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Id1 Ablation Protects Hematopoietic Stem Cells from Stress-Induced Exhaustion and Aging

  1. Author:
    Singh, Satyendra K
    Singh, Shweta
    Gadomski, Stephen
    Sun, Lei
    Pfannenstein, Alexander
    Magidson, Valentin
    Chen, Jack
    Kozlov, Serguei
    Tessarollo, Lino
    Klarmann, Kimberly
    Keller, Jonathan

  2. Author Address

    Mouse Cancer Genetics Program, Center for Cancer Research, NCI, Frederick, MD 21702, USA; Department of Stem Cell and Cell Culture, Center for Advanced Research, King George 39;s Medical University, Lucknow 226003, India., Mouse Cancer Genetics Program, Center for Cancer Research, NCI, Frederick, MD 21702, USA., Optical Microscopy and Analysis Lab, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., Advanced Biomedical and Computation Sciences, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., Center for Advanced Preclinical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., Mouse Cancer Genetics Program, Center for Cancer Research, NCI, Frederick, MD 21702, USA; Basic Science Program and Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., Mouse Cancer Genetics Program, Center for Cancer Research, NCI, Frederick, MD 21702, USA; Basic Science Program and Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. Electronic address: kellerjo@mail.nih.gov.,
    1. Year: 2018
    2. Date: Aug 02
    3. Epub Date: 2018 06 28
  2. Journal: Cell Stem Cell
    1. 23
    2. 2
    3. Pages: 252-265.e8
  4. Type of Article: Article
  1. Abstract:

    Defining mechanisms that maintain tissue stem cells during homeostasis, stress, and aging is important for improving tissue regeneration and repair and enhancing cancer therapies. Here, we show that Id1 is induced in hematopoietic stem cells (HSCs) by cytokines that promote HSC proliferation and differentiation, suggesting that it functions in stress hematopoiesis. Genetic ablation of Id1 increases HSC self-renewal in serial bone marrow transplantation (BMT) assays, correlating with decreases in HSC proliferation, mitochondrial biogenesis, and reactive oxygen species (ROS) production. Id1-/- HSCs have a quiescent molecular signature and harbor less DNA damage than control HSCs. Cytokines produced in the hematopoietic microenvironment after ?-irradiation induce Id1 expression. Id1-/- HSCs display a blunted proliferative response to such cytokines and other inducers of chronic proliferation including genotoxic and inflammatory stress and aging, protecting them from chronic stress and exhaustion. Thus, targeting Id1 may be therapeutically useful for improving HSC survival and function during BMT, chronic stress, and aging. Copyright © 2018 Elsevier Inc. All rights reserved.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.stem.2018.06.001
  3. PMID: 30082068
  4. View record in Web of Science®
  5. WOS: 000440583900015
  6. PII : S1934-5909(18)30283-2

Library Notes

  1. Fiscal Year: FY2017-2018
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