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J Invest Dermatol ; 140(12): 2343-2352.e3, 2020 12.
Article in English | MEDLINE | ID: mdl-32339540

ABSTRACT

Knowing the damage that particulate matter (PM) can cause in skin is important for tightly controlling the release of air pollutants and preventing more serious diseases. This study investigates if such alterations are present in reconstructed human epidermis exposed to coarse air PM. Exposure of reconstructed human epidermis to increasing concentrations (2.2, 8.9, and 17.9 µg/cm2) of standard urban PM over time led to decreased cell viability at 48 hours. The barrier function was shown to be compromised by 24 hours of exposure to high doses (17.9 µg/cm2). Morphological alterations included cytoplasm vacuolization and partial loss of epidermal stratification. Cytokeratin 10, involucrin, loricrin, and filaggrin protein levels were significantly decreased. We confirmed an inflammatory process by IL-1α release and found a significant increase in AQP3 expression. We also demonstrated changes in NOTCH1 and AhR expression of epidermis treated with coarse air PM. The use of hydrogen peroxide altered AQP3 and NOTCH1 expression, and the use of N-acetyl-L-cysteine altered NOTCH1 expression, suggesting that this is a redox-dependent process. These results demonstrate that coarse air PM induces dose-dependent inflammatory response and alterations in protein markers of differentiation and water transport in the epidermis that could ultimately compromise the structural integrity of the skin, promoting or exacerbating various skin diseases.


Subject(s)
Air Pollutants/toxicity , Epidermis/drug effects , Particulate Matter/toxicity , Water Loss, Insensible/drug effects , Biomarkers/analysis , Biomarkers/metabolism , Cell Differentiation/drug effects , Cell Differentiation/immunology , Cells, Cultured , Epidermis/immunology , Epidermis/metabolism , Filaggrin Proteins , Humans , Keratinocytes , Primary Cell Culture , Skin Diseases/chemically induced , Skin Diseases/immunology , Skin Diseases/prevention & control , Water Loss, Insensible/immunology
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