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Id1 and Id3 Maintain Steady-State Hematopoiesis by Promoting Sinusoidal Endothelial Cell Survival and Regeneration

  1. Author:
    Gadomski,Stephen
    Singh, Satyendra K.
    Singh,Shweta
    Sarkar,Tanmoy
    Klarmann,Kim
    Berenschot, Maximillian
    Seaman,Steven
    Jakubison,Brad
    Gudmundsson,Kristbjorn
    Lockett,Stephen
    Keller,Jonathan

  2. Author Address

    NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Basic Sci Program, Frederick, MD 21702 USA.Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Opt Microscopy & Anal Lab, Frederick, MD 21702 USA.Univ Cambridge, Cambridge Stem Cell Inst, Dept Haematol, Cambridge CB2 0AW, England.King Georges Med Univ, Ctr Adv Res, Dept Stem Cell & Cell Culture, Lucknow 226003, Uttar Pradesh, India.
    1. Year: 2020
    2. Date: Apr 28
  2. Journal: Cell reports
  3. CELL PRESS,
    1. 31
    2. 4
  5. Type of Article: Article
  6. Article Number: 107572
  7. ISSN: 2211-1247
  1. Abstract:

    Investigating mechanisms that regulate endothelial cell (EC) growth and survival is important for understanding EC homeostasis and how ECs maintain stem cell niches. We report here that targeted loss of Id genes in adult ECs results in dilated, leaky sinusoids and a pro-inflammatory state that increases in severity over time. Disruption in sinusoidal integrity leads to increased hematopoietic stem cell (HSC) proliferation, differentiation, migration, and exhaustion. Mechanistically, sinusoidal ECs (SECs) show increased apoptosis because of reduced Bcl2-family gene expression following Id gene ablation. Furthermore, Id1(-/-) Id3(-/-) SECs and upstream type H vessels show increased expression of cyclin-dependent kinase inhibitors p21 and p27 and impaired ability to proliferate, which is rescued by reducing E2-2 expression. Id1(-/-) Id3(-/-) mice do not survive sublethal irradiation because of impaired vessel regeneration and hematopoietic failure. Thus, Id genes are required for the survival and regeneration of BM SECs during homeostasis and stress to maintain HSC development.

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External Sources

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  2. DOI: 10.1016/j.celrep.2020.107572
  3. PMID: 32348770
  4. View record in Web of Science®
  5. WOS: 000529070000011

Library Notes

  1. Fiscal Year: FY2019-2020
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