DP receptor signaling を介するマクロファージによるLPS誘導性TNF-α産生能増強

• 大東 希好

  大阪歯科大学小児歯科学講座

• 東 泰孝

  大阪歯科大学薬理学講座

• 渡邉 京子

  大阪歯科大学小児歯科学講座

• 白数 慎也

  大阪歯科大学小児歯科学講座

• 嘉藤 幹夫

  大阪歯科大学小児歯科学講座

• 大東 道治

  大阪歯科大学小児歯科学講座

• 大浦 清

  大阪歯科大学薬理学講座

書誌事項

タイトル別名

• DP recptor signaling increased LPS-induced TNF-.ALPHA. production by macrophages.

抄録

Prostaglandin D₂ (PGD₂) acts via the adenyl cyclase-coupled receptor for PGD₂ (DP receptor) . Previously, we presented evidence that BW245C, a DP receptor agonist, inhibited chemotaxis, phagocytosis, superoxide anion production and nitrite production, and potentiated TNF-α production by macrophages. To gain information on the mechanism through which agonist of DP receptor potentiated LPS-stimulated TNF-αproduction by macrophages, in this study, we sought to identify downstream effectors of DP receptor-potentiated TNF-αproduction. Both SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor, and PD98059, an extracellular signal-related kinase (ERK) 1/2 inhibitor, prevented LPS-induced TNF-αproduction and BW245C-increased TNFαproduction in the presence of LPS, respectively. In contrast, LY294002, a phosphoinositide 3-kinase (PI3K) inhibitor, D609, a phospholipase C (PLC) inhibitor, and suramin, a PLD inhibitor, all did not affect LPS-induced TNF-αproduction, whereas they markedly inhibited BW245C-increased TNFαproduction in the presence of LPS. These results suggest that LPS evidently induced the production of TNF-αthrough p38 MAPK and ERK 1/2 signaling pathways, and that BW245C further increased LPS-induced TNF-αproduction through PI3K, PLC, and PLD.

収録刊行物

• 歯科薬物療法

  歯科薬物療法 22 (3), 153-159, 2003

  日本歯科薬物療法学会

キーワード

• マクロファージ
• ホスホリパーゼ

詳細情報

• CRID: 1390001204734484992
• NII論文ID: 130003840817
• NII論文ID: 10016242459
• NII書誌ID: AN0023517X
• DOI: 10.11263/jsotp1982.22.153
• ISSN: 18844928
• ISSN: 02881012
• Web Site: https://search.jamas.or.jp/link/ui/2004268833
• 本文言語コード: en
• データソース種別:
  • JaLC
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可