ArticleExperimental and therapeutic medicine2020
PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Mitigating PM2.5-induced skin injury and aging: botanical strategies targeting redox and inflammatory pathways.Redox report : communications in free radical research · 2026Review
- Atmospheric Aerosol Neurotoxicity and Parkinson's Disease: Mechanisms and Perspectives.Journal of biochemical and molecular toxicology · 2026Review
- Particulate Matter-Induced Skin Injury: A Dual-Pathway AhR-Nrf2 Framework for Epidermal Homeostasis and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Heat Stress Modulates WDR5-Mediated H3K4me3 Modification to Induce Melanogenesis via Activating CX3CL1/CX3CR1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A semi-analytical approach for solving a fractional-order mathematical model of skin cell damage and repair driven by environmental pollutants.Scientific reports · 2026Article
- Seasonal Variation in PMAntioxidants (Basel, Switzerland) · 2026Article
- Long-Term PMLife (Basel, Switzerland) · 2025Review
- Fine Particulate Matter (PM2.5) Disrupts Intestinal Barrier Function by Inducing Oxidative Stress and PI3K/AKT-Mediated Inflammation in Caco-2 Cells.International journal of molecular sciences · 2025Article
- PM2.5 Exposure Aggravates Inflammatory Response and Mucus Production in 16HBE Cells through Inducing Oxidative Stress and RAGE Expression.Cell biochemistry and biophysics · 2025Article
- Causal association between air pollution and autoimmune diseases: a two-sample Mendelian randomization study.Frontiers in public health · 2024Article
- NO-induced apoptosis in human melanocytes from lightly and darkly pigmented skin.Postepy dermatologii i alergologii · 2023Article
- Promoting New Approach Methodologies (NAMs) for research on skin color changes in response to environmental stress factors: tobacco and air pollution.Frontiers in toxicology · 2023Review
- Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy.Redox report : communications in free radical research · 2022Article
- A cross-sectional study of Chinese women facial skin status with environmental factors and individual lifestyles.Scientific reports · 2022Article
- Review
- Recent Insights into Particulate Matter (PMInternational journal of environmental research and public health · 2022Review
- The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death.Oxidative medicine and cellular longevity · 2022Review
- Arbutin as a Skin Depigmenting Agent with Antimelanogenic and Antioxidant Properties.Antioxidants (Basel, Switzerland) · 2021Review
- Autophagy attenuates particulate matter 2.5-induced damage in HaCaT cells.Annals of translational medicine · 2021Article
- Curcumin protects BEAS‑2B cells from PMInternational journal of molecular medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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