Stem Cells
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First published online December 7, 2006
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2006-0405v1
25/4/828    most recent
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Submitted on July 4, 2006
Accepted on November 29, 2006

Tissue-Specific Stem Cells

Age dependent increase in SP distribution within Hematopoiesis: implications for our understanding of the mechanism of aging

Daniel J. Pearce 1, Fernando Anjos-Afonso 1, Christopher M. Ridler 1, Ayad Eddaoudi 2, Dominique Bonnet 1*

1 Hematopoietic Stem Cell Laboratory, London Research Institute, Cancer Research UK, London, United Kingdom
2 FACS Laboratory, London Research Institute, Cancer Research UK, London, United Kingdom

* To whom correspondence should be addressed. E-mail: d.bonnet{at}cancer.org.uk.


  Abstract

It is thought that as we age, damage to our stem cells may lead to diminished stem cell pool function and consequently a reduced organ regeneration potential that contributes to somatic senescence. Stem cells have evolved many anti-toxicity mechanisms and certain mechanisms may be utilized to isolate hematopoietic stem cells. One method exploits the activity of the ABCG2 transporter to efflux Hoechst 33342 and results in a stem cell population known as the side population. The SP subset represents a remarkable enrichment for hematopoietic stem cells and provides an opportunity to re-evaluate age-based changes in hematopoietic stem cells.

We report here that the frequency of SP cells steadily increases with age, as does the proportion of Lin-/Sca-1+/c-kit+ cells that is capable of Hoechst efflux. Phenotyping, progenitor and long-term repopulation assays have indicated that SP cells in older mice are still stem cells, albeit with a lower homing efficiency than SP cells from younger mice. Analysis of apoptosis within SP cells has revealed an apoptosis-resistant population in SP cells from old mice. Gene expression analysis has determined that SP cells from old mice have a reduced expression of apoptosis-promoting genes than SP cells from young mice.

This increase in SP cells with age seems to be an intrinsic property that may be independent of the age of the microenvironment (niche) and our data might provide some clues as to how this alteration in the proportion of stem/progenitor cells occurs. A possible selection-based mechanism of stem cell pool aging is discussed.


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