Item type |
デフォルトアイテムタイプ_(フル)(1) |
公開日 |
2023-03-18 |
タイトル |
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タイトル |
Irsogladine maleate regulates neutrophil migration and E-cadherin expression in gingival epithelium stimulated by Aggregatibacter actinomycetemcomitans |
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言語 |
en |
作成者 |
Fujita, Tsuyoshi
Kishimoto, Akiyoshi
Shiba, Hideki
Hayashida, Kouichi
Kajiya, Mikihito
Uchida, Yuushi
Matsuda, Shinji
Takeda, Katsuhiro
Ouhara, Kazuhisa
Kawaguchi, Hiroyuki
Abiko, Yoshimitsu
Kurihara, Hidemi
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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 |
権利情報 |
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権利情報 |
Copyright (c) 2010 Elsevier Inc. |
主題 |
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主題Scheme |
Other |
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主題 |
Irsogladine maleate |
主題 |
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主題Scheme |
Other |
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主題 |
Aggregatibacter actinomycetemcomitans |
主題 |
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主題Scheme |
Other |
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主題 |
E-cadherin |
主題 |
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主題Scheme |
Other |
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主題 |
Neutrophil migration |
主題 |
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主題Scheme |
Other |
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主題 |
CXC-chemokine |
主題 |
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主題Scheme |
Other |
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主題 |
Gingival epithelial cells |
主題 |
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主題Scheme |
NDC |
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主題 |
490 |
内容記述 |
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内容記述 |
Irsogladine maleate (IM) counters Aggregatibacter actinomycetemcomitans-induced reduction of the gap junction intercellular communication and the expression of zonula occludens-1, which is a major tight junction structured protein, in cultured human gingival epithelial cells (HGEC). In addition, IM obviates the A. actinomycetemcomitans-induced increase in interleukin (IL)-8 levels in HGEC. Thus, by regulating the intercellular junctional complex and chemokine secretion in HGEC, IM may be useful to prevent periodontal disease. To clarify the effects and regulatory mechanism of IM in vivo and in vitro, we examined the expression of E-cadherin and neutrophil chemotaxis induced by A. actinomycetemcomitans under IM pretreatment. Immunohistochemical studies revealed that A. actinomycetemcomitans application to the gingival sulcus decreased the number of cells positive for E-cadherin and increased those positive for cytokine-induced neutrophil chemoattractant-2α (CINC-2α) in rat gingival epithelium. However, in IM-pretreated rats, A. actinomycetemcomitans application had little effect on CINC-2α and E-cadherin in gingival epithelium. In cultured HGEC, real-time PCR and Western blotting showed that IM and the ERK inhibitor PD98059 abolished the A. actinomycetemcomitans-induced increase in CXCL-1 and IL-8 in HGEC. On the other hand, IM, PD98059, and the p38 MAP kinase inhibitor SB203580 recovered the decrease in E-cadherin expression. In addition, conditioned medium from A. actinomycetemcomitans-stimulated HGEC enhanced human neutrophil chemotaxis, compared to that from un-stimulated HGEC or that from A. actinomycetemcomitans-stimulated HGEC under IM pretreatment. Furthermore, IM down-regulated the p38 MAP kinase and ERK phosphorylations induced by A. actinomycetemcomitans. In conclusion, IM may control A. actinomycetemcomitans-induced gingival inflammation by regulating neutrophil migration and E-cadherin expression in gingival epithelium. |
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言語 |
en |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
第23回歯科基礎医学会賞受賞論文 |
出版者 |
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出版者 |
Elsevier |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
出版タイプ |
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出版タイプ |
AO |
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出版タイプResource |
http://purl.org/coar/version/c_b1a7d7d4d402bcce |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
10.1016/j.bcp.2010.01.017 |
関連情報 |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
http://dx.doi.org/10.1016/j.bcp.2010.01.017 |
収録物識別子 |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00564486 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
0006-2952 |
開始ページ |
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開始ページ |
1496 |
書誌情報 |
Biochemical pharmacology
Biochemical pharmacology
巻 79,
号 10,
p. 1496-1505,
発行日 2010-05
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旧ID |
32185 |