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circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p
BACKGROUND: Circular RNAs (circRNAs) are involved in the pathogenesis of many diseases, and circ_0041795 was shown to promote the progression of diabetic retinopathy (DR). The aim of this study was to explore the molecular mechanism of circ_0041795 in DR. METHODS: Human retinal pigment epithelial ce...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9410931/ https://www.ncbi.nlm.nih.gov/pubmed/36035287 http://dx.doi.org/10.1155/2022/8519664 |
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author | Sun, Xiaoyan Liu, Dan Wei, Wei |
author_facet | Sun, Xiaoyan Liu, Dan Wei, Wei |
author_sort | Sun, Xiaoyan |
collection | PubMed |
description | BACKGROUND: Circular RNAs (circRNAs) are involved in the pathogenesis of many diseases, and circ_0041795 was shown to promote the progression of diabetic retinopathy (DR). The aim of this study was to explore the molecular mechanism of circ_0041795 in DR. METHODS: Human retinal pigment epithelial cells ARPE-19 were treated with high glucose (HG). circ_0041795, miR-589-5p, and Yes-associated protein 1 (YAP1) levels were measured by reverse transcription-quantitative polymerase chain reaction assay. Biological behaviors were examined by Cell Counting Kit-8 assay for cell viability, EdU assay for cell proliferation, flow cytometry for cell apoptosis, and enzyme-linked immunosorbent assay for cell inflammation. Oxidative stress was assessed via the commercial kits. Western blot was performed for analysis of protein expression. The molecular binding was assessed via dual-luciferase reporter assay and pull-down assay. RESULTS: HG-induced inhibiting effects on cell viability and proliferation but promoting effects on cell apoptosis, inflammation, and oxidative stress were ameliorated by silence of circ_0041795. circ_0041795 was identified to act as a miR-589-5p sponge. The regulation of circ_0041795 in HG-induced cell injury was achieved by inhibiting miR-589-5p. miR-589-5p targeted YAP1 and relieved HG-induced cell dysfunction via downregulating YAP1. circ_0041795 sponged miR-589-5p to regulate YAP1 level and activated the NF-κB pathway through the miR-589-5p/YAP1 axis. CONCLUSION: All these results elucidated that circ_0041795 facilitated the development of DR by inducing miR-589-5p-mediated YAP1 upregulation. |
format | Online Article Text |
id | pubmed-9410931 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-94109312022-08-26 circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p Sun, Xiaoyan Liu, Dan Wei, Wei Comput Math Methods Med Research Article BACKGROUND: Circular RNAs (circRNAs) are involved in the pathogenesis of many diseases, and circ_0041795 was shown to promote the progression of diabetic retinopathy (DR). The aim of this study was to explore the molecular mechanism of circ_0041795 in DR. METHODS: Human retinal pigment epithelial cells ARPE-19 were treated with high glucose (HG). circ_0041795, miR-589-5p, and Yes-associated protein 1 (YAP1) levels were measured by reverse transcription-quantitative polymerase chain reaction assay. Biological behaviors were examined by Cell Counting Kit-8 assay for cell viability, EdU assay for cell proliferation, flow cytometry for cell apoptosis, and enzyme-linked immunosorbent assay for cell inflammation. Oxidative stress was assessed via the commercial kits. Western blot was performed for analysis of protein expression. The molecular binding was assessed via dual-luciferase reporter assay and pull-down assay. RESULTS: HG-induced inhibiting effects on cell viability and proliferation but promoting effects on cell apoptosis, inflammation, and oxidative stress were ameliorated by silence of circ_0041795. circ_0041795 was identified to act as a miR-589-5p sponge. The regulation of circ_0041795 in HG-induced cell injury was achieved by inhibiting miR-589-5p. miR-589-5p targeted YAP1 and relieved HG-induced cell dysfunction via downregulating YAP1. circ_0041795 sponged miR-589-5p to regulate YAP1 level and activated the NF-κB pathway through the miR-589-5p/YAP1 axis. CONCLUSION: All these results elucidated that circ_0041795 facilitated the development of DR by inducing miR-589-5p-mediated YAP1 upregulation. Hindawi 2022-08-05 /pmc/articles/PMC9410931/ /pubmed/36035287 http://dx.doi.org/10.1155/2022/8519664 Text en Copyright © 2022 Xiaoyan Sun et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Sun, Xiaoyan Liu, Dan Wei, Wei circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title | circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title_full | circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title_fullStr | circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title_full_unstemmed | circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title_short | circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p |
title_sort | circ_0041795 induces yap1 upregulation to accelerate the progression of diabetic retinopathy through binding to mir-589-5p |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9410931/ https://www.ncbi.nlm.nih.gov/pubmed/36035287 http://dx.doi.org/10.1155/2022/8519664 |
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