Abstract
Purpose :
According to the recent article, high sodium intake may affect the development of age-related cataracts. We aimed to introduce a tonicity response gene regulator, tonicity-responsive binding-protein (TonEBP or NFAT5) and determine its expression mechanism and specific roles in human lens epithelial cells (HLECs) exposed to hyperosmolar stress.
Methods :
TonEBP expression was determined in various hyperosmolar conditions in HLECs by RT-PCR and Western immunoblot analyses. TonEBP translocation during hyperosmolar stress was examined by immunocytochemistry. TonEBP-related signal transduction activity was measured on the basis of inhibition of p38 MAPK activity. Hyperosmotic apoptosis of HLECs was measured by flow cytometry.
Results :
TonEBP was upregulated and translocated to the nucleus under conditions of hyperosmolar stress. Activation of p38 MAPK by hypertonicity played key roles in TonEBP acitivation and p65 nuclear. Moreover, most of the HLECs underwent cell death on dual inhibition of p38 MAPK and TonEBP.
Conclusions :
We demonstrate TonEBP is induced and translocates to the nucleus in HLECs undergoing hyperosmolar stress through activation of p38 MAPK. Our results indicate that TonEBP may be an important gene regulator in hyperosmolar stressed HLECs.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.