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Effect of exposure to Asian sand dust-Particulate matter on liver Tenascin-C expression in human cancer cell and mouse hepatic tissue

Authors
Lee, Yong HyunKim, Dae YoungJeong, Sung HwanHwang, You Jin
Issue Date
Sep-2019
Publisher
JAPANESE SOC TOXICOLOGICAL SCIENCES
Keywords
Asian sand dust (ASD) - Particulate matter (PM); Fibrosis; Tenascin-C (Tn-C); TGF-β1
Citation
The Journal of toxicological sciences, v.44, no.9, pp.633 - 641
Journal Title
The Journal of toxicological sciences
Volume
44
Number
9
Start Page
633
End Page
641
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/2710
DOI
10.2131/jts.44.633
ISSN
1880-3989
Abstract
Asian Sand Dust-Particulate Matter (ASD-PM) aerosol brings large amounts of wind-eroded soil particles containing high concentrations of metallic components caused by industrialization and vehicles. Proinflammatory and cytotoxic cytokines trigger local inflammatory responses and cause a systematically high incidence of cardiovascular and other diseases. Tenascin C (Tn-C) is known to be expressed in damaged tissue or in a developmental stage of tissue. In this study, we examined the expression of Tn-C and Fibronectin in human cancer-cell lines and in liver tissue of mice treated with ASD-PM to investigate the inflammatory and cell-damage effects of ASD-PM. In our in vivo study, mice were intratracheally instilled with saline suspensions of ASD-PM particles. Instillation of these particles was repeated twice a week for 12 weeks and the liver tissues were stained with hematoxylin, eosin, and Masson's trichrome, and we carried out an IF. Tn-C expression in liver tissues was detected by RT-PCR and western blot analysis. In the results, the expression of Tn-C increased in a dose-dependent manner in both RNA and Immunofluorescence assay (IF). In our in vitro study, A549 and Hep3B cell lines were incubated in culture media with Transforming Growth Factor-Beta1(TGF-β1) and ASD-PM. Immunofluorescence microscopy images showed a two times stronger expression of fluorescence in the ASD-treated group than in that treated with TGF-β1. They also showed a stronger expression of Tn-C in proportion to the concentration of ASD-PM. We confirmed that ASD-PM when inhaled formally migrated to other organs and induced Tn-C expression. ASD-PM containing metals causes expression of Tn-C in liver tissue in proportion to the concentration of ASD-PM.
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