nature-medicine201212-3

来自美国宾夕法尼亚大学医学院的科学家最新研究表明激活Wnt–β-catenin并抑制mTOR信号有助于造血干细胞的维持。

-2012年12月《自然-医学》


中文翻译


【题目】通过调控Wnt和mTOR通路维持造血干细胞

【译文】造血干细胞(HSC)自我更新和谱系定型取决于与微环境的复杂相互作用。因为这些相互作用并未被很好的界定,临床应用或基础研究中维持或扩展HSC的能力受到严重限制了。近期证据表明HSC存在于低灌注营养减少的生境中,而且营养传感通路有助于HSC的稳态。 本研究报道mTOR通路(已确立的营养感受器)的抑制,联合典型Wnt–β-catenin信号的激活,在无细胞因子条件下,使得人和鼠长期HSC的体外维持变为可能。研究还表明同时激活Wnt–β-catenin并抑制mTOR信号的两种临床上批准的给药方法在体内增加了长期HSC的数量(但非比例)。

英文原稿


[Title]: Maintenance of hematopoietic stem cells through regulation of Wnt and mTOR pathways

[Authors]:Jian Huang,1 Michelle Nguyen-McCarty,2 Elizabeth O Hexner,1, 3 Gwenn Danet-Desnoyers1 & Peter S Klein1, 2

[Abstract]Hematopoietic stem cell (HSC) self renewal and lineage commitment depend on complex interactions with the microenvironment. The ability to maintain or expand HSCs for clinical applications or basic research has been substantially limited because these interactions are not well defined. Recent evidence suggests that HSCs reside in a low-perfusion, reduced-nutrient niche and that nutrient-sensing pathways contribute to HSC homeostasis. Here we report that suppression of the mTOR pathway, an established nutrient sensor, combined with activation of canonical Wnt–β-catenin signaling, allows for the ex vivo maintenance of human and mouse long-term HSCs under cytokine-free conditions. We also show that the combination of two clinically approved medications that together activate Wnt–β-catenin and inhibit mTOR signaling increases the number (but not the proportion) of long-term HSCs in vivo.

原文地址

http://www.nature.com/nm/journal/v18/n12/abs/nm.2984.html

 

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