南方医科大学学报2024，Vol.44Issue(8)：1459-1466,8.DOI:10.12122/j.issn.1673-4254.2024.08.04
康柏西普可逆转TGF-β2诱导的晶状体上皮细胞发生上皮间质转化:基于调节TGF-β/Smad信号通路
Conbercept reverses TGF-β2-induced epithelial-mesenchymal transition in human lens epithelial cells by regulating the TGF-β/Smad signaling pathway
摘要
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.关键词
后发性白内障/康柏西普/上皮间质转化/转化生长因子-β2Key words
posterior capsule opacification/conbercept/epithelial-to-mesenchymal transition/transforming growth factor-β2引用本文复制引用
朱梦云,王剑锋..康柏西普可逆转TGF-β2诱导的晶状体上皮细胞发生上皮间质转化:基于调节TGF-β/Smad信号通路[J].南方医科大学学报,2024,44(8):1459-1466,8.基金项目
安徽省高校自然科学重点项目(KJ2021A0341) （KJ2021A0341）
