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Dickkopf-1 参与了地塞米松介导的毛囊退化。

Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression.

机构信息

Department of Immunology, Kyungpook National University School of Medicine, Daegu, Korea.

出版信息

Exp Dermatol. 2017 Oct;26(10):952-954. doi: 10.1111/exd.13308. Epub 2017 Apr 27.

DOI:10.1111/exd.13308
PMID:28155238
Abstract

The stress-related neurohormones including glucocorticoids (GCs) are secreted by hair follicles (HFs), and GCs suppress murine hair growth in vivo. In this study, we found that dexamethasone (Dex), a synthetic GC, increased the expression of dickkopf-1 (DKK1), a known catagen inducer, in dermal papilla (DP) cells, but not in follicular keratinocytes. The neutralizing DKK1 antibody significantly attenuated the Dex-induced inhibition of human hair shaft elongation. In addition, the neutralizing Dkk1 antibody delayed Dex-induced catagen in mice. Collectively, our data strongly suggest that stress-related neurohormones cause DP cells to secrete DKK1, thereby leading to stress-associated disturbances in hair growth.

摘要

压力相关的神经激素包括糖皮质激素(GCs),由毛囊(HFs)分泌,GCs 在体内抑制小鼠毛发生长。在这项研究中,我们发现地塞米松(Dex),一种合成的 GC,增加了真皮乳头(DP)细胞中已知的休止期诱导物 dickkopf-1(DKK1)的表达,但不在毛囊角质形成细胞中。中和 DKK1 抗体显著减弱了 Dex 诱导的人毛干伸长抑制。此外,中和 Dkk1 抗体延迟了 Dex 诱导的小鼠休止期。总的来说,我们的数据强烈表明,压力相关的神经激素导致 DP 细胞分泌 DKK1,从而导致与压力相关的毛发生长紊乱。

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