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    The hemogenic competence of endothelial progenitors is restricted by Runx1 silencing during embryonic development.

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    Authors
    Eliades, Alexia
    Wareing, Sarah
    Marinopoulou, Elli
    Fadlullah, Muhammad Z H
    Patel, Rahima
    Grabarek, J
    Plusa, B
    Lacaud, Georges
    Kouskoff, Valerie
    Affiliation
    Cancer Research UK Stem Cell Hematopoiesis Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester M20 4BX
    Issue Date
    2016-06-07
    
    Metadata
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    Abstract
    It is now well-established that hematopoietic stem cells (HSCs) and progenitor cells originate from a specialized subset of endothelium, termed hemogenic endothelium (HE), via an endothelial-to-hematopoietic transition. However, the molecular mechanisms determining which endothelial progenitors possess this hemogenic potential are currently unknown. Here, we investigated the changes in hemogenic potential in endothelial progenitors at the early stages of embryonic development. Using an ETV2::GFP reporter mouse to isolate emerging endothelial progenitors, we observed a dramatic decrease in hemogenic potential between embryonic day (E)7.5 and E8.5. At the molecular level, Runx1 is expressed at much lower levels in E8.5 intra-embryonic progenitors, while Bmi1 expression is increased. Remarkably, the ectopic expression of Runx1 in these progenitors fully restores their hemogenic potential, as does the suppression of BMI1 function. Altogether, our data demonstrate that hemogenic competency in recently specified endothelial progenitors is restrained through the active silencing of Runx1 expression.
    Citation
    The hemogenic competence of endothelial progenitors is restricted by Runx1 silencing during embryonic development. 2016, 15 (10):2185-99 Cell Rep
    Journal
    Cell Reports
    URI
    http://hdl.handle.net/10541/614554
    DOI
    10.1016/j.celrep.2016.05.001
    PubMed ID
    27239041
    Type
    Article
    Language
    en
    ISSN
    2211-1247
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.celrep.2016.05.001
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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