Item type |
学位論文 / Thesis or Dissertation(1) |
公開日 |
2020-03-25 |
タイトル |
|
|
タイトル |
The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium. |
|
言語 |
en |
言語 |
|
|
言語 |
eng |
キーワード |
|
|
主題 |
レチノイン酸 |
キーワード |
|
|
主題 |
角化細胞 |
キーワード |
|
|
主題 |
三次元培養 |
キーワード |
|
|
主題 |
角化 |
キーワード |
|
|
主題 |
密着結合 |
キーワード |
|
|
主題 |
クローディン |
キーワード |
|
|
言語 |
en |
|
主題 |
retinoic acid |
キーワード |
|
|
言語 |
en |
|
主題 |
keratinocyte |
キーワード |
|
|
言語 |
en |
|
主題 |
three-dimensional culture |
キーワード |
|
|
言語 |
en |
|
主題 |
keratinization |
キーワード |
|
|
言語 |
en |
|
主題 |
tight junction |
キーワード |
|
|
言語 |
en |
|
主題 |
claudin |
資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_db06 |
|
資源タイプ |
doctoral thesis |
アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
著者 |
Miyazono, Shoji
Otani, Takahito
Ogata, Kayoko
Kitagawa, Norio
Iida, Hiroshi
Inai, Yuko
Matsuura, Takashi
Inai, Tetsuichiro
|
抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). We previously reported that serum-affected keratinocyte differentiation and function; namely, it inhibited keratinization, decreased loricrin (LOR) and claudin (CLDN) 1 expression, increased keratin (K) 4 and CLDN4 levels, and reduced paracellular permeability in three-dimensional (3D) cultures of mouse keratinocytes (COCA). Contrarily, RAR inhibition reversed these changes. Here, we aimed to examine whether atRA exerted the same effects as serum, and whether it was involved in the differential oral mucosa keratinization among animal species. Porcine oral mucosal keratinocytes, which form non-keratinized epithelium in vivo, established keratinized epithelium in 3D cultures. Both mouse and porcine sera induced non-keratinized epithelium at 0.1% in COCA 3D cultures. Although atRA caused the same changes as serum, its effective concentration differed. atRA inhibited keratinization at 0.1 nM and 1 nM in porcine or human keratinocytes and COCA, respectively. Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell-cell contacts. These atRA-induced changes were reverted by RAR inhibition. The results indicate that serum-induced changes are probably due to the effect of serum-derived atRA, and that mouse keratinocytes require higher atRA concentrations to suppress keratinization than porcine and human keratinocytes. We propose that the lower susceptibility of mouse keratinocytes to atRA, rather than a lower retinol concentration, is a possible reason for the keratinization of mouse oral mucosal epithelium. |
学位名 |
|
|
学位名 |
博士(歯学) |
学位授与大学 |
|
|
|
学位授与機関識別子 |
37114 |
|
|
学位授与機関名 |
福岡歯科大学 |
学位授与年度 |
|
|
内容記述 |
2019年度 |
学位授与年月日 |
|
|
学位授与年月日 |
2020-03-14 |
報告番号 |
|
|
学位授与番号 |
甲第315号 |
関連サイト |
|
|
|
識別子タイプ |
URI |
|
|
関連識別子 |
https://dx.doi.org/10.1007/s00418-020-01845-1 |
|
|
関連名称 |
Springer |
著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |