PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanism...

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Bibliographic Details
Published in:Experimental and therapeutic medicine Vol. 19; no. 5; pp. 3227 - 3238
Main Authors: Suo, Danfeng, Zeng, Sanwu, Zhang, Junling, Meng, Linghe, Weng, Lishuo
Format: Journal Article
Language:English
Published: Greece Spandidos Publications 01-05-2020
Spandidos Publications UK Ltd
D.A. Spandidos
Subjects:
Air pollution
Apoptosis
Cell adhesion & migration
Cytochrome c
Enzyme-linked immunosorbent assay
Fibroblast growth factors
Free radicals
Heme
Investigations
Metabolic disorders
Neomycin
Outdoor air quality
Oxidative stress
Peroxidase
Skin
Stem cells
Superoxides
Vitiligo
China
melanin metabolic disorder
vitiligo
apoptosis
oxidative stress injury
human melanocytes
particulate matter 2.5
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Summary:Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanisms of PM2.5 on vitiligo. Human keratinocytes (HaCaT cells) and human melanocytes (PIG1 cells and PIG3V cells) were exposed to PM2.5 (0-200 µg/ml) for 24 h. The cell viability of the three cell lines was measured by a Cell Counting Kit-8 assay. The secretions of stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in HaCaT cells were evaluated by ELISA. The melanin contents, cellular tyrosinase activity, apoptosis, cell migration, malondialdehyde (MDA) contents, superoxide dismutase (SOD) levels, glutathione peroxidase (GSH-Px) levels and related protein expressions in PIG1 cells and PIG3V cells were evaluated by a NaOH assay, DOPA assay, Annexin V-FITC/Propidium Iodide staining, MDA assay, SOD assay, GSH-Px assay and western blotting, respectively. It was demonstrated that PM2.5 exposure inhibited cell viability of all three cell lines (HaCaT, PIG1 and PIG3V cells). PM2.5 exposure attenuated the secretions of SCF and bFGF in HaCaT cells. Moreover, PM2.5 exposure attenuated the activation of tyrosinase and melanogenesis, inhibited cell migration, and induced apoptosis and oxidative stress injury in PIG1 cells and PIG3V cells. In addition, PM2.5 exposure caused upregulated cytosolic cytochrome C and activated caspase-3 in PIG1 cells and PIG3V cells. Furthermore, PM2.5 exposure activated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 signaling pathway. The present results suggested that PM2.5 exposure could inhibit the secretions of SCF and bFGF in keratinocytes, and cause oxidative stress injury and melanin metabolic disorder in melanocytes. Therefore, PM2.5 could be a new risk factor for vitiligo.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2020.8590