FIP200 is required for the cell-autonomous maintenance of fetal hematopoietic stem cells

Fei Liu, Jae Y. Lee, Huijun Wei, Osamu Tanabe, James D. Engel, Sean J. Morrison, Jun Lin Guan

研究成果: Article査読

139 被引用数 (Scopus)

抄録

Little is known about whether autophagic mechanisms are active in hematopoietic stem cells (HSCs) or how they are regulated. FIP200 (200-kDa FAK-family interacting protein) plays important roles in mammalian autophagy and other cellular functions, but its role in hematopoietic cells has not been examined. Here we show that conditional deletion of FIP200 in hematopoietic cells leads to perinatal lethality and severe anemia. FIP200 was cell-autonomously required for the maintenance and function of fetal HSCs. FIP200-deficient HSC were unable to reconstitute lethally irradiated recipients. FIP200 ablation did not result in increased HSC apoptosis, but it did increase the rate of HSC proliferation. Consistent with an essential role for FIP200 in autophagy, FIP200-null fetal HSCs exhibited both increased mitochondrial mass and reactive oxygen species. These data identify FIP200 as a key intrinsic regulator of fetal HSCs and implicate a potential role for autophagy in the maintenance of fetal hematopoiesis and HSCs.

本文言語English
ページ(範囲)4806-4814
ページ数9
ジャーナルBlood
116
23
DOI
出版ステータスPublished - 2010 12 2

ASJC Scopus subject areas

  • 生化学
  • 免疫学
  • 血液学
  • 細胞生物学

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