[Conbercept reverses TGF-β 2 -induced epithelial-mesenchymal transition in human lens epithelial cells by regulating the TGF-β/Smad signaling pathway].

Autor: Zhu M; Department of Ophthalmology, Fuyang Hospital of Anhui Medical University, Fuyang 236000, China., Wang J; Department of Ophthalmology, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.
Jazyk: čínština
Zdroj: Nan fang yi ke da xue xue bao = Journal of Southern Medical University [Nan Fang Yi Ke Da Xue Xue Bao] 2024 Aug 20; Vol. 44 (8), pp. 1459-1466.
DOI: 10.12122/j.issn.1673-4254.2024.08.04
Abstrakt: Objective: To investigate the mechanism by which conbercept reverses transforming growth factor-β 2 (TGF-β 2 )-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLECs).
Methods: Cultured HLEC SRA01/04 cells were treated with TGF-β 2 , conbercept, or both, and the changes in cell proliferation, apoptosis, and migration were observed using MTT assay, flow cytometry, scratch assay, and Transwell assay. Western blotting and qRT-PCR were used to detect the changes in the expression of EMT-related epithelial cell markers (E-Cadherin, α-SMA, and Snail), extracellular matrix components, and genes related to the TGF-β/Smad signaling pathway.
Results: Conbercept significantly reduced TGF-β 2 -induced EMT of SRA01/04 cells, decreased the expression levels of mesenchymal and extracellular matrix markers α-SMA, Snail, collagen I, collagen IV, and FN1, and upregulated the protein and mRNA expressions of E-cadherin ( P <0.05). Transwell assay showed significantly lower cell migration ability in TGF-β 2 +conbercept group than in TGF-β 2 group ( P <0.05). Conbercept also inhibited the increase in Smad2/3 phosphorylation levels in HLEC-SRA01/04 cells with TGF-β 2 -induced EMT ( P <0.01).
Conclusion: Conbercept inhibits TGF-β 2 induced EMT by downregulating the expression of pSmad2/3 in TGF-β/Smad signaling pathway, indicating a potential therapeutic strategy against visual loss induced by posterior capsule opacification.
Databáze: MEDLINE
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