本研究の目的は, 早産児におけるネフロン数の減少の発生機序の解明である。早産児は子宮外での相対的高酸素に暴露されることから, hypoxia inducible factor(HIF)の発現・活性低下がネフロン形成早期停止に影響するという仮説を立てた。低酸素環境下で飼育した新生児マウスのネフロン形成とHIF発現, 活性の比較検討を予定したが検証に値する期間の飼育は困難であった。早産モデルマウスの飼育も困難で, ネフロン形成早期停止が示唆された個体もあったが, 全体として有意差は出なかった。生きながらえても全身状態不良で, HIFの発現・活性以外の因子の影響が強いと判断し, 十分な結果を得られなかった。
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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