[Conbercept reverses TGF-β₂-induced epithelial-mesenchymal transition in human lens epithelial cells by regulating the TGF-β/Smad signaling pathway].

Q3 Medicine Nan fang yi ke da xue xue bao = Journal of Southern Medical University Pub Date : 2024-08-20 DOI:10.12122/j.issn.1673-4254.2024.08.04

M Zhu, J Wang

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Abstract

Objective: To investigate the mechanism by which conbercept reverses transforming growth factor-β₂ (TGF-β₂)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLECs).

Methods: Cultured HLEC SRA01/04 cells were treated with TGF-β₂, 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-β₂-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-β₂+conbercept group than in TGF-β₂ group (P <0.05). Conbercept also inhibited the increase in Smad2/3 phosphorylation levels in HLEC-SRA01/04 cells with TGF-β₂-induced EMT (P <0.01).

Conclusion: Conbercept inhibits TGF-β₂ 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.

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[康柏西普通过调节TGF-β/Smad信号通路逆转TGF-β2-诱导的人晶状体上皮细胞上皮-间质转化】。］

目的研究康柏西汀逆转转化生长因子-β2（TGF-β2）诱导的人晶状体上皮细胞（HLECs）上皮-间质转化（EMT）的机制：用TGF-β2、康柏西汀或两者同时处理培养的HLEC SRA01/04细胞，用MTT试验、流式细胞术、划痕试验和Transwell试验观察细胞增殖、凋亡和迁移的变化。用 Western 印迹和 qRT-PCR 检测与 EMT 相关的上皮细胞标记物（E-Cadherin、α-SMA 和 Snail）、细胞外基质成分和 TGF-β/Smad 信号通路相关基因的表达变化：结果：康柏西普明显降低了TGF-β2-诱导的SRA01/04细胞的EMT，降低了间充质和细胞外基质标志物α-SMA、Snail、胶原蛋白I、胶原蛋白IV和FN1的表达水平，并上调了E-cadherin（P 2+康柏西普组）的蛋白和mRNA表达（P 2-诱导的EMT组）（P 结论：康柏西普抑制了TGF-β2-诱导的SRA01/04细胞的EMT，并降低了间充质和细胞外基质标志物α-SMA、Snail、胶原蛋白I、胶原蛋白IV和FN1的表达水平：康柏西普通过下调TGF-β/Smad信号通路中pSmad2/3的表达，抑制了TGF-β2诱导的EMT，为后囊变引起的视力下降提供了一种潜在的治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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