| Project/Area Number |
16K10074
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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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| Research Field |
Pediatrics
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| Research Institution | Keio University |
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Principal Investigator |
Maeda Jun 慶應義塾大学, 医学部(信濃町), 専任講師 (00255506)
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| Co-Investigator(Kenkyū-buntansha) |
内田 敬子 慶應義塾大学, 保健管理センター(日吉), 講師 (50286522)
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| Research Collaborator |
YAMAGISHI Hiroyuki
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 肺血管幹細胞 / 肺血管形成 / 幹細胞マーカー / Sca-1 / 血管内皮細胞 / 肺血管内皮前駆細胞 / CD31 / 肺間葉系細胞 / 先天性心疾患 / 小児循環器学 |
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| Outline of Final Research Achievements |
We analyzed the temporospational expression pattern of adult murine pulmonary cells both positive for stem cell antigen, Sca-1 and endothelial cell marker, CD31. The cells positive for both Sca-1 and CD31 were expressed in alveolar wall and vascular wall in alveolar interstitial space. Fluorescent antigen cell sorting using anti-Sca-1 and anti-CD31 antibodies could separate a subset of both antigen-positive cells. These cells were differentiated to characteristic luminal structure, suggesting potential for differentiation to pulmonary vascular cells. However, the Sca-1-negative and CD31-positive cells were more robustly able to give rise to vascular cells. These results suggested that Sca-1 could be expressed in pulmonary vascular stem cells but might repress the angiogenesis in adult murine lungs.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究において、肺組織における正常な肺血管内皮への分化する幹細胞、すなわちガス交換を担う気道系（肺胞）と血管系（肺毛細血管網）のネットワークの発生および再生機構の少なくとも一部が解明され、肺血管幹細胞分画が特定された。肺血管低形成、肺動静脈奇形、肺動脈性高血圧症などの肺血管疾患は、単独でも有効な治療法が少なく、また先天性心疾患に合併すると、その予後を不良にする。本研究の成果は、これら難治性肺血管疾患に対して、肺血管幹細胞と肺血管発生の分子機序を応用した新たな再生医療や内科的治療の分子標的検索のための基礎的知見として、臨床にもつながる意義がある。
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