Indications for a brain-hair follicle axis: inhibition of keratinocyte proliferation and up-regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P
Indications for a brain-hair follicle axis: inhibition of keratinocyte proliferation and up-regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P
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DOI：
10.1096/fj.00-0699fje
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发表时间：
2001-09-01
期刊：
影响因子：
4.8
通讯作者：
Paus, R
中科院分区：
文献类型：
--
作者：
Arck, PC;Handjiski, B;Paus, R
长期以来，人们一直怀疑压力会导致脱发，尽管目前还没有令人信服的证据。在这里，我们发现在小鼠声学应激显著增加毛囊含有凋亡细胞的数量，并抑制毛囊内角化细胞原位增殖。超声应激还显著增加了活化的滤泡周围巨噬细胞簇的数量和脱颗粒肥大细胞的数量，而下调了上皮内γ δ T淋巴细胞的数量。这些应激诱导的免疫变化可以通过在非应激小鼠中注射神经肽P物质来模拟，而在应激小鼠中被选择性P物质受体拮抗剂所消除。我们得出结论，压力确实可以抑制毛发生长，可能是通过脑毛囊轴中巨噬细胞和/或肥大细胞的物质p依赖性激活。
It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte proliferation in situ. Sonic stress also significantly increased the number of activated perifollicular macrophage clusters and the number of degranulated mast cells, whereas it down-regulated the number of intraepithelial gamma delta T lymphocytes. These stress-induced immune changes could be mimicked by injection of the neuropeptide substance P in nonstressed mice and were abrogated by a selective substance P receptor antagonist in stressed mice. We conclude that stress can indeed inhibit hair growth in vivo, probably via a substance P-dependent activation of macrophages and/or mast cells in the context of a brain-hair follicle axis.