Item type |
学位論文 / Thesis or Dissertation(1) |
公開日 |
2019-04-11 |
タイトル |
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タイトル |
Anisomycin, a JNK and p38 activator, suppresses cell-cell junction formation in 2D cultures of K38 mouse keratinocyte cells and reduces claudin-7 expression, with an increase of paracellular permeability in 3D cultures. |
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言語 |
en |
言語 |
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言語 |
eng |
キーワード |
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主題 |
c-Jun NH2-terminal protein kinase (JNK) |
キーワード |
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主題 |
p38 mitogen-activated protein kinase (MAPK) |
キーワード |
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主題 |
tight junction; claudin |
キーワード |
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主題 |
keratinocyte |
キーワード |
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主題 |
three-dimensional culture |
キーワード |
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言語 |
en |
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主題 |
c-Jun NH2-terminal protein kinase (JNK) |
キーワード |
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言語 |
en |
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主題 |
p38 mitogen-activated protein kinase (MAPK) |
キーワード |
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言語 |
en |
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主題 |
tight junction; claudin |
キーワード |
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言語 |
en |
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主題 |
keratinocyte |
キーワード |
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言語 |
en |
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主題 |
three-dimensional culture |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_db06 |
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資源タイプ |
doctoral thesis |
アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
著者 |
Nikaido, Misaki
Otani, Takahito
Kitagawa, Norio
Ogata, Kayoko
Iida, Hiroshi
Anan, Hisashi
Inai, Tetsuichiro
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抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Keratinocytes in the oral mucosal epithelium, which is a non-keratinized stratified epithelium, are exposed to various stimuli from the oral cavity. JNK and p38 are stress-activated mitogen-activated protein kinases (MAPKs) that are phosphorylated by various stimuli and are involved in the assembly and disassembly of tight junctions (TJs) in keratinocytes. Therefore, we investigated the effects of stress-activated MAPKs on TJs in a mouse keratinocyte cell line during cell-cell junction formation in two-dimensional (2D) cultures or stratification to form non-keratinized epithelium in 3D cultures. In 2D cultures, calcium induced zipper-like staining for ZO-1 at 2 h and string-like staining for ZO-1 at 12 h, which indicated immature and mature cell-cell junctions, respectively. Anisomycin (AM), a JNK and p38 activator, inhibited formation of string-like staining for ZO-1, whereas inhibition of JNK, but not p38, after AM treatment restored string-like staining for ZO-1, although claudins (CLDNs) 4, 6, and 7 did not completely colocalize to ZO-1-positive sites. In 3D cultures, AM treatment for 2 weeks activated only p38, suppressed flattening of the superficial cells, removed CLDN7 from ZO-1-positive spots on the surface of 3D cultures, which represent TJs, and decreased transepithelial electrical resistance. Thus, short-term AM treatment inhibited maturation of cell-cell junctions by JNK, but not p38, activation. p38 activation by long-term AM treatment affected morphology of stratified structures and paracellular permeability, which was increased by CLDN7 removal from TJs. Various chronic stimuli that activate stress-activated MAPKs may weaken the keratinocyte barrier and be involved in TJ-related diseases. |
学位名 |
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学位名 |
博士(歯学) |
学位授与大学 |
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学位授与機関識別子 |
37114 |
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学位授与機関名 |
福岡歯科大学 |
学位授与年度 |
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内容記述 |
2018年度 |
学位授与年月日 |
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学位授与年月日 |
2019-03-02 |
報告番号 |
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学位授与番号 |
甲第305号 |
関連サイト |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1007/s00418-018-1736-z |
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関連名称 |
SpringerLink |
著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |