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    HDAC1 and HDAC2 modulate TGF-β signaling during endothelial-to-hematopoietic transition.

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    Authors
    Thambyrajah, Roshana
    Fadlullah, Muhammad Z H
    Proffitt, Martin
    Patel, Rahima
    Cowley, S
    Kouskoff, Valerie
    Lacaud, Georges
    Affiliation
    CRUK Stem Cell Biology Group, CRUK Manchester Institute, 555 Wilmslow Road, Manchester M20 4GJ, UK
    Issue Date
    2018-04-10
    
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    Abstract
    The first hematopoietic stem and progenitor cells are generated during development from hemogenic endothelium (HE) through trans-differentiation. The molecular mechanisms underlying this endothelial-to-hematopoietic transition (EHT) remain poorly understood. Here, we explored the role of the epigenetic regulators HDAC1 and HDAC2 in the emergence of these first blood cells in vitro and in vivo. Loss of either of these epigenetic silencers through conditional genetic deletion reduced hematopoietic transition from HE, while combined deletion was incompatible with blood generation. We investigated the molecular basis of HDAC1 and HDAC2 requirement and identified TGF-β signaling as one of the pathways controlled by HDAC1 and HDAC2. Accordingly, we experimentally demonstrated that activation of this pathway in HE cells reinforces hematopoietic development. Altogether, our results establish that HDAC1 and HDAC2 modulate TGF-β signaling and suggest that stimulation of this pathway in HE cells would be beneficial for production of hematopoietic cells for regenerative therapies.
    Citation
    HDAC1 and HDAC2 modulate TGF-β signaling during endothelial-to-hematopoietic transition. 2018, 10(4): 1369-1383 Stem Cell Rep
    Journal
    Stem Cell Reports
    URI
    http://hdl.handle.net/10541/620986
    DOI
    10.1016/j.stemcr.2018.03.011
    PubMed ID
    29641990
    Type
    Article
    Language
    en
    ISSN
    2213-6711
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.stemcr.2018.03.011
    Scopus Count
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