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Min Zhao, Fatemeh Valamanesh, Nicolette Farman, Jean-Claude Jeanny, Francine Behar-Cohen; Differential Regulation of AQP4 and Kir4.1 by Triamcinolone Acetonide and Dexamethasone in The Rat Retina: Guiding The Choice for An Antiedematous Steroid?. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5639.
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We have showed that aldosterone acts through the mineralocorticoid (MR) or/and the glucocorticoid receptor (GR) to regulate Kir4.1 and aquaporin AQP4 which contribute to the fluid homeostasis of the neuroretina. In the present study, we investigated the differential effects of dexamethasone (dex) and triamcinolone acetonide (TA), two mostly used glucocorticoids (Gs) in the treatment of macular edema, on ion/water channels in the rat normal retina.
Primary cultured rat retinal Muller glial cells, rat retinal explants and rat retinas from dex or TA injected eyes were used to evaluate the 24h effects on ion/water channel expression using real-time PCR, immunohistochemistry and western blot.
We showed that while dex and TA both enhance expression of sodium channel ENaC-α, they exert different effects on Kir4.1 and AQP4. Dex up-regulates Kir4.1 and enhances perivascular and end-feet localization, however TA does not. TA induces a down-regulation of AQP4 and reduces localization in every level of the retina, whilst dex increases the perivascular localization but does not modify its expression level.
Dex and TA regulate differentially the ion/water channel expression, thus may act differently in the control of the retina hydration. Further investigations on underlying mechanism of macular edema and on anti-edematous effects of different Gs are necessary to guide a rational use of the Gs.
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