Journal
DRUG DESIGN DEVELOPMENT AND THERAPY
Volume 12, Issue -, Pages 4149-4161Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DDDT.S185618
Keywords
proliferative vitreoretinopathy; quercetin; epithelial-mesenchymal transition; transforming growth factor-beta 1
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Funding
- National Natural Science Foundation of China [81470648]
- Fundamental Research Funds for the Central Universities
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Purpose: The purpose of this study was to evaluate the effect and mechanism of quercetin on TGF-beta 1-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-beta 1-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-beta 1-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.
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