期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 209, 期 8, 页码 1457-1468出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20120225
关键词
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资金
- FPI predoctoral fellowship [SAF2004-03198]
- ISCIII program [02/30279]
- Ministerio de Economia y Competitividad [SAF2007-60080, PLE2009-0111, SAF2010-15450]
- AGAUR [2009SGR-23]
- Instituto de Salud Carlos III, RTICC [RD06/0020/0098]
Understanding how hematopoietic stem cells (HSCs) are generated and the signals that control this process is a crucial issue for regenerative medicine applications that require in vitro production of HSC. HSCs emerge during embryonic life from an endothelial-like cell population that resides in the aorta-gonad-mesonephros (AGM) region. We show here that beta-catenin is nuclear and active in few endothelial nonhematopoietic cells closely associated with the emerging hematopoietic clusters of the embryonic aorta during mouse development. Importantly, Wnt/beta-catenin activity is transiently required in the AGM to generate long-term HSCs and to produce hematopoietic cells in vitro from AGM endothelial precursors. Genetic deletion of beta-catenin from the embryonic endothelium stage (using VE-cadherin-Cre recombinase), but not from embryonic hematopoietic cells (using Vav1-Cre), precludes progression of mutant cells toward the hematopoietic lineage; however, these mutant cells still contribute to the adult endothelium. Together, those findings indicate that Wnt/beta-catenin activity is needed for the emergence but not the maintenance of HSCs in mouse embryos.
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