4.7 Article

Particulate matter promotes hyperpigmentation via AhR/MAPK signaling activation and by increasing a-MSH paracrine levels in keratinocytes

期刊

ENVIRONMENTAL POLLUTION
卷 278, 期 -, 页码 -

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2021.116850

关键词

Particulate matter; Aryl hydrocarbon receptor; Melanogenesis; a-MSH

资金

  1. National Natural Science Foundation of China [81773333, 82073449]
  2. National Natural Science Foundation of Hunan Province [2019JJ50853]
  3. Hunan Development and Reform Commission Innovation Project [2019412]
  4. Hunan Provincial Innovation Foundation For Postgraduate [CX20190158]
  5. Fundamental Research Funds for the Central Universities of Central South University [2020zzts290]

向作者/读者索取更多资源

PM2.5 has become a global concern for public health and the environment, with the ability to induce skin aging and hyperpigmentation. By activating specific signaling pathways, PM2.5 can induce melanogenesis and promote hyperpigmentation.
Particulate matter with an aerodynamic equivalent diameter of 2.5 mm or less in ambient air (PM2.5) has become a global public and environmental problem, and the control of the PM2.5 concentration in air is an urgent problem. PM2.5 can easily penetrate the skin, activating the inflammatory response in skin, unbalancing the skin barrier function, and inducing skin aging. Hyperpigmentation is the main manifestation of skin aging and has a considerable impact on quality of life worldwide. To date, no research on the influence of PM2.5 on hyperpigmentation has been conducted. Here, we illustrate that PM2.5 can induce melanogenesis in vivo and in vitro by regulating TYR, TYRP1, TYRP2, and MITF expression via AhR/ MAPK signaling activation. Furthermore, PM2.5 increased a-MSH paracrine levels, which in turn promote hyperpigmentation. Our results provide a deeper understanding of how PM2.5 disrupts skin homeostasis and function. Treatment with AhR antagonists may be a potential therapeutic strategy for hyperpigmentation induced by PM2.5. (c) 2021 Elsevier Ltd. All rights reserved.

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