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干细胞动员的氧化还原调控。

Redox regulation of stem cell mobilization.

机构信息

Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA.

出版信息

Can J Physiol Pharmacol. 2009 Dec;87(12):989-95. doi: 10.1139/Y09-102.

DOI:10.1139/Y09-102
PMID:20029535
Abstract

A growing body of evidence supports the role of redox signaling in the mechanisms of hematopoietic stem cell mobilization and homing. Cytokines and adhesion molecules control stem cell mobilization through a redox-regulated process. The FoxO-SirT network appears to be intimately involved in redox-regulated stem cell homeostasis, whereas the process of stem cell differentiation is regulated by redox effector factor-1 (Ref-1) protein. Lack of oxygen (hypoxia), specifically controlled hypoxia, can stimulate the growth of the stem cells in their niche, and hypoxia-inducible factor (HIF)-1alpha appears to play a significant role in their maintenance and homing mechanism.

摘要

越来越多的证据支持氧化还原信号在造血干细胞动员和归巢机制中的作用。细胞因子和黏附分子通过氧化还原调节过程控制干细胞的动员。FoxO-SirT 网络似乎密切参与氧化还原调节干细胞的动态平衡,而干细胞分化的过程则受到氧化还原效应因子-1(Ref-1)蛋白的调节。缺氧(低氧),特别是受控缺氧,可以刺激干细胞在其龛位中的生长,缺氧诱导因子(HIF)-1alpha 似乎在它们的维持和归巢机制中发挥重要作用。

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The nucleotide sugar UDP-glucose mobilizes long-term repopulating primitive hematopoietic cells.尿苷二磷酸葡萄糖可动员长期重建造血祖细胞。
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