Expression of Estrogen Receptor-alpha in Nasal Polyps and the Effects of Dexamethasone on Estrogen Receptor-alpha Expression in RPMI 2650 Cells

초록

Background: Studies have reported that epithelial cell proliferation may be involved in the pathogenesis of nasal polyps (NPs). Estrogen receptor (ER)-alpha, one type of ER, is related to anti-inflammatory action and cell survival in certain tissues. In this study, we examined the presence or absence of ER-alpha in NPs and healthy inferior turbinate mucosae. We also investigated the effect of dexamethasone on ER-alpha expression, cell viability, and apoptosis in RPMI 2650 cells. Methods: Immunohistochemical staining and Western blot analysis were conducted to determine the expression of ER-alpha in 15 NPs and 15 healthy inferior turbinate mucosae. After treating RPMI 2650 cells with dexamethasone, ER-alpha expression was analyzed using Western blot analysis and cell viability was determined using the MTT assay. Western blot analysis and annexin V-phycoerythrin (PE) staining were used to examine apoptotic cell death. Results: Western blot analysis showed that ER-alpha expression was upregulated in 13 of the 15 NP tissues. Immunohistochemical staining for ER-alpha confirmed the results of the Western blot analysis. When RPMI 2650 cells were treated with dexamethasone, both ER-alpha expression and cell viability were decreased. Furthermore, the treatment of RPMI 2650 cells with dexamethasone increased apoptotic cell death, as shown by increased levels of BAX and cleaved caspase-3, decreased levels of Bcl-2, and an increased percentage of positive annexin V-PE stained cells. Conclusion: ER-alpha expression was higher in NPs than in healthy inferior turbinate mucosae. When RPMI 2650 cells were treated with dexamethasone, ER-alpha expression was downregulated, cell viability decreased, and apoptosis increased. The decreased cell viability may be related, at least in part, to the decreased ER-alpha protein levels, which likely contributed to the induction of apoptotic cell death in RPMI 2650 cells.

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