Suppr超能文献

延长的ras激活参与血小板生成素诱导的人因子依赖性造血细胞系巨核细胞分化。

Involvement of prolonged ras activation in thrombopoietin-induced megakaryocytic differentiation of a human factor-dependent hematopoietic cell line.

作者信息

Matsumura I, Nakajima K, Wakao H, Hattori S, Hashimoto K, Sugahara H, Kato T, Miyazaki H, Hirano T, Kanakura Y

机构信息

Department of Hematology and Oncology, Osaka University Medical School, Suita, Osaka 565-0871, Kirin Brewery Co. Ltd., Takasaki, Gunma 370-1202, Japan.

出版信息

Mol Cell Biol. 1998 Jul;18(7):4282-90. doi: 10.1128/MCB.18.7.4282.

Abstract

Thrombopoietin (TPO) is a hematopoietic growth factor that plays fundamental roles is both megakaryopoiesis and thrombopoiesis through binding to its receptor, c-mpl. Although TPO has been shown to activate various types of intracellular signaling molecules, such as the Janus family of protein tyrosine kinases, signal transducers and activators of transcription (STATs), and ras, the precise mechanisms underlying TPO-induced proliferation and differentiation remain unknown. In an effort to clarify the mechanisms of TPO-induced proliferation and differentiation, c-mpl was introduced into F-36P, a human interleukin-3 (IL-3)-dependent erythroleukemia cell line, and the effects of TPO on the c-mpl-transfected F-36P (F-36P-mpl) cells were investigated. F-36P-mpl cells were found to proliferate and differentiate at a high rate into mature megakaryocytes in response to TPO. Dominant-negative (dn) forms of STAT1, STAT3, STAT5, and ras were inducibly expressed in F-36P-mpl cells, and their effects on TPO-induced proliferation and megakaryocytic differentiation were analyzed. Among these dn molecules, both dn ras and dn STAT5 reduced TPO- or IL-3-induced proliferation of F-36P-mpl cells by approximately 30%, and only dn ras could inhibit TPO-induced megakaryocytic differentiation. In accord with this result, overexpression of activated ras (H-rasG12V) for 5 days led to megakaryocytic differentiation of F-36P-mpl cells. In a time course analysis on H-rasG12V-induced differentiation, activation of the ras pathway for 24 to 28 h was required and sufficient to induce megakaryocytic differentiation. Consistent with this result, the treatment of F-36P-mpl cells with TPO was able to induce prolonged activation of ras for more than 24 h, whereas IL-3 had only a transient effect. These results suggest that prolonged ras activation may be involved in TPO-induced megakaryocytic differentiation.

摘要

血小板生成素(TPO)是一种造血生长因子,通过与它的受体c-mpl结合,在巨核细胞生成和血小板生成过程中发挥着重要作用。尽管TPO已被证明能激活多种类型的细胞内信号分子,如Janus家族的蛋白酪氨酸激酶、信号转导子和转录激活子(STATs)以及ras,但TPO诱导增殖和分化的精确机制仍不清楚。为了阐明TPO诱导增殖和分化的机制,将c-mpl导入F-36P,一种依赖人白细胞介素-3(IL-3)的红白血病细胞系,并研究了TPO对转染c-mpl的F-36P(F-36P-mpl)细胞的影响。发现F-36P-mpl细胞在TPO作用下能以高速度增殖并分化为成熟的巨核细胞。在F-36P-mpl细胞中可诱导表达STAT1、STAT3、STAT5和ras的显性负性(dn)形式,并分析它们对TPO诱导的增殖和巨核细胞分化的影响。在这些dn分子中,dn ras和dn STAT5都使TPO或IL-3诱导的F-36P-mpl细胞增殖降低约30%,并且只有dn ras能抑制TPO诱导的巨核细胞分化。与该结果一致,激活的ras(H-rasG12V)过表达5天导致F-36P-mpl细胞向巨核细胞分化。在对H-rasG12V诱导分化的时间进程分析中,ras途径激活24至28小时是诱导巨核细胞分化所必需且足够的。与该结果一致,用TPO处理F-36P-mpl细胞能够诱导ras持续激活超过24小时,而IL-3只有短暂的作用。这些结果表明,ras的持续激活可能参与TPO诱导的巨核细胞分化。

相似文献

4
Thrombopoietin activates a STAT5-like factor in hematopoietic cells.
EMBO J. 1995 Jun 15;14(12):2847-56. doi: 10.1002/j.1460-2075.1995.tb07284.x.
7
Dissecting the thrombopoietin receptor: functional elements of the Mpl cytoplasmic domain.
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2350-5. doi: 10.1073/pnas.94.6.2350.
10
Lnk inhibits Tpo-mpl signaling and Tpo-mediated megakaryocytopoiesis.
J Exp Med. 2004 Sep 6;200(5):569-80. doi: 10.1084/jem.20040762. Epub 2004 Aug 30.

引用本文的文献

2
Deciphering the Role of the Coagulation Cascade and Autophagy in Cancer-Related Thrombosis and Metastasis.
Front Oncol. 2020 Dec 7;10:605314. doi: 10.3389/fonc.2020.605314. eCollection 2020.
3
Role of Erk1/2 signaling in the regulation of neutrophil versus monocyte development in response to G-CSF and M-CSF.
J Biol Chem. 2015 Oct 2;290(40):24561-73. doi: 10.1074/jbc.M115.668871. Epub 2015 Aug 20.
4
Phosphorylated c-Mpl tyrosine 591 regulates thrombopoietin-induced signaling.
Exp Hematol. 2014 Jun;42(6):477-86.e4. doi: 10.1016/j.exphem.2014.02.007. Epub 2014 Mar 4.
5
7
An ENU-induced recessive mutation in Mpl leads to thrombocytopenia with overdominance.
Exp Hematol. 2009 Feb;37(2):276-84. doi: 10.1016/j.exphem.2008.10.005. Epub 2008 Dec 6.
8
Extracellular signal-regulated kinase induces the megakaryocyte GPIIb/CD41 gene through MafB/Kreisler.
Mol Cell Biol. 2004 May;24(10):4534-45. doi: 10.1128/MCB.24.10.4534-4545.2004.
9
Structure of the receptor-binding domain of human thrombopoietin determined by complexation with a neutralizing antibody fragment.
Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1816-21. doi: 10.1073/pnas.0308530100. Epub 2004 Feb 9.
10
STAT5 and Oct-1 form a stable complex that modulates cyclin D1 expression.
Mol Cell Biol. 2003 Dec;23(24):8934-45. doi: 10.1128/MCB.23.24.8934-8945.2003.

本文引用的文献

4
A possible involvement of Stat5 in erythropoietin-induced hemoglobin synthesis.
Biochem Biophys Res Commun. 1997 May 8;234(1):198-205. doi: 10.1006/bbrc.1997.6486.
5
Dissecting the thrombopoietin receptor: functional elements of the Mpl cytoplasmic domain.
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2350-5. doi: 10.1073/pnas.94.6.2350.
9
Minimal Ras-binding domain of Raf1 can be used as an activation-specific probe for Ras.
Oncogene. 1997 Feb 6;14(5):623-5. doi: 10.1038/sj.onc.1201005.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验