Oxygen levels epigenetically regulate fate switching of neural precursor cells via hypoxia-inducible factor 1α-Notch signal interaction in the developing brain

Tetsuji Mutoh, Tsukasa Sanosaka, Kei Ito, Kinichi Nakashima

研究成果: Article査読

37 被引用数 (Scopus)

抄録

Oxygen levels in tissues including the embryonic brain are lower than those in the atmosphere. We reported previously that Notch signal activation induces demethylation of astrocytic genes, conferring astrocyte differentiation ability on midgestational neural precursor cells (mgNPCs). Here, we show that the oxygen sensor hypoxia-inducible factor 1α (HIF1α) plays a critical role in astrocytic gene demethylation in mgNPCs by cooperating with the Notch signaling pathway. Expression of constitutively active HIF1α and a hyperoxic environment, respectively, promoted and impeded astrocyte differentiation in the developing brain. Our findings suggest that hypoxia contributes to the appropriate scheduling of mgNPC fate determination.

本文言語English
ページ(範囲)561-569
ページ数9
ジャーナルStem Cells
30
3
DOI
出版ステータスPublished - 2012 3月
外部発表はい

ASJC Scopus subject areas

  • 分子医療
  • 発生生物学
  • 細胞生物学

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