Electric field exposure promotes epithelial‑mesenchymal transition in human lens epithelial cells via integrin β1‑FAK signaling.

Electric field (EF) exposure can affect the elongation, migration, orientation, and division of cells. The present study tested the hypothesis that EF may also affect epithelial‑mesenchymal transition (EMT) in lens epithelial cells and that this effect may be an important inducer in the pathological process of posterior capsule opacification (PCO). Human lens epithelial (HLE)‑B3 cells were exposed to an EF. Experiments were performed in the presence or absence of an anti‑integrin β1 blocking antibody or a small molecule inhibitor targeting focal adhesion kinase (FAK). Cell morphology changes were observed by microscopy. The expression levels of integrin β1, FAK, phosphorylated (p)FAK and of EMT markers, E‑cadherin and Vimentin, were examined by immunofluorescence, reverse transcription‑quantitative polymerase chain reaction and western blotting. Following exposure to EF, HLE‑B3 cells appeared elongated and resembled more fibroblast‑like cells. Expression of E‑cadherin was decreased, while expression of Vimentin was increased in HLE‑B3 cells exposed to EF, compared with control cells. In addition, the mRNA expression levels of integrin β1 were increased, and the protein expression levels of integrin β1 and pFAK were increased in HLE‑B3 cells exposed to EF, compared with control cells. Blocking of integrin β1 suppressed the EMT‑related morphological changes of HLE‑B3 cells and reduced the activation of FAK following EF exposure. However, blocking of pFAK did not affect the EMT status of HLE‑B3 cells induced by EF. In conclusion, the present study demonstrated that EF exposure induced EMT in HLE‑B3 cells and that this effect may partially be mediated by the activation of integrin β1‑FAK signaling. The present results may provide a new mechanistic approach to prevent the development of PCO.