Expression of Estrogen Receptor-alpha in Nasal Polyps and the Effects of Dexamethasone on Estrogen Receptor-alpha Expression in RPMI 2650 Cells
반원우, 이윤진, 이상한, 정재엽, 백병준,
소속 상세정보
반원우 ( Ban Won-Woo ) - Soonchunhyang University College of Medicine Soonchunhyang University Cheonan Hospital Department of Otorhinolaryngology-Head and Neck Surgery
이윤진 ( Lee Yoon-Jin ) - Soonchunhyang University College of Medicine Department of Biochemistry
이상한 ( Lee Sang-Han ) - Soonchunhyang University College of Medicine Department of Biochemistry
정재엽 ( Jung Jae-Yeop ) - Soonchunhyang University College of Medicine Soonchunhyang University Cheonan Hospital Department of Otorhinolaryngology-Head and Neck Surgery
백병준 ( Baek Byoung-Joon ) - Soonchunhyang University College of Medicine Soonchunhyang University Cheonan Hospital Department of Otorhinolaryngology-Head and Neck Surgery
Abstract
Background: Studies have reported that epithelial cell proliferation may be involved in the pathogenesis of nasal polyps (NPs). Estrogen receptor (ER)-α, 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-α in NPs and healthy inferior turbinate mucosae. We also investigated the effect of dexamethasone on ER-α expression, cell viability, and apoptosis in RPMI 2650 cells.
Methods: Immunohistochemical staining and Western blot analysis were conducted to determine the expression of ER-α in 15 NPs and 15 healthy inferior turbinate mucosae. After treating RPMI 2650 cells with dexamethasone, ER-α 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-α expression was upregulated in 13 of the 15 NP tissues. Immunohistochemical staining for ER-α confirmed the results of the Western blot analysis. When RPMI 2650 cells were treated with dexamethasone, both ER-α 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-α expression was higher in NPs than in healthy inferior turbinate mucosae. When RPMI 2650 cells were treated with dexamethasone, ER-α expression was downregulated, cell viability decreased, and apoptosis increased. The decreased cell viability may be related, at least in part, to the decreased ER-α protein levels, which likely contributed to the induction of apoptotic cell death in RPMI 2650 cells.
키워드
Estrogen Receptor-α; Nasal Polyp; Apoptosis; RPMI 2650 Cells; Cell Viability
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