Abstract
Purpose :
Recent research showed that ER stress induces EMT in different cellular systems. However, it remains unclear whether ER stress effects EMT or cell immigration on LECs.In this study, we aime to investigate the role of ER Stress on lens epithelium EMT and cell immigration.
Methods :
Human LECs were cultured and treated with TM/TG to induce ER stress. PBA／TUDCA is usedto inhibit the TM/TG induced UPR activation in the LECs.Western blot analysis and immunohistochemistry assay were used to detect the related proteins levels.Wound healing assay was used to see the cell immigration manner.
Results :
Human LECs were cultured and treated with TM/TG to induce ER stress. Western blot analysis and immunohistochemistry assay were used to detect the related proteins levels. Proteins levels on three pathways of UPR including GRP78, P-eIf2α, ATF6, ATF4, P-IRE1α were significantly increased. In the meantime, we detected the increased level of F-cadherin, fibronectin (FN), vimentin, α-SMA, and decreased protein level of E-cadherin. We then use PBA & TUDCA to inhibit the TM/TG induced UPR activation in the LECs, and found the recovered protein level of F-cadherin, fibronectin (FN), vimentin, α-SMA, and E-cadherin. Wound healing assay was used to see the cell immigration manner. We found that the TM/TG induced ER stress can facilitate the LECs immigration, on the contrary, the LECs immigration is suppressed when the ER stress is inhibited with PBA/TUDCA.
Conclusions :
These results indicate that prolonged ER stress is involved in lens capsular opacification through regulating EMT in lens epithelium.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.