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Raheleh Rahimi Darabad, David A. Sullivan; Influence of Estradiol-17ß on Estrogen Receptor mRNA in Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):304.
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Estrogens have been reported to induce photophobia, blurred vision, foreign body sensation, heightened sensitivity, contact lens intolerance and fluctuations in corneal thickness, edema and curvature. In addition, hormone replacement therapy in postmenopausal women may decrease visual acuity. However, the mechanism(s) underlying these estrogen-eye interactions are unknown. We hypothesize that these estrogen actions are mediated primarily through estrogen receptors (ER) in corneal epithelial cells, leading to an altered expression of specific genes and proteins. To begin to test this hypothesis, we examined whether estradiol-17ß (E2) modulates ER mRNA levels in human corneal epithelial cells. The ER, at least in non-ocular epithelia, is a classic target for estrogen autoregulation.
Immortalized human corneal (passages 67-69; from James Jester) and breast (MCF7 cells, passages 48-50; from Ana Soto and Carlos Sonnenschein) epithelial cells were cultured in phenol red- and serum-free medium until confluence, and then treated with vehicle or 10 nM E2 for 2 days. Alternatively, confluent cells were first exposed to dextran-coated charcoal-stripped FBS for 48 hours, then administered the vehicle or E2. Cellular RNA was extracted and processed for the analysis of ERα-, ERß- and ß2-microglobulin (housekeeping gene) mRNA by real time PCR.
Our results show that, as in published research, E2 causes a significant decrease in ERα mRNA levels in the control MCF7 cells. However, E2 had no discernable effect on ERα mRNA content in corneal epithelial cells, irrespective of whether cells had been exposed to serum. Moreover, our initial, preliminary studies suggest that corneal epithelial cell treatment with E2 for different time periods (i.e. 6 and 24 hours) and doses (i.e. 0.1 nM and 1 pM) may also have no effect on ERα mRNA expression. In these experiments the level of ERß mRNA in corneal and breast cells was invariably too low for comparative analyses.
These findings do not support our hypothesis that E2 action in corneal epithelial cells involves an alteration in ERα gene expression. It is possible that E2 influence on the cornea is mediated through non-genomic mechanisms.
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