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Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway

Epithelial-melancholy transition (EMT) is the main cause of organ fibrosis and a common pathogenetic mechanism in most cataracts. This study aimed to explore the molecular mechanism of Toll-like receptor (TLR)-3 in the occurrence and development of post-cataract EMT and to provide new ideas for the...

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Autores principales: Xie, Weiwei, Yu, Qihua, Wang, Layi, Shao, Yongqing, Bo, Qingyun, Wu, Guohai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9342145/
https://www.ncbi.nlm.nih.gov/pubmed/35758265
http://dx.doi.org/10.1080/21655979.2022.2085391
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author Xie, Weiwei
Yu, Qihua
Wang, Layi
Shao, Yongqing
Bo, Qingyun
Wu, Guohai
author_facet Xie, Weiwei
Yu, Qihua
Wang, Layi
Shao, Yongqing
Bo, Qingyun
Wu, Guohai
author_sort Xie, Weiwei
collection PubMed
description Epithelial-melancholy transition (EMT) is the main cause of organ fibrosis and a common pathogenetic mechanism in most cataracts. This study aimed to explore the molecular mechanism of Toll-like receptor (TLR)-3 in the occurrence and development of post-cataract EMT and to provide new ideas for the prevention and treatment of posterior capsule opacification (PCO). In the presence or absence of TLR3, the human lens epithelial cell (LEC) line, SRA01/04, was treated with the transforming growth factor (TGF)-β2. Cell counting kit-8 (CCK-8) and Transwell assays were used to analyze the cell proliferation, migration, and invasion. The expression levels of proteins and RNAs were detected by western blotting and quantitative polymerase chain reaction (qPCR) experiments. Functional gain and loss studies showed that TLR3 regulates the proliferation, migration, and invasion of LECs and EMT induced by TGF-β2. Moreover, TLR3 regulates the expression of Jagged-1, Notch-1, and Notch-3 These findings indicate that TLR3 prevents the progression of lens fibrosis by targeting the Jagged-1/Notch signaling pathway to regulate the proliferation, migration, and invasion of LECs, and TGF-β2-induced EMT. Therefore, the TLR3-Jagged-1/Notch signaling axis may be a potential therapeutic target for the treatment of fibrotic cataracts.
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spelling pubmed-93421452022-08-02 Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway Xie, Weiwei Yu, Qihua Wang, Layi Shao, Yongqing Bo, Qingyun Wu, Guohai Bioengineered Research Paper Epithelial-melancholy transition (EMT) is the main cause of organ fibrosis and a common pathogenetic mechanism in most cataracts. This study aimed to explore the molecular mechanism of Toll-like receptor (TLR)-3 in the occurrence and development of post-cataract EMT and to provide new ideas for the prevention and treatment of posterior capsule opacification (PCO). In the presence or absence of TLR3, the human lens epithelial cell (LEC) line, SRA01/04, was treated with the transforming growth factor (TGF)-β2. Cell counting kit-8 (CCK-8) and Transwell assays were used to analyze the cell proliferation, migration, and invasion. The expression levels of proteins and RNAs were detected by western blotting and quantitative polymerase chain reaction (qPCR) experiments. Functional gain and loss studies showed that TLR3 regulates the proliferation, migration, and invasion of LECs and EMT induced by TGF-β2. Moreover, TLR3 regulates the expression of Jagged-1, Notch-1, and Notch-3 These findings indicate that TLR3 prevents the progression of lens fibrosis by targeting the Jagged-1/Notch signaling pathway to regulate the proliferation, migration, and invasion of LECs, and TGF-β2-induced EMT. Therefore, the TLR3-Jagged-1/Notch signaling axis may be a potential therapeutic target for the treatment of fibrotic cataracts. Taylor & Francis 2022-06-26 /pmc/articles/PMC9342145/ /pubmed/35758265 http://dx.doi.org/10.1080/21655979.2022.2085391 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
Xie, Weiwei
Yu, Qihua
Wang, Layi
Shao, Yongqing
Bo, Qingyun
Wu, Guohai
Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title_full Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title_fullStr Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title_full_unstemmed Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title_short Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway
title_sort toll-like receptor 3 gene regulates cataract-related mechanisms via the jagged-1/notch signaling pathway
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9342145/
https://www.ncbi.nlm.nih.gov/pubmed/35758265
http://dx.doi.org/10.1080/21655979.2022.2085391
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