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

Hair Follicle Bulge Stem Cells Appear Dispensable for the Acute Phase of Wound Re-epithelialization.
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DOI:
10.1002/stem.2289
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发表时间:
2016-05
期刊:
Stem cells (Dayton, Ohio)
影响因子:
--
通讯作者:
Hardman MJ
Hardman MJ
中科院分区:
其他
文献类型:
--
作者:
Garcin CL;Ansell DM;Headon DJ;Paus R;Hardman MJ

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皮肤愈合反应已经发展到迅速发生,以最大限度地减少感染并重新建立上皮稳态。快速愈合是通过多种细胞类型的复杂协调来实现的,其中重要的是包括毛囊(HF)内的特定细胞群。在生理条件下,HF和滤泡间表皮的上皮隔室保持离散,K15 + ve隆突干细胞在毛发周期期间为HF重建贡献后代,并作为生长期期间毛干产生的基础。只有在受伤时,HF细胞才从毛囊迁移到新表皮。然而,第一反应细胞的身份,特别是这个过程是否涉及K15 + ve隆突细胞对表皮伤口修复早期阶段的直接贡献仍然不清楚。在这里,我们证明,在小鼠皮肤表皮损伤不诱导隆突活化在早期表皮伤口修复。具体而言,未受伤的高频隆突细胞既不增殖,也没有出现迁移出隆起的壁龛后,表皮创伤。为支持这些观察结果,白喉毒素介导的K15 + ve隆突细胞部分消融未能延迟伤口愈合。我们的数据表明,隆突细胞只在修复的后期对表皮损伤作出反应。我们讨论,这种反应可能已经演变为一种保护性的保障机制,对隆突干细胞耗竭和肿瘤发生。干细胞2016; 34:1377 - 1385
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