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烟草烟雾引起的皮肤色素沉着是由芳香烃受体介导的。

Tobacco smoke-induced skin pigmentation is mediated by the aryl hydrocarbon receptor.

出版信息

Exp Dermatol. 2013 Aug;22(8):556-8. doi: 10.1111/exd.12170. Epub 2013 Jun 27.

DOI:10.1111/exd.12170
PMID:23802610
Abstract

It is widely recognized that tobacco smoke causes skin pigmentation. No studies, however, have directly evaluated the mechanisms of the changes in smoker's skin pigmentation. In this study, when cultured with water-soluble tobacco smoke extract, the human epidermal melanocytes grew to a large size and produced more melanins. We evaluated melanocyte activation by quantifying microphthalmia-associated transcription factor (MITF) expression by real-time polymerase chain reaction. MITF expression was significantly and dose-dependently increased by exposure to tobacco smoke extract. The Wnt/β-catenin signalling pathway seemed to mediate the tobacco smoke extract-induced melanocyte activation. Immunocytochemical studies revealed that the activated melanocytes actively expressed aryl hydrocarbon receptors (AhR) around the nuclear membrane. The tobacco smoke extract-induced MITF activation was inhibited by RNA silencing of the AhR. This study provides the evidence that tobacco smoke enhances pigmentation in vitro and that the increase in pigmentation may involve β-catenin- and AhR-mediated mechanisms inside human melanocytes.

摘要

人们普遍认为,烟草烟雾会导致皮肤色素沉着。然而,目前尚无研究直接评估吸烟者皮肤色素沉着变化的机制。在这项研究中,当与水溶性烟草烟雾提取物一起培养时,人类表皮黑素细胞生长到较大的大小并产生更多的黑色素。我们通过实时聚合酶链反应定量测定小眼畸形相关转录因子(MITF)的表达来评估黑素细胞的激活。暴露于烟草烟雾提取物可显著且剂量依赖性地增加 MITF 的表达。Wnt/β-catenin 信号通路似乎介导了烟草烟雾提取物诱导的黑素细胞激活。免疫细胞化学研究显示,激活的黑素细胞在核膜周围积极表达芳香烃受体(AhR)。用 AhR 的 RNA 沉默抑制了烟草烟雾提取物诱导的 MITF 激活。这项研究提供了证据表明,烟草烟雾在体外增强色素沉着,并且色素沉着的增加可能涉及β-连环蛋白和 AhR 介导的人黑素细胞内的机制。

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