Loading...
Hair follicle bulge stem cells appear dispensable for the acute phase of wound re-epithelialization
Garcin, C.L. Headon, D.J. Paus, R. Hardman, M.J.
Garcin, C.L.
Headon, D.J.
Paus, R.
Hardman, M.J.
Publication Date
2016-05
End of Embargo
Supervisor
Keywords
Rights
© 2016 The Authors. Stem Cells published by Wiley Periodicals, Inc. on behalf of AlphaMed Press.
This is an open access article under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Peer-Reviewed
Yes
Open Access status
openAccess
Accepted for publication
01/12/2015
Institution
Department
Awarded
Embargo end date
Collections
Additional title
Abstract
The cutaneous healing response has evolved to occur rapidly, in order to minimize infection and to re‐establish epithelial homeostasis. Rapid healing is achieved through complex coordination of multiple cell types, which importantly includes specific cell populations within the hair follicle (HF). Under physiological conditions, the epithelial compartments of HF and interfollicular epidermis remain discrete, with K15+ve bulge stem cells contributing progeny for HF reconstruction during the hair cycle and as a basis for hair shaft production during anagen. Only upon wounding do HF cells migrate from the follicle to contribute to the neo‐epidermis. However, the identity of the first‐responding cells, and in particular whether this process involves a direct contribution of K15+ve bulge cells to the early stage of epidermal wound repair remains unclear. Here we demonstrate that epidermal injury in murine skin does not induce bulge activation during early epidermal wound repair. Specifically, bulge cells of uninjured HFs neither proliferate nor appear to migrate out of the bulge niche upon epidermal wounding. In support of these observations, Diphtheria toxin‐mediated partial ablation of K15+ve bulge cells fails to delay wound healing. Our data suggest that bulge cells only respond to epidermal wounding during later stages of repair. We discuss that this response may have evolved as a protective safeguarding mechanism against bulge stem cell exhaust and tumorigenesis.
Version
Published version
Citation
Garcin CL, Ansell DM, Headon DJ et al (2016) Hair follicle bulge stem cells appear dispensable for the acute phase of wound re-epithelialization. Stem Cells. 34(5): 1377-1385.
Link to publisher’s version
Link to published version
Link to Version of Record
Type
Article