دورية أكاديمية

Hair Follicle Bulge Stem Cells Appear Dispensable for the Acute Phase of Wound Re-epithelialization

التفاصيل البيبلوغرافية
العنوان: Hair Follicle Bulge Stem Cells Appear Dispensable for the Acute Phase of Wound Re-epithelialization
المؤلفون: Garcin, Clare L, Ansell, David M, Headon, Denis J, Paus, Ralf, Hardman, Matthew J
المصدر: Garcin , C L , Ansell , D M , Headon , D J , Paus , R & Hardman , M J 2016 , ' Hair Follicle Bulge Stem Cells Appear Dispensable for the Acute Phase of Wound Re-epithelialization ' , Stem Cells , vol. 34 , no. 5 , pp. 1377-1385 . https://doi.org/10.1002/stem.2289Test
سنة النشر: 2016
المجموعة: The University of Manchester: Research Explorer - Publications
الوصف: 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. Stem Cells 2016;34:1377-1385.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1002/stem.2289
الإتاحة: https://doi.org/10.1002/stem.2289Test
https://research.manchester.ac.uk/en/publications/66303e56-b48f-47e9-91ef-92425b260ab3Test
حقوق: info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.281FD5D5
قاعدة البيانات: BASE