Distinct contribution of stem and progenitor cells to epidermal maintenance

Guilhem Mascré, Sophie Dekoninck, Benjamin Drogat, Khalil Kass Youssef, Sylvain Brohée, Panagiota A. Sotiropoulou, Benjamin D. Simons () and Cédric Blanpain ()
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Guilhem Mascré: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Sophie Dekoninck: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Benjamin Drogat: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Khalil Kass Youssef: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Sylvain Brohée: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Panagiota A. Sotiropoulou: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium
Benjamin D. Simons: Cavendish Laboratory, J. J. Thomson Avenue, Cambridge CB3 0HE, UK
Cédric Blanpain: Université Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium

Nature, 2012, vol. 489, issue 7415, 257-262

Abstract: Abstract The skin interfollicular epidermis (IFE) is the first barrier against the external environment and its maintenance is critical for survival. Two seemingly opposite theories have been proposed to explain IFE homeostasis. One posits that IFE is maintained by long-lived slow-cycling stem cells that give rise to transit-amplifying cell progeny, whereas the other suggests that homeostasis is achieved by a single committed progenitor population that balances stochastic fate. Here we probe the cellular heterogeneity within the IFE using two different inducible Cre recombinase–oestrogen receptor constructs targeting IFE progenitors in mice. Quantitative analysis of clonal fate data and proliferation dynamics demonstrate the existence of two distinct proliferative cell compartments arranged in a hierarchy involving slow-cycling stem cells and committed progenitor cells. After wounding, only stem cells contribute substantially to the repair and long-term regeneration of the tissue, whereas committed progenitor cells make a limited contribution.

Date: 2012
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DOI: 10.1038/nature11393

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