Quercetin inhibits transforming growth factor β1-induced epithelial–mesenchymal transition in human retinal pigment epithelial cells via the Smad pathway
Received 28 August 2018
Accepted for publication 24 October 2018
Published 6 December 2018 Volume 2018:12 Pages 4149—4161
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Qiongyu Guo
Wenting Cai,1,* Donghui Yu,1,* Jiaqi Fan,2 Xiuwei Liang,3 Huizi Jin,1 Chang Liu,2 Meijiang Zhu,1 Tianyi Shen,1 Ruiling Zhang,1 Weinan Hu,4 Qingquan Wei,1 Jing Yu1,5
1Department of Ophthalmology, Shanghai Tenth People’s Hospital Affiliated with Tongji University, Shanghai, People’s Republic of China; 2Department of Ophthalmology, Nanjing Medical University, Nanjing, People’s Republic of China; 3Department of Ophthalmology, Nanchang University, Nanchang, People’s Republic of China; 4Department of Ophthalmology, Anhui University of Science and Technology, Huainan, People’s Republic of China; 5Department of Ophthalmology, Ninghai First Hospital, Zhejiang, People’s Republic of China
*These authors contributed equally to this work
Purpose: The purpose of this study was to evaluate the effect and mechanism of quercetin on TGF-β1-induced retinal pigment epithelial (RPE) cell proliferation, migration, and extracellular matrix secretion.
Materials and methods: Cell counting kit-8, transwell, wound-healing assays, and ELISA were used to assess viability, migration, and collagen I secretion, respectively. Western blot analysis and qPCR were employed to detect mRNA and protein expression levels, respectively.
Results: Quercetin suppressed TGF-β1-induced cell proliferation, migration, and collagen I secretion. The results also showed that mRNA and protein expression of epithelial–mesenchymal transition (EMT)-related markers such as alpha-smooth muscle actin and N-cadherin was downregulated by quercetin in TGF-β1-treated RPE cells; conversely, quercetin upregulated the expression of E-cadherin and tight junction protein 1 (ZO-1). In addition, quercetin could inhibit mRNA and protein expression of matrix metalloproteinases. Quercetin may reverse the progression of EMT via the Smad2/3 pathway.
Conclusion: Our results demonstrate the protective effects of quercetin on RPE cell EMT, revealing a potential therapeutic agent for proliferative vitreoretinopathy treatment.
Keywords: proliferative vitreoretinopathy, quercetin, epithelial–mesenchymal transition, transforming growth factor-β1
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. 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.Download Article [PDF] View Full Text [HTML][Machine readable]