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GFI1 和 GFI1B 控制造血定向期间造血内皮细胞内皮特性的丧失。

GFI1 and GFI1B control the loss of endothelial identity of hemogenic endothelium during hematopoietic commitment.

机构信息

Cancer Research UK Stem Cell Biology Group, Paterson Institute for Cancer Research, University of Manchester, Manchester, United Kingdom.

出版信息

Blood. 2012 Jul 12;120(2):314-22. doi: 10.1182/blood-2011-10-386094. Epub 2012 Jun 5.

Abstract

Recent studies have established that during embryonic development, hematopoietic progenitors and stem cells are generated from hemogenic endothelium precursors through a process termed endothelial to hematopoietic transition (EHT). The transcription factor RUNX1 is essential for this process, but its main downstream effectors remain largely unknown. Here, we report the identification of Gfi1 and Gfi1b as direct targets of RUNX1 and critical regulators of EHT. GFI1 and GFI1B are able to trigger, in the absence of RUNX1, the down-regulation of endothelial markers and the formation of round cells, a morphologic change characteristic of EHT. Conversely, blood progenitors in Gfi1- and Gfi1b-deficient embryos maintain the expression of endothelial genes. Moreover, those cells are not released from the yolk sac and disseminated into embryonic tissues. Taken together, our findings demonstrate a critical and specific role of the GFI1 transcription factors in the first steps of the process leading to the generation of hematopoietic progenitors from hemogenic endothelium.

摘要

最近的研究已经证实,在胚胎发育过程中,造血祖细胞和干细胞是通过一个称为内皮向造血转化(EHT)的过程从造血内皮前体中产生的。转录因子 RUNX1 对这个过程至关重要,但它的主要下游效应物在很大程度上仍然未知。在这里,我们报告了鉴定出 Gfi1 和 Gfi1b 是 RUNX1 的直接靶标和 EHT 的关键调节因子。GFI1 和 GFI1B 能够在没有 RUNX1 的情况下触发内皮标记物的下调和圆形细胞的形成,这是 EHT 的特征形态变化。相反,GFI1 和 GFI1B 缺陷胚胎中的血液祖细胞仍然表达内皮基因。此外,这些细胞不会从卵黄囊中释放出来并散布到胚胎组织中。总之,我们的研究结果表明,GFI1 转录因子在导致造血内皮产生造血祖细胞的过程的最初步骤中起着关键和特定的作用。

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