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首页> 外文期刊>Nature immunology >Hematopoietic stem cell and multilineage defects generated by constitutive beta-catenin activation
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Hematopoietic stem cell and multilineage defects generated by constitutive beta-catenin activation

机译：组成性β-catenin激活产生的造血干细胞和多系缺陷

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摘要

Gain of Wnt signaling through b-catenin has been ascribed a critical function in the stimulation of hematopoietic stem cell self-renewal, whereas loss of b-catenin is reportedly dispensable for hematopoiesis. Here we have used conditional mouse genetics and transplantation assays to demonstrate that constitutive activation of b-catenin blocked multilineage differentiation, leading to the death of mice. Blood cell depletion was accompanied by failure of hematopoietic stem cells to repopulate irradiated hosts and to differentiate into mature cells. Activation of b-catenin enforced cell cycle entry of hematopoietic stem cells, thus leading to exhaustion of the long-term stem cell pool. Our data suggest that fine-tuned Wnt stimulation is essential for hematopoiesis and is thus critical for therapeutic hematopoietic stem cell population expansion.
机译：通过β-连环蛋白获得的Wnt信号转导已被认为在刺激造血干细胞自我更新中起关键作用，而据报道，β-连环蛋白的丧失对于造血是必不可少的。在这里，我们已经使用条件小鼠遗传学和移植实验来证明b-catenin的组成性激活会阻止多谱系分化，从而导致小鼠死亡。血细胞耗竭的同时，造血干细胞也无法重现受辐照的宿主并分化为成熟细胞。 b-catenin的激活会迫使造血干细胞进入细胞周期，从而导致长期干细胞库耗尽。我们的数据表明，微调的Wnt刺激对于造血至关重要，因此对于治疗性造血干细胞群体的扩展至关重要。

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