| Project/Area Number |
25670493
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | National Center for Child Health and Development |
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Principal Investigator |
Fujinaga Hideshi 国立研究開発法人国立成育医療研究センター, その他部局等, その他 (60623733)
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| Co-Investigator(Renkei-kenkyūsha) |
Umezawa Akihiro 独立行政法人国立成育医療研究センター, 再生医療センター, センター長 (70213486)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 肺低形成 / 血管内皮前駆細胞 / ECFC / VEGF / SDF1 / 血管内皮成長因子 |
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| Outline of Final Research Achievements |
Vascular growth is necessary for normal lung development. We hypothesized that the function of endothelial colony-forming cells (ECFCs), a type of endothelial progenitor cells (EPCs), is impaired in congenital diaphragmatic hernia (CDH), that is associated with lung hypoplasia. Cord blood (CB) was collected from CDH patients and healthy controls. We assessed CB progenitor cell populations and CB ECFC functions. CB ECFCs were decreased in CDH. CDH ECFCs had reduced potential for self-renewal, proliferation and migration. Their capacity for nitric oxide (NO) production was enhanced but response to VEGF was blunted. The in vivo potential for vasculogenesis was reduced in CDH ECFCs. There was no difference in VEGF and SDF1α levels in CB plasma and culture media, and ECFC mRNA expression associated with VEGF-NO and SDF1-CXCR4 signaling between groups. In conclusion, CB ECFC function is disrupted in CDH, probably due to mechanisms other than alteration of VEGF-NO and SDF1-CXCR4 signaling.
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