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地塞米松增加血管生成素-1和静止造血干细胞:地塞米松诱导血液保护的新机制。

Dexamethasone increases angiopoietin-1 and quiescent hematopoietic stem cells: a novel mechanism of dexamethasone-induced hematoprotection.

作者信息

Kim Hyongbum, Choi Ji-Young, Lee Jung Min, Park Yoon Shin, Suh Hwal, Song Hae-Ryong, Jo Sangmee Ahn, Jo Inho

机构信息

Department of Biomedical Sciences, National Institute of Health, Seoul, South Korea.

出版信息

FEBS Lett. 2008 Oct 15;582(23-24):3509-14. doi: 10.1016/j.febslet.2008.09.021. Epub 2008 Sep 18.

Abstract

Angiopoietin-1 (Ang-1) is known to have hematoprotective effects by increasing the quiescence of hematopoietic stem cells. However, it remains to be determined if the upregulation of Ang-1 and the subsequent increase in the quiescence of hematopoietic stem cells are also involved in the dexamethasone (Dex)-mediated bone marrow protection. Here Western blotting and flow cytometric analyses demonstrate that Dex increases the levels of Ang-1 in mouse bone marrow and the quiescence of hematopoietic stem cells. Our data for the first time suggest that the increased quiescence of hematopoietic stem cells provides a novel mechanism of Dex-induced hematoprotection.

摘要

已知血管生成素-1(Ang-1)通过提高造血干细胞的静止状态而具有血液保护作用。然而,Ang-1的上调以及随后造血干细胞静止状态的增加是否也参与地塞米松(Dex)介导的骨髓保护作用仍有待确定。在此,蛋白质印迹法和流式细胞术分析表明,Dex可提高小鼠骨髓中Ang-1的水平以及造血干细胞的静止状态。我们的数据首次表明,造血干细胞静止状态的增加为Dex诱导的血液保护提供了一种新机制。

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