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Sarah Farukhi, Abbas Haider, Marc Yonkers; 17-beta Estradiol Specifically Increases Aquaporin-1 Function in a Xenopus Model for Idiopathic Intracranial Hypertension. Invest. Ophthalmol. Vis. Sci. 2016;57(12):4548.
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© ARVO (1962-2015); The Authors (2016-present)
The mechanism of rises in intracranial pressure in patients with Idiopathic Intracranial Hypertension (IIH) is unknown, but increased systemic estrogen concentrations is a known risk factors. Aquaporin-1 (AQP-1) is one of two key water transport channels that have been shown to regulate cerebrospinal fluid (CSF) pressure. Here we use an experimental model to test the effect of three naturally occurring forms of estrogen (17-b estradiol, estrone, and estriol) on AQP-1 function.
AQP1 cRNA was injected into xenopus oocytes and channel function was assessed with a swelling assay. In ND96 hypotonic solution, xenopus oocytes were assessed for increase in cross sectional area over time indicating increased permeability after a 48 hour incubation period. Oocytes were exposed to each of the three different forms of naturally occurring estrogen, added externally, and compared to control oocytes exposed to vehicle solution.
Oocytes injected with AQP1 cRNA in 17-b estradiol solution swelled faster than those exposed to estrone and estriol. The increased permeability rate of AQP-1 to estradiol was almost 2-fold the permeability rate of AQP-1 exposed to estrone and estriol (P<0.05). Oocytes exposed to estrone and estriol demonstrated a permeability rate similar to control oocytes exposed to vehicle solution.
17-b Estradiol is the predominant estrogen form during female reproductive years both in absolute serum levels and in estrogenic activity. Our study shows increased permeability rates of AQP-1 in response to estradiol when compared to estrone and estriol. The hormonal preference of AQP-1 may help explain the increased prevalence of idiopathic intracranial hypertension in women of childbearing age.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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