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在稳态下，血小板生成素信号传导是白细胞介素-11反应性造血祖细胞体内扩增所必需的。

Thrombopoietin signaling is required for in vivo expansion of IL-11--responsive hematopoietic progenitor cells in the steady state.

作者信息

Scott C L, Robb L, Nandurkar H H, Mansfield R, Alexander W S, Begley C G

机构信息

The Walter and Eliza Hall Institute of Medical Research, P.O. Royal Melbourne Hospital, Victoria, Australia.

出版信息

Exp Hematol. 2001 Feb;29(2):138-45. doi: 10.1016/s0301-472x(00)00622-6.

DOI:10.1016/s0301-472x(00)00622-6
PMID:11166452
Abstract

OBJECTIVE

mpl(-/-) mice have a profound defect in platelets and megakaryocytes and a defect in hematopoietic progenitor cells and stem cells. However, no specific subset of the progenitor/stem cell compartment has been shown to be particularly affected by this deficiency in mpl(-/-) mice. In this article, we identified a specific subset of bone marrow progenitor/stem cells that was altered in mpl(-/-) mice.

MATERIALS AND METHODS

In vitro and in vivo hematopoietic assays were utilized to examine the response to interleukin-11 in mice lacking the receptor for thrombopoietin (TPO) (mpl(-/-) mice).

RESULTS

The interleukin (IL)-11-responsive subset of progenitor cells was not detected in clonal cultures of bone marrow cells from mpl(-/-) mice. However, mpl(-/-) mice responded to IL-11 in vivo as evidenced by a rise in platelet count and an increase in spleen weight. Experiments were performed to address this paradox: administration of 5-fluorouracil with consequent "expansion" of early hematopoietic cells resulted in the appearance of IL-11-responsive cells in mpl(-/-) mice when assayed in in vitro cultures.

CONCLUSIONS

Thus, although mpl(-/-) mice have the capacity to produce IL-11-responsive progenitor cells, under steady state conditions their expansion is dependent on TPO. This is the first evidence that a specific subset of bone marrow progenitor/stem cells is altered in mpl(-/-) mice.

摘要

目的

mpl(-/-)小鼠在血小板和巨核细胞方面存在严重缺陷，在造血祖细胞和干细胞方面也有缺陷。然而，尚未发现祖细胞/干细胞区室的特定亚群受到mpl(-/-)小鼠这种缺陷的特别影响。在本文中，我们鉴定出了mpl(-/-)小鼠中发生改变的骨髓祖细胞/干细胞的一个特定亚群。

材料与方法

利用体外和体内造血试验来检测缺乏血小板生成素（TPO）受体的小鼠（mpl(-/-)小鼠）对白介素-11的反应。

结果

在mpl(-/-)小鼠骨髓细胞的克隆培养物中未检测到祖细胞的白介素（IL）-11反应性亚群。然而，mpl(-/-)小鼠在体内对白介素-11有反应，血小板计数升高和脾脏重量增加证明了这一点。进行实验以解决这一矛盾：给予5-氟尿嘧啶从而使早期造血细胞“扩增”，结果在体外培养检测时，mpl(-/-)小鼠中出现了白介素-11反应性细胞。

结论

因此，尽管mpl(-/-)小鼠有能力产生对白介素-11有反应的祖细胞，但在稳态条件下它们的扩增依赖于血小板生成素。这是mpl(-/-)小鼠中骨髓祖细胞/干细胞的一个特定亚群发生改变的首个证据。

相似文献

1
Thrombopoietin signaling is required for in vivo expansion of IL-11--responsive hematopoietic progenitor cells in the steady state.在稳态下，血小板生成素信号传导是白细胞介素-11反应性造血祖细胞体内扩增所必需的。
Exp Hematol. 2001 Feb;29(2):138-45. doi: 10.1016/s0301-472x(00)00622-6.
2
The residual megakaryocyte and platelet production in c-mpl-deficient mice is not dependent on the actions of interleukin-6, interleukin-11, or leukemia inhibitory factor.c-mpl基因缺陷小鼠中的残余巨核细胞和血小板生成并不依赖于白细胞介素-6、白细胞介素-11或白血病抑制因子的作用。
Blood. 2000 Jan 15;95(2):528-34.
3
Thrombopoietin, the ligand for the Mpl receptor, synergizes with steel factor and other early acting cytokines in supporting proliferation of primitive hematopoietic progenitors of mice.血小板生成素，即Mpl受体的配体，可与干细胞因子及其他早期起作用的细胞因子协同作用，以支持小鼠原始造血祖细胞的增殖。
Blood. 1996 Jun 1;87(11):4544-51.
4
Hematopoietic stem cell deficiencies in mice lacking c-Mpl, the receptor for thrombopoietin.缺乏血小板生成素受体c-Mpl的小鼠中的造血干细胞缺陷。
Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1195-200. doi: 10.1073/pnas.95.3.1195.
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Thrombopoietin does not induce lineage-restricted commitment of Mpl-R expressing pluripotent progenitors but permits their complete erythroid and megakaryocytic differentiation.血小板生成素不会诱导表达Mpl-R的多能祖细胞发生谱系限制的定向分化，但能使其完全向红系和巨核系分化。
Blood. 1997 May 15;89(10):3544-53.
6
Promegapoietin, a family of chimeric growth factors, supports megakaryocyte development through activation of IL-3 and c-Mpl ligand signaling pathways.促血小板生成素，一种嵌合生长因子家族，通过激活白细胞介素-3和c-Mpl配体信号通路来支持巨核细胞的发育。
Exp Hematol. 2001 Oct;29(10):1177-84. doi: 10.1016/s0301-472x(01)00694-4.
7
Low levels of erythroid and myeloid progenitors in thrombopoietin-and c-mpl-deficient mice.血小板生成素和c-mpl基因缺陷小鼠中红系和髓系祖细胞水平较低。
Blood. 1996 Aug 1;88(3):803-8.
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Deficiencies in progenitor cells of multiple hematopoietic lineages and defective megakaryocytopoiesis in mice lacking the thrombopoietic receptor c-Mpl.缺乏血小板生成受体c-Mpl的小鼠中多种造血谱系祖细胞的缺陷及巨核细胞生成缺陷。
Blood. 1996 Mar 15;87(6):2162-70.
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Soluble thrombopoietin receptor (Mpl) and granulocyte colony-stimulating factor receptor directly stimulate proliferation of primitive hematopoietic progenitors of mice in synergy with steel factor or the ligand for Flt3/Flk2.可溶性血小板生成素受体（Mpl）和粒细胞集落刺激因子受体与Steel因子或Flt3/Flk2配体协同作用，可直接刺激小鼠原始造血祖细胞的增殖。
Blood. 1996 Dec 1;88(11):4124-31.
10
Thrombopoietin stimulates colony-forming unit-megakaryocyte proliferation and megakaryocyte maturation independently of cytokines that signal through the gp130 receptor subunit.血小板生成素可独立于通过gp130受体亚基发出信号的细胞因子，刺激巨核细胞集落形成单位增殖和巨核细胞成熟。
Blood. 1996 Sep 15;88(6):2026-32.

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