| 목적 : Subconjunctival fibrosis at the surgical site determines the outcome of glaucoma surgery. Epithelial-mesenchymal transition (EMT) is now thought to have a significant role in fibrosis and vascular endothelial growth factor (VEGF) is reported to trigger EMT by inducing TGF-β1.방법 : In the present study, we used immunohistochemistry, western blot analysis, enzyme-linked immunosorbent assay, and electron microscopy to elucidate whether EMT is involved in subconjunctival fibrosis after glaucoma surgery and to determine the contribution of VEGF to subconjunctival fibrosis. A rabbit trabeculectomy model was created and VEGF stimulation or VEGF inhibition was performed during surgery.결과 : VEGF stimulation induced TGF-β1 expression in a dose-dependent manner. Down-regulation of epithelial markers (E-cadherin and β-catenin) and up-regulation of mesenchymal marker (α-SMA) were observed in the conjunctival and subconjunctival layers after trabeculectomy with VEGF stimulation. Up-regulation of Smad and Snail, which plays a central role in EMT and myofibroblast transdifferentiation, were observed in the conjunctival and subconjunctival layers at the site of trabeculectomy. Electron microscopy revealed changes of the conjunctival epithelial cells.결론 : These findings suggest that EMT may have a role in subconjunctival fibrosis after glaucoma surgery. EMT and myofibroblast transdifferentiation were mediated by Smad and Snail signaling pathway. VEGF potentially affected the TGF-β1/Smad/Snail pathway, thereby triggering EMT and myofibroblast transdifferentiation. Therapeutic approaches modulating VEGF may control EMT and myofibroblast transdifferentiation and reduce subconjunctival fibrosis after glaucoma surgery. |