2017 Fiscal Year Final Research Report
Analysis of the role of HIF in early termination of nephrogenesis due to prematurity and development of treatment.
Project/Area Number |
15K09726
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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 |
Embryonic/Neonatal medicine
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Research Institution | Keio University |
Principal Investigator |
Hida Mariko 慶應義塾大学, 医学部(信濃町), 共同研究員 (20276306)
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Co-Investigator(Kenkyū-buntansha) |
粟津 緑 慶應義塾大学, 医学部(信濃町), 講師 (20129315)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 糸球体減少 / 早産児 / 低酸素環境 |
Outline of Final Research Achievements |
We have been analyzing the mechanism of early termination of nephrogenesis in preterm infants. Since a neonate is exposed to higher level of oxygen than in utero, we had hypothesized that the change in expression and activity of hypoxia inducible factor (HIF) would influence on maintenance of nephron progenitor cells, vasculisation, and nephrogenesis. We planned to create preterm model mice and to raise them under hypoxic condition. We had examined the expression and activity of HIF in those model mice. Unfortunately to create preterm mice had been quite difficult. We have succeeded to create one-day-preterm mice, which pathological study suggested that nephrogenesis may terminate earlier than term mice, but we could not raise enough number of model mice for examination. To raise mice under hypoxic condition was also quite difficult. Since they were quite sick under hypoxic condition, we could not make enough assessment. We need to analyze in vitro with organ culture specimens.
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Free Research Field |
小児科、新生児・胎児
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