Blood:c-Myc单倍体剂量不足在HSC维持中的作用

2020-09-02 MedSci原创 MedSci原创

近日,《血液》杂志上发表了一篇新研究,报道了c-Myc对造血作用的剂量效应及其在造血干细胞(HSC)和骨髓壁龛细胞中介导Wnt/b-catenin通路的独特作用。

中心点:

c-Myc通过调节Nr4a1、Nr4a2和Jmjd3的表达来控制HSC的自我更新、静止和存活。

Apc单倍体剂量不足丢失通过上调c-Myc所介导的骨髓内皮细胞的IL6的分泌来阻碍红系分化。

摘要:

近日,《血液》杂志上发表了一篇新研究,报道了c-Myc对造血作用的剂量效应及其在造血干细胞(HSC)和骨髓壁龛细胞中介导Wnt/b-catenin通路的独特作用。

研究人员发现c-Myc单倍体剂量不足可通过抑制HSC自我更新和静止以及促进其凋亡来导致无效造血,而且还发现对维持HSC功能至关重要的三个基因Nr4a1、Nr4a2和Jmjd3,是c-Myc在HSC中的下游靶基因。

c-Myc直接与Nr4a1、Nr4a2和Jmjd3的启动子区域结合,调控其表达。三个基因都参与c-Myc对HSC存活的维持功能,另外Nr4a1和Nr4a2还介导c-Myc对HSC静止的调控功能。

肿瘤抑制蛋白Apc是Wnt/b-catenin通路的负性调控因子。研究人员首次发现,Apc单倍体剂量不足可通过促进骨髓内皮细胞表达和分泌IL-6来诱导红系分化阻滞。且c-Myc单倍体剂量不足不能恢复体内Apc-缺陷型HSC的功能缺陷,但可有效阻止Apc杂合型小鼠重度贫血的发展,显著延长这类小鼠的存活期。

此外,研究人员还证明了c-Myc介导内皮细胞Apc缺失诱导性的IL-6分泌,c-Myc单倍体剂量不足可逆转Apc缺陷型内皮细胞对红系细胞分化的负性作用。

综上所述,该研究表明,c-Myc在介导Apc在造血中的功能具有上下相关的作用。

原始出处:

Yue Sheng,et al. Role of c-Myc haploinsufficiency in the maintenance of HSCs. Blood. August 21, 2020.

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    2021-08-06 sjq035
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    2020-09-04 guihongzh
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    2020-09-04 lixiaol
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    2020-09-03 韩杰

    学习

    0

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    2020-09-02 146a24b1m26(暂无昵称)

    very good

    0

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    2020-09-02 ms7000002041401517

    good

    0

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