Irsogladine maleate regulates neutrophil migration and E-cadherin expression in gingival epithelium stimulated by Aggregatibacter actinomycetemcomitans
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ID | 32185 |
本文ファイル | |
著者 |
Kishimoto, Akiyoshi
Hayashida, Kouichi
Kawaguchi, Hiroyuki
Abiko, Yoshimitsu
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キーワード | Irsogladine maleate
Aggregatibacter actinomycetemcomitans
E-cadherin
Neutrophil migration
CXC-chemokine
Gingival epithelial cells
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NDC |
医学
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抄録(英) | 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. |
内容記述 | 第23回歯科基礎医学会賞受賞論文
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掲載誌名 |
Biochemical pharmacology
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巻 | 79巻
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号 | 10号
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開始ページ | 1496
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終了ページ | 1505
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出版年月日 | 2010-05
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出版者 | Elsevier
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ISSN | 0006-2952
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NCID | |
出版者DOI | |
言語 |
英語
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NII資源タイプ |
学術雑誌論文
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広大資料タイプ |
学術雑誌論文
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DCMIタイプ | text
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フォーマット | application/pdf
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著者版フラグ | author
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権利情報 | Copyright (c) 2010 Elsevier Inc.
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関連情報URL(IsVersionOf) | http://dx.doi.org/10.1016/j.bcp.2010.01.017
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部局名 |
医歯薬学総合研究科
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