Purinergic signaling is a novel target of sepsis therapy
Project/Area Number |
24590125
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biological pharmacy
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Research Institution | Tokyo University of Science |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | 敗血症 / 炎症 / プリン受容体 / P2X7受容体 / P2Y11受容体 / ATP / サイトカイン / マクロファージ / 国際情報交換 スペイン / P2Y受容体 / 国際情報交換 |
Outline of Final Research Achievements |
Sepsis is known as systemic inflammatory response syndorome (SIRS) with symptoms such as hypercytokinemi. Now, it is need to improve the therapy of sepsis. To establish effective therapy of sepsis, we investigated a role of purinergic signaling on sepsis by using immune cells and sepsis model mice in this study. We found that activation of P2Y11 receptor by exocytic ATP release in macrophage is involved in production of pro-inflammatory cytokine. P2Y11 receptor antagonist suppressed an increase of cytokine in LPS-treated mice. On the other hand, we also found that activation of P2X7 receptor play an important role in sepsis, suggesting that P2Y11 and P2X7 receptor antagonists would become a novel candidate of sepsis therapy.
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] Extracellular ATP induces P2X7 receptor activation in mouse Kupffer cells, leading to release of IL-1β, HMGB1, and PGE2, decreased MHC class I expression and necrotic cell death.2015
Author(s)
Toki Y, Takenouchi T, Harada H, Tanuma S, Kitani H, Kojima S, Tsukimoto M.
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Journal Title
Biochemical and Biophysical Research Communications
Volume: 458(4)
Issue: 4
Pages: 771-776
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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