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Epilation induces hair and skin pigmentation through an EDN3/EDNRB-dependent regenerative response of melanocyte stem cells

机译:脱毛通过黑素细胞干细胞的EDN3 / EDNRB依赖性再生反应诱导头发和皮肤色素沉着

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摘要

In response to various types of injury, melanocyte stem cells (McSCs) located in the bulge of hair follicles can regenerate mature melanocytes for hair and skin pigmentation. How McSCs respond to injury, however, remains largely unknown. Here we show that after epilation of mice, McSCs regenerate follicular and epidermal melanocytes, resulting in skin and hair hyperpigmentation. We further show that epilation leads to endogenous EDN3 upregulation in the dermal papilla, the secondary hair germ cells, and the epidermis. Genetic and pharmacological disruption of the EDN3 receptor EDNRB in vivo significantly blocks the effect of epilation on follicular and epidermal melanocyte regeneration as well as skin and hair hyperpigmentation. Taken together, these results indicate that epilation induces McSCs activation through EDN3/EDNRB signaling and in turn leads to skin and hair hyperpigmentation. The findings suggest that EDN/EDNRB signaling may serve as a potential therapeutic target to promote repigmentation in hypopigmentation disorders.
机译:为了应对各种类型的损伤,位于毛囊隆起处的黑素细胞干细胞(McSC)可以再生成熟的黑素细胞,使头发和皮肤色素沉着。然而,McSCs如何对伤害做出反应仍然未知。在这里,我们显示了小鼠脱毛后,McSCs再生了卵泡和表皮黑素细胞,导致皮肤和头发色素沉着过度。我们进一步表明,脱毛导致真皮乳头,次生毛发细胞和表皮中的内源性EDN3上调。 EDN3受体EDNRB在体内的遗传和药理学破坏显着阻断了脱毛对卵泡和表皮黑素细胞再生以及皮肤和头发色素沉着的影响。两者合计,这些结果表明脱毛通过EDN3 / EDNRB信号传导诱导McSCs活化,进而导致皮肤和头发色素沉着过度。这些发现表明,EDN / EDNRB信号传导可能是促进色素沉着障碍中色素沉着的潜在治疗靶标。

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