细胞生物学
毛囊
收缩(语法)
生物
内皮素1
内皮素受体
祖细胞
内科学
内分泌学
化学
受体
干细胞
医学
生物化学
作者
Pieter Martino,Raghava R. Sunkara,Nicholas Heitman,Martina Rangl,Alexia Brown,Nivedita Saxena,Laura Grisanti,Donald E. Kohan,Masashi Yanagisawa,Michael Rendl
标识
DOI:10.1038/s41556-022-01065-w
摘要
Substantial follicle remodelling during the regression phase of the hair growth cycle is coordinated by the contraction of the dermal sheath smooth muscle, but how dermal-sheath-generated forces are regulated is unclear. Here, we identify spatiotemporally controlled endothelin signalling—a potent vasoconstriction-regulating pathway—as the key activating mechanism of dermal sheath contraction. Pharmacological blocking or genetic ablation of both endothelin receptors, ETA and ETB, impedes dermal sheath contraction and halts follicle regression. Epithelial progenitors at the club hair–epithelial strand bottleneck produce the endothelin ligand ET-1, which is required for follicle regression. ET signalling in dermal sheath cells and downstream contraction is dynamically regulated by cytoplasmic Ca2+ levels through cell membrane and sarcoplasmic reticulum calcium channels. Together, these findings illuminate an epithelial–mesenchymal interaction paradigm in which progenitors—destined to undergo programmed cell death—control the contraction of the surrounding sheath smooth muscle to orchestrate homeostatic tissue regression and reorganization for the next stem cell activation and regeneration cycle. Martino, Sunkara et al. report that endothelin produced by hair follicle progenitors binds to endothelin receptors on dermal sheath cells to trigger their contraction and hair follicle regression.
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