Aim
To study the effect of discoidin I-like domaincontaining protein 3 (EDIL3) depletion on the proliferation and epithelial-mesenchymal transition (EMT) in human lens epithelial cells (LECs).
Conclusion
The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.
Methods
RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using EdU kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β (TGFβ) pathway was investigated using Western blotting.
Results
The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation (P<0.05) and migration (P<0.01). Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin (α-SMA) (P<0.001) and vimentin (P<0.01), while increased the expression of E-cadherin (P<0.001). EDIL3 depletion could suppress the phosphorylation of Smad2 (P<0.01) and Smad3 (P<0.01) and the activation of exracellular signal regulated kinase (ERK) (P<0.05).