{"title":"[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】。］","authors":"M Zhu, J Wang","doi":"10.12122/j.issn.1673-4254.2024.08.04","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanism by which conbercept reverses transforming growth factor-β<sub>2</sub> (TGF-β<sub>2</sub>)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLECs).</p><p><strong>Methods: </strong>Cultured HLEC SRA01/04 cells were treated with TGF-β<sub>2</sub>, 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.</p><p><strong>Results: </strong>Conbercept significantly reduced TGF-β<sub>2</sub>-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 (<i>P</i> <0.05). Transwell assay showed significantly lower cell migration ability in TGF-β<sub>2</sub>+conbercept group than in TGF-β<sub>2</sub> group (<i>P</i> <0.05). Conbercept also inhibited the increase in Smad2/3 phosphorylation levels in HLEC-SRA01/04 cells with TGF-β<sub>2</sub>-induced EMT (<i>P</i> <0.01).</p><p><strong>Conclusion: </strong>Conbercept inhibits TGF-β<sub>2</sub> 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.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378053/pdf/","citationCount":"0","resultStr":"{\"title\":\"[Conbercept reverses TGF-β<sub>2</sub>-induced epithelial-mesenchymal transition in human lens epithelial cells by regulating the TGF-β/Smad signaling pathway].\",\"authors\":\"M Zhu, J Wang\",\"doi\":\"10.12122/j.issn.1673-4254.2024.08.04\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the mechanism by which conbercept reverses transforming growth factor-β<sub>2</sub> (TGF-β<sub>2</sub>)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLECs).</p><p><strong>Methods: </strong>Cultured HLEC SRA01/04 cells were treated with TGF-β<sub>2</sub>, 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.</p><p><strong>Results: </strong>Conbercept significantly reduced TGF-β<sub>2</sub>-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 (<i>P</i> <0.05). Transwell assay showed significantly lower cell migration ability in TGF-β<sub>2</sub>+conbercept group than in TGF-β<sub>2</sub> group (<i>P</i> <0.05). Conbercept also inhibited the increase in Smad2/3 phosphorylation levels in HLEC-SRA01/04 cells with TGF-β<sub>2</sub>-induced EMT (<i>P</i> <0.01).</p><p><strong>Conclusion: </strong>Conbercept inhibits TGF-β<sub>2</sub> 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.</p>\",\"PeriodicalId\":18962,\"journal\":{\"name\":\"Nan fang yi ke da xue xue bao = Journal of Southern Medical University\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-08-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378053/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nan fang yi ke da xue xue bao = Journal of Southern Medical University\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12122/j.issn.1673-4254.2024.08.04\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12122/j.issn.1673-4254.2024.08.04","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
[Conbercept reverses TGF-β2-induced epithelial-mesenchymal transition in human lens epithelial cells by regulating the TGF-β/Smad signaling pathway].
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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