Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age

Derrick J. Rossi (), David Bryder, Jun Seita, Andre Nussenzweig, Jan Hoeijmakers and Irving L. Weissman
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Derrick J. Rossi: and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
David Bryder: and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Jun Seita: and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Andre Nussenzweig: Experimental Immunology Branch and Laboratory for Receptor Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Jan Hoeijmakers: Erasmus Medical Center, PO Box 1738, 3000DR, Rotterdam, The Netherlands
Irving L. Weissman: and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA

Nature, 2007, vol. 447, issue 7145, 725-729

Abstract: DNA damage does not significantly impact in the establishment, maintenance or expansion of long-term reconstituting haematopoietic stem cells (LT-HSC), it is instead a physiological mechanism of stem cell ageing that may underlie the diminished capacity of aged tissues to return to homeostasis after exposure to acute stress or injury.

Date: 2007
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DOI: 10.1038/nature05862

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