Expression of RANKL and Proliferation Abilities of Cultured Human Middle Ear Cholesteatoma Epithelial Cells
Hiroshima Journal of Medical Sciences Volume 62 Issue 1
Page 1-6
published_at 2013-03
アクセス数 : 1468 件
ダウンロード数 : 205 件
今月のアクセス数 : 1 件
今月のダウンロード数 : 0 件
この文献の参照には次のURLをご利用ください : https://ir.lib.hiroshima-u.ac.jp/00035022
File |
HiroshimaJMedSci_62_1.pdf
470 KB
種類 :
fulltext
|
Title ( eng ) |
Expression of RANKL and Proliferation Abilities of Cultured Human Middle Ear Cholesteatoma Epithelial Cells
|
Creator | |
Source Title |
Hiroshima Journal of Medical Sciences
|
Volume | 62 |
Issue | 1 |
Start Page | 1 |
End Page | 6 |
Journal Identifire |
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
|
Abstract |
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.
|
Keywords |
Cholesteatoma
Lipopolysaccharide
RANKL
Dexamethasone
|
NDC |
Medical sciences [ 490 ]
|
Language |
eng
|
Resource Type | departmental bulletin paper |
Publisher |
Hiroshima University Medical Press
|
Date of Issued | 2013-03 |
Rights |
(c) Hiroshima University Medical Press.
|
Publish Type | Version of Record |
Access Rights | open access |
Source Identifier |
[ISSN] 0018-2052
[NCID] AA00664312
|