Expression of RANKL and Proliferation Abilities of Cultured Human Middle Ear Cholesteatoma Epithelial Cells
Hiroshima Journal of Medical Sciences 62 巻 1 号
1-6 頁
2013-03 発行
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タイトル ( eng ) |
Expression of RANKL and Proliferation Abilities of Cultured Human Middle Ear Cholesteatoma Epithelial Cells
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作成者 | |
収録物名 |
Hiroshima Journal of Medical Sciences
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巻 | 62 |
号 | 1 |
開始ページ | 1 |
終了ページ | 6 |
収録物識別子 |
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
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抄録 |
One of the most distinct characteristics of middle ear cholesteatomas is their capacity for bone destruction during the growth process. In this study, we examined the relationship between inflammatory mechanisms and both bone absorption and the proliferation of epithelial cholesteatoma cells. Cultured cholesteatoma epithelial cells were stimulated by lipopolysaccharide (LPS) and dexamethasone (Dex). We found that the expression of receptor activator of NF-κB ligand (RANKL) and Ki-67 in cultured cholesteatoma cells was increased by LPS stimulation, indicating that LPS promotes not only bone destruction but also the proliferative activities of these cells. The constitutive expression of RANKL and Ki-67 and the production of IL-6 and IL-8 were significantly inhibited by Dex treatment. Further, Dex significantly suppressed the stimulatory effects of LPS on RANKL and Ki-67 expression and on IL-6 and IL-8 production. Based on results so far, Dex likely exerts a beneficial action against acute inflammation. However, further studies might be required to assess its clinical features.
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著者キーワード |
Cholesteatoma
Lipopolysaccharide
RANKL
Dexamethasone
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NDC分類 |
医学 [ 490 ]
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言語 |
英語
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資源タイプ | 紀要論文 |
出版者 |
Hiroshima University Medical Press
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発行日 | 2013-03 |
権利情報 |
(c) Hiroshima University Medical Press.
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出版タイプ | Version of Record(出版社版。早期公開を含む) |
アクセス権 | オープンアクセス |
収録物識別子 |
[ISSN] 0018-2052
[NCID] AA00664312
|