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Adv Drug Deliv Rev. 2020 Jan 1;153:65-71. doi: 10.1016/j.addr.2020.02.002. Epub 2020 Feb 21.
2
Hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells.交感神经的过度激活导致黑素细胞干细胞耗竭。
Nature. 2020 Jan;577(7792):676-681. doi: 10.1038/s41586-020-1935-3. Epub 2020 Jan 22.
3
Nociceptor sensory neurons suppress neutrophil and γδ T cell responses in bacterial lung infections and lethal pneumonia.伤害感受器感觉神经元可抑制细菌肺部感染和致死性肺炎中的中性粒细胞和 γδ T 细胞反应。
Nat Med. 2018 May;24(4):417-426. doi: 10.1038/nm.4501. Epub 2018 Mar 5.
4
A UV-Independent Topical Small-Molecule Approach for Melanin Production in Human Skin.一种不依赖紫外线的局部小分子方法用于人类皮肤黑色素生成
Cell Rep. 2017 Jun 13;19(11):2177-2184. doi: 10.1016/j.celrep.2017.05.042.
5
Brain-skin connection: stress, inflammation and skin aging.脑-皮联系:压力、炎症与皮肤衰老
Inflamm Allergy Drug Targets. 2014;13(3):177-90. doi: 10.2174/1871528113666140522104422.
6
Direct migration of follicular melanocyte stem cells to the epidermis after wounding or UVB irradiation is dependent on Mc1r signaling.创伤或 UVB 照射后,滤泡黑素细胞干细胞向表皮的直接迁移依赖于 Mc1r 信号。
Nat Med. 2013 Jul;19(7):924-9. doi: 10.1038/nm.3194. Epub 2013 Jun 9.
7
NFIB is a governor of epithelial-melanocyte stem cell behaviour in a shared niche.NFIB 是上皮细胞-黑素细胞干细胞在共享生态位中行为的一个调控因子。
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8
An ultraviolet-radiation-independent pathway to melanoma carcinogenesis in the red hair/fair skin background.红发/白皙皮肤背景下黑色素瘤发生的紫外线辐射非依赖性途径。
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9
Defining MC1R regulation in human melanocytes by its agonist α-melanocortin and antagonists agouti signaling protein and β-defensin 3.通过其激动剂α-黑素细胞刺激素和拮抗剂刺鼠相关蛋白及β-防御素 3 来定义人类黑素细胞中的 MC1R 调节。
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黑素皮质素 1 受体对于急性应激诱导的小鼠毛发变白是可有可无的。

Melanocortin 1 receptor is dispensable for acute stress induced hair graying in mice.

机构信息

Department of Stem Cell and Regenerative Biology, Harvard University and Harvard Stem Cell Institute, Cambridge, MA, USA.

Westlake Laboratory of Life Sciences and Biomedicine, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.

出版信息

Exp Dermatol. 2021 Apr;30(4):572-577. doi: 10.1111/exd.14264. Epub 2020 Dec 31.

DOI:10.1111/exd.14264
PMID:33382172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8016727/
Abstract

Stress is a risk factor for many skin conditions, but the cellular and molecular mechanisms of its impacts have only begun to be revealed. In mice, acute stress induces loss of melanocyte stem cells (MeSCs) and premature hair greying. Our previous work demonstrated that the loss of MeSCs upon acute stress is caused by the hyperactivation of the sympathetic nervous system. Stress also induces the secretion of stress hormones from the hypothalamic-pituitary-adrenal (HPA) axis; however, whether stress hormones are involved in the hair greying process has not been fully examined. In particular, the adrenocorticotropic hormone (ACTH) is released from the pituitary glands upon stress. ACTH is a ligand for the melanocortin 1 receptor (MC1R), which plays critical roles in regulating MeSC migration and skin pigmentation. We investigated whether the MC1R pathway is required for the stress-induced hair greying. We confirmed that MC1R is the major melanocortin receptor expressed in MeSCs. However, induction of acute stress via resiniferatoxin (RTX) injection still leads to hair greying in Mc1r mutant mice, suggesting that the ACTH-MC1R pathway is not a major contributor in acute stress-induced premature hair greying.

摘要

压力是许多皮肤状况的一个风险因素,但它的影响的细胞和分子机制才刚刚开始被揭示。在小鼠中,急性压力会导致黑素细胞干细胞(MeSCs)的丧失和过早的头发变白。我们之前的工作表明,急性压力下 MeSCs 的丧失是由于交感神经系统的过度激活所致。压力还会导致下丘脑-垂体-肾上腺(HPA)轴分泌应激激素;然而,应激激素是否参与了头发变白的过程尚未得到充分研究。特别是,促肾上腺皮质激素(ACTH)在应激时从垂体中释放。ACTH 是黑素皮质素 1 受体(MC1R)的配体,在调节 MeSC 迁移和皮肤色素沉着中发挥着关键作用。我们研究了 MC1R 途径是否是应激诱导的头发变白所必需的。我们证实 MC1R 是 MeSCs 中表达的主要黑素皮质素受体。然而,通过树脂毒素(RTX)注射诱导急性压力仍然会导致 Mc1r 突变小鼠的头发变白,这表明 ACTH-MC1R 途径不是急性压力诱导的过早头发变白的主要贡献者。