.nlm.nih.gov/pubmed/35510503
http://dx.doi.org/10.1080/21655979.2022.2070997
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