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L. Luo, M. Wadehra, P. Coulam, R. Levinson, L. Gordon; Regulation of Epithelial Membrane Protein–2 (EMP2) Expression in Human Corneal Epithelium . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2105.
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Purpose: Epithelial membrane protein– 2 (EMP2) is highly expressed in ocular tissues. EMP2 has an important role in modulation of cell surface protein expression including specific integrin isoforms and changes in expression levels may coordinately alter biologic behavior in specific epithelial cells. The purpose of this study is to explore expression of epithelial membrane protein–2 (EMP2) after exposure to estrogen or the inflammatory mediators, interleukin–1alpha (IL–1α) and interleukin–1beta (IL–1ß), in cultured human corneal epithelial cells. Methods: A human transformed corneal epithelial cell line was exposed to estrogen or inflammatory mediators and analyzed for EMP2 expression by quantitative Western blot analysis. Expression of estrogen receptor alpha (ERα) in the cell line was confirmed by Western blot analysis. For estrogen exposure, the cells were cultured in charcoal treated serum supplemented either with 10 uM/L, 20 uM/L estrogen or vehicle control for 72 hours. Other cells were cultured for 72 hours in the presence of either 10 ng/ml, 20 ng/ml IL–1α or 10 ng/ml, 20 ng/ml IL–1ß. Results: Expression of ERa was found in human transformed corneal epithelial cell line by Western blots. Compared with untreated cells and vehicle treated cells, estrogen markedly stimulated expression of EMP–2. Exposure to IL–1b markedly decreased the expression of EMP–2 to about 10% of the control, while IL–1a did not significantly affect expression of EMP2 when compared with the control. Conclusions: These findings demonstrate that estrogen and IL–1ß may modulate expression of EMP–2 in human corneal epithelium. The consequence of increased EMP2 may directly or indirectly modulate cell–cell or cell–extracellular matrix interactions and regulate cell adhesion. Stimulation of EMP–2 by estrogen is hypothesized to play a role in the pathogenesis of dry eye. CR: N. Support: Research to Prevent Blindness
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