U.S. Department of EnergyOffice of Scientific and Technical Information
Ionizing Particle Radiation as a Modulator of Endogenous Bone Marrow Cell Reprogramming: Implications for Hematological Cancers [Ionizing radiation as a modulator of bone marrow cell reprogramming: low doses as a driver for associated hematological cancers]
Abstract
Exposure of individuals to ionizing radiation (IR), as in the case of astronauts exploring space or radiotherapy cancer patients, increases their risk of developing secondary cancers and other health-related problems. Bone marrow (BM), the site in the body where hematopoietic stem cell (HSC) self-renewal and differentiation to mature blood cells occurs, is extremely sensitive to low-dose IR, including irradiation by high-charge and high-energy particles. Low-dose IR induces DNA damage and persistent oxidative stress in the BM hematopoietic cells. Inefficient DNA repair processes in HSC and early hematopoietic progenitors can lead to an accumulation of mutations whereas long-lasting oxidative stress can impair hematopoiesis itself, thereby causing long-term damage to hematopoietic cells in the BM niche. We report here that low-dose 1H- and 56Fe-IR significantly decreased the hematopoietic early and late multipotent progenitor (E- and L-MPP, respectively) cell numbers in mouse BM over a period of up to 10 months after exposure. Both 1H- and 56Fe-IR increased the expression of pluripotent stem cell markers Sox2, Nanog, and Oct4 in L-MPPs and 10 months post-IR exposure. We postulate that low doses of 1H- and 56Fe-IR may induce endogenous cellular reprogramming of BM hematopoietic progenitor cells to assume a more primitive pluripotent phenotype andmore »
- Authors:
-
- Boston University School of Medicine, Boston, MA (United States). Whitaker Cardiovascular Institute
- GeneSys Research Institute, Boston, MA (United States). Cardiovascular Research Center
- Yale School of Medicine, New Haven, CT (United States). Yale Cardiovascular Research Center
- Wake Forest School of Medicine, Winston-Salem, NC (United States). Wake Forest Institute for Regenerative Medicine
- University of California Davis, Sacramento, CA (United States). Radiation Oncology, School of Medicine; Lawrence Livermore National Lab. (LLNL), Livermore, CA (United States)
- GeneSys Research Institute, Boston, MA (United States). Cardiovascular Research Center ; Tufts University School of Medicine, Boston, MA (United States)
- Boston University School of Medicine, Boston, MA (United States). Whitaker Cardiovascular Institute; GeneSys Research Institute, Boston, MA (United States). Cardiovascular Research Center; Tufts University School of Medicine, Boston, MA (United States)
- Publication Date:
- Research Org.:
- Lawrence Livermore National Laboratory (LLNL), Livermore, CA (United States)
- Sponsoring Org.:
- USDOE National Nuclear Security Administration (NNSA)
- OSTI Identifier:
- 1466139
- Report Number(s):
- LLNL-JRNL-737728
Journal ID: ISSN 2234-943X; 890200
- Grant/Contract Number:
- AC52-07NA27344
- Resource Type:
- Journal Article: Accepted Manuscript
- Journal Name:
- Frontiers in Oncology
- Additional Journal Information:
- Journal Volume: 5; Journal Issue: no. 231; Journal ID: ISSN 2234-943X
- Publisher:
- Frontiers Research Foundation
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 62 RADIOLOGY AND NUCLEAR MEDICINE
Citation Formats
Muralidharan, Sujatha, Sasi, Sharath P., Zuriaga, Maria A., Hirschi, Karen K., Porada, Christopher D., Coleman, Matthew A., Walsh, Kenneth X., Yan, Xinhua, and Goukassian, David A. Ionizing Particle Radiation as a Modulator of Endogenous Bone Marrow Cell Reprogramming: Implications for Hematological Cancers [Ionizing radiation as a modulator of bone marrow cell reprogramming: low doses as a driver for associated hematological cancers]. United States: N. p., 2015.
Web. doi:10.3389/fonc.2015.00231.
Muralidharan, Sujatha, Sasi, Sharath P., Zuriaga, Maria A., Hirschi, Karen K., Porada, Christopher D., Coleman, Matthew A., Walsh, Kenneth X., Yan, Xinhua, & Goukassian, David A. Ionizing Particle Radiation as a Modulator of Endogenous Bone Marrow Cell Reprogramming: Implications for Hematological Cancers [Ionizing radiation as a modulator of bone marrow cell reprogramming: low doses as a driver for associated hematological cancers]. United States. https://doi.org/10.3389/fonc.2015.00231
Muralidharan, Sujatha, Sasi, Sharath P., Zuriaga, Maria A., Hirschi, Karen K., Porada, Christopher D., Coleman, Matthew A., Walsh, Kenneth X., Yan, Xinhua, and Goukassian, David A. 2015.
"Ionizing Particle Radiation as a Modulator of Endogenous Bone Marrow Cell Reprogramming: Implications for Hematological Cancers [Ionizing radiation as a modulator of bone marrow cell reprogramming: low doses as a driver for associated hematological cancers]". United States. https://doi.org/10.3389/fonc.2015.00231. https://www.osti.gov/servlets/purl/1466139.
@article{osti_1466139,
title = {Ionizing Particle Radiation as a Modulator of Endogenous Bone Marrow Cell Reprogramming: Implications for Hematological Cancers [Ionizing radiation as a modulator of bone marrow cell reprogramming: low doses as a driver for associated hematological cancers]},
author = {Muralidharan, Sujatha and Sasi, Sharath P. and Zuriaga, Maria A. and Hirschi, Karen K. and Porada, Christopher D. and Coleman, Matthew A. and Walsh, Kenneth X. and Yan, Xinhua and Goukassian, David A.},
abstractNote = {Exposure of individuals to ionizing radiation (IR), as in the case of astronauts exploring space or radiotherapy cancer patients, increases their risk of developing secondary cancers and other health-related problems. Bone marrow (BM), the site in the body where hematopoietic stem cell (HSC) self-renewal and differentiation to mature blood cells occurs, is extremely sensitive to low-dose IR, including irradiation by high-charge and high-energy particles. Low-dose IR induces DNA damage and persistent oxidative stress in the BM hematopoietic cells. Inefficient DNA repair processes in HSC and early hematopoietic progenitors can lead to an accumulation of mutations whereas long-lasting oxidative stress can impair hematopoiesis itself, thereby causing long-term damage to hematopoietic cells in the BM niche. We report here that low-dose 1H- and 56Fe-IR significantly decreased the hematopoietic early and late multipotent progenitor (E- and L-MPP, respectively) cell numbers in mouse BM over a period of up to 10 months after exposure. Both 1H- and 56Fe-IR increased the expression of pluripotent stem cell markers Sox2, Nanog, and Oct4 in L-MPPs and 10 months post-IR exposure. We postulate that low doses of 1H- and 56Fe-IR may induce endogenous cellular reprogramming of BM hematopoietic progenitor cells to assume a more primitive pluripotent phenotype and that IR-induced oxidative DNA damage may lead to mutations in these BM progenitors. This could then be propagated to successive cell lineages. Persistent impairment of BM progenitor cell populations can disrupt hematopoietic homeostasis and lead to hematologic disorders, and these findings warrant further mechanistic studies into the effects of low-dose IR on the functional capacity of BM-derived hematopoietic cells including their self-renewal and pluripotency.},
doi = {10.3389/fonc.2015.00231},
url = {https://www.osti.gov/biblio/1466139},
journal = {Frontiers in Oncology},
issn = {2234-943X},
number = no. 231,
volume = 5,
place = {United States},
year = {Wed Oct 14 00:00:00 EDT 2015},
month = {Wed Oct 14 00:00:00 EDT 2015}
}
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Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age
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DNA damage response in adult stem cells: pathways and consequences
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CD133 is a modifier of hematopoietic progenitor frequencies but is dispensable for the maintenance of mouse hematopoietic stem cells
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Long-term changes in rat hematopoietic and other physiological systems after high-energy iron ion irradiation
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A role for NANOG in G1 to S transition in human embryonic stem cells through direct binding of CDK6 and CDC25A
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The risk of developing a second cancer after receiving craniospinal proton irradiation
journal, March 2009
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Notch signalling via RBP-J promotes myeloid differentiation
journal, June 2000
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Fucosyltransferase VII improves the function of selectin ligands on cord blood hematopoietic stem cells
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Relative biological effectiveness of simulated solar particle event proton radiation to induce acute hematological change in the porcine model
journal, September 2013
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Role of isolated and clustered DNA damage and the post-irradiating repair process in the effects of heavy ion beam irradiation
journal, February 2015
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Oxidative DNA damage: mechanisms, mutation, and disease
journal, July 2003
- Cooke, Marcus S.; Evans, Mark D.; Dizdaroglu, Miral
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Induced Pluripotent Stem Cell Lines Derived from Human Somatic Cells
journal, December 2007
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Radiation Will Make Astronauts' Trip to Mars Even Riskier
journal, May 2013
- Kerr, R. A.
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Elemental and Isotopic Composition of the Galactic Cosmic Rays
journal, December 1983
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NOTCH Signaling Is Required for Formation and Self-Renewal of Tumor-Initiating Cells and for Repression of Secretory Cell Differentiation in Colon Cancer
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Surface fucosylation of human cord blood cells augments binding to P-selectin and E-selectin and enhances engraftment in bone marrow
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Host defence during Klebsiella pneumonia relies on haematopoietic-expressed Toll-like receptors 4 and 2
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Analysis of Cell Cycle in Mouse Bone Marrow Cells Following Acute in vivo Exposure to 56Fe Ions
journal, January 2008
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- Journal of Radiation Research, Vol. 49, Issue 4
Recent Advances in the Biology of Heavy-Ion Cancer Therapy
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- Journal of Radiation Research, Vol. 51, Issue 4
Carbon Ion Radiotherapy: Clinical Experiences at National Institute of Radiological Science (NIRS)
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High Expression of SOX2 and OCT4 Indicates Radiation Resistance and an Independent Negative Prognosis in Cervical Squamous Cell Carcinoma
journal, April 2014
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- Journal of Histochemistry & Cytochemistry, Vol. 62, Issue 7
Mammalian Stem Cells Reprogramming in Response to Terahertz Radiation
journal, December 2010
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