AI Article Synopsis
- The study aimed to understand how conbercept affects the TGF-β-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells, a process that can lead to visual impairment.
- Through experiments using cultured HLEC SRA01/04 cells, researchers treated the cells with TGF-β, conbercept, or both to measure changes in their growth, death, and movement, along with examining specific protein and gene expressions related to EMT.
- Results showed that conbercept effectively reduced the EMT caused by TGF-β by lowering the levels of certain biomarkers and inhibiting the signaling pathway associated with cell transition, suggesting it could be a promising treatment for conditions like posterior capsule opacification that can result
Article Abstract
Objective: To investigate the mechanism by which conbercept reverses transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLECs).
Methods: Cultured HLEC SRA01/04 cells were treated with TGF-β, 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-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 ( <0.05). Transwell assay showed significantly lower cell migration ability in TGF-β+conbercept group than in TGF-β group ( <0.05). Conbercept also inhibited the increase in Smad2/3 phosphorylation levels in HLEC-SRA01/04 cells with TGF-β-induced EMT ( <0.01).
Conclusion: Conbercept inhibits TGF-β 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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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378053 | PMC |
| http://dx.doi.org/10.12122/j.issn.1673-4254.2024.08.04 | DOI Listing |
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