| Project/Area Number |
18K08167
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | University of Yamanashi (2019-2022)
Tohoku University (2018) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大河内 眞也 東北大学, 事業支援機構, 講師 (40375035)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | リゾホスファチジン酸 / 慢性閉塞性肺疾患 / 加齢 / 細胞老化 / 呼吸器 / オルガノイド / COPD / 肺幹細胞 / 呼吸器疾患 |
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| Outline of Final Research Achievements |
In LPAR3-deficient mice, lung compliance, a feature commonly associated with COPD, was significantly increased compared to wild-type mice. In addition, the number of spheroid colony derived from bronchioalveolar progenitor cells (BASCs) in LPAR3-/- mice was a third less than that in WT mice. Also, the spheroid colonies derived from BASCs in LPAR3-/- mice possessed almost same ability to those in WT mice in terms of differentiating into type I and II alveolar cells. These results suggest that BASCs in LPAR3-/- mice, which showed COPD-like phenotype, had a propensity to lose their stemness, especially self-renewing capacity, compared those collected from WT mice.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、脂質メディエーターの一種であるリゾホスファチジン酸によるシグナル、特にLPAR3を介したシグナルが、肺の組織幹細胞（気管支肺胞前駆細胞）を細胞老化から保護し、ステムネスを維持していることが示唆された。この結果は、リゾホスファチジン酸による肺の恒常性維持という新しい概念を提唱するものであり、その学術的意義は大きいと思われる。また、現在明確な治療法がない慢性閉塞性肺疾患（COPD）の新たな治療法の突破口となりうる点で、社会的意義も同様に大きいと思われる。
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