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Copper oxide nanoparticle induces inflammatory response and mucus production via MAPK signaling in human bronchial epithelial cells

Authors
Ko, Je-WonPark, Ji-WonShin, Na-RaeKim, Jae-HongCho, Young-KwonShin, Dong-HoKim, Jong-ChoonLee, In-ChulOh, Sei-RyangAhn, Kyung-SeopShin, In-Sik
Issue Date
4월-2016
Publisher
ELSEVIER
Keywords
Copper oxide nanoparticles; Inflammatory response; MUC5AC; Mitogen-activated protein kinases
Citation
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, v.43, pp.21 - 26
Indexed
SCIE
SCOPUS
Journal Title
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume
43
Start Page
21
End Page
26
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/89059
DOI
10.1016/j.etap.2016.02.008
ISSN
1382-6689
Abstract
Copper nanoparticles (CuONPs) can pose risks to industrial workers. With increase of its applications especially in electronic fields, it is necessary to assess the toxicity of CuONPs, including pulmonary toxicity. In this study, we investigated the effect of CuONPs on human epithelial cell line H292. CuONPs treatment caused a significant increase in IL-6 and IL-8 mRNA expression and protein levels in H292 cells in a concentration-dependent manner. The mRNA expression and protein levels of MUC5AC were consistent with those of proinflammatory mediators. Additionally, CuONPs treatment increased phosphorylation of mitogen-activated protein kinases (MAPKs), Erk, JNK, and p-38 compared to that of control in a concentration-dependent manner. However, co-treatment with CuONPs and each MAPK inhibitor significantly decreased the phosphorylation of each MAPK, resulting in decreased mRNA expression and protein levels of proinflammatory mediators and MUC5AC compared to that in H292 cells only treated with CuONPs. In summary, CuONPs-induced inflammatory mediators and MUC5AC associated with MAPKs phosphorylation. Our results will provide useful information on CuONPs-induced pulmonary toxicity. (C) 2016 Elsevier B.V. All rights reserved.
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생명과학대학 (생명과학부)
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