| Project/Area Number |
18K14604
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 42030:Animal life science-related
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| Research Institution | Azabu University (2019-2021)
The University of Tokyo (2018) |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | カハール介在細胞 / 消化管運動 / 炎症 / 一酸化窒素 / 消化管 / 老化 / 腸管神経 |
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| Outline of Final Research Achievements |
Interstitial cells of Cajal (ICC) are pacemaker cells for gastrointestinal motility. Nitric oxide (NO) can disrupt ICC during intestinal inflammation, while it is required for maintaining of the ICC network during healthy conditions. However, the mechanism by which NO exerts completely opposite effects on ICC, survival and disruption, is not well understood. In this study, we hypothesized that the amount of NO exposure to ICC determines the fate of ICC. The results suggest that large amounts of NO impaired ICC and small amounts of NO were necessary for ICC survival. However, the mechanism of ICC survival by NO may not be a direct action on ICC, but may be an indirect action via other types of cells. We examined the possible involvement of apelin signaling in NO-induced ICC survival, but further investigations are needed.
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| Academic Significance and Societal Importance of the Research Achievements |
ICCは正常な消化管運動を生み出すために欠かすことができない機能を担っているが、炎症性疾患や糖尿病時にはICCの減少や機能障害が生じることが報告されている。このようなICC障害を治療する方法は未だ確立されておらず、ICCを標的とした消化管運動不全の治療法確立が期待されている。本研究によりNOへの暴露の程度がICCの生存や障害を左右する要因であることが示唆された。本研究の成果はNOの制御によりICC障害の予防や治療が行える可能性を示すとともに、治療戦略構築における基盤的知見となると考えられる。
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