Epidermal Growth Factor Inhibits The Epithelial-mesenchymal Transition And The Potential Mechanism In Corneal Epithelial Cells

BackgroundThe aims of this study were to evaluate the effects of epidermal growth factor(EGF)on the transforming growth factor(TGF)-β1-induced epithelial-mesenchymal transition(EMT)and cell movement in human corneal epithelial cells(HCECs),and to determine the combined role of EGF and TGF-β1 in corneal epithelium wound healing.MethodsHCECs were cultured and treated with TGF-β1 or EGF in different concentrations or for different periods of time,with or without 10μM SB431542(a Smad2 inhibitor),20μM PD98059(an ERK inhibitor),10μM SB202190(a p38 inhibitor),10μM SP600125(a JNK inhibitor),and 1μWortmannin(an AKT inhibitor).The relative protein expression using western blotting,RNA expression using RT-PCR,cell viability using the CCK-8 assay,and migratio1.using the Transwell(?)cell migration and cell scratch wound healing assays were used to characterize the cells.ResultsAfter treatment with TGF-β1,three EMT-related proteins(fibronectin,N-cadherin,and E-cadherin)and mRNA expression showed that the EMT was upregulated in a concentration-dependent and time-dependent manner,with decreasing cell viability and increasing cell migration.The phosphorylation of Smad2 and p38 was a key process of the TGF-β1-induced EMT.Additionally,the expression of EMT-related proteins and mRNAs showed that EGF inhibited the TGF-β1-indued EMT,with increasing cell viability.Although the EMT was inhibited,EGF enhanced cell movement,and the blockage of p38(by SB202190,a P38 inhibitor)was a possible mechanism of this process.ConclusionsEGF inhibited the TGF-β1-induced EMT via suppression of p38,and promoted cell proliferation and migration in a non-EMT process by inhibiting the p38 pathway...