Abstract
Purpose: :
Glucocorticoids have been used to treat macular edema. The exact mechanism by which glucocorticoids reduce edema still remain unknown. The aim of this study was to evaluate the genomic regulation of glucocorticoids proteins involved on ion and water transport.
Methods: :
Human RPE cell (ARPE-19) cultured for 6 weeks were exposed to either triamcinolone (TA) (10µM) or dexamethasone (DEX) (25µM) in serum-free medium for various periods of time up to 24 hours. To study whether glucocorticoid receptor is involved, the glucocorticoid receptor antagonist, RU38486 (100 µM) was added 3 hours prior addition of triamcinolone acetonide or dexamethasone. Expression of ENaC alpha, SGK-1 and AQP-1 quantified at 1, 6 and 24 hours in RPE cells using quantitative real-time PCR.
Results: :
Expression SGK1 was significantly increased by TA and DEX at 1 and 6 hours and return to control levels at 24 hours. Expression of ENAC alpha was increased by 6 to 8 times at 6 and 24 hours by TA and DEX, and RU38486 reversed the effect of TA and DEX. No significant difference in AQP-1 expression was induced by any the glucocorticoids used.
Conclusions: :
These data indicate that TA and DEX may regulate sodium transport in RPE cells through the gluoccorticoid receptor.
Keywords: corticosteroids • retinal pigment epithelium • gene/expression