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

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Title: Copper oxide nanoparticle induces inflammatory response and mucus production via MAPK signaling in human bronchial epithelial cells.
Authors: Ko, Je-Won1, Park, Ji-Won2,3, Shin, Na-Rae1,2, Kim, Jae-Hong3, Cho, Young-Kwon4, Shin, Dong-Ho1, Kim, Jong-Choon1, Lee, In-Chul1, Oh, Sei-Ryang2, Ahn, Kyung-Seop2 ksahn@kribb.re.kr, Shin, In-Sik1 dvmmk79@gmail.com
Source: Environmental Toxicology & Pharmacology. Apr2016, Vol. 43, p21-26. 6p.
Subject Terms: *Physiology, Copper oxide, Nanomedicine, Mucus, Mitogen-activated protein kinases, Cellular signal transduction, Epithelial cells
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. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Copper oxide nanoparticle induces inflammatory response and mucus production via MAPK signaling in human bronchial epithelial cells.
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  Data: <searchLink fieldCode="AR" term="%22Ko%2C+Je-Won%22">Ko, Je-Won</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Park%2C+Ji-Won%22">Park, Ji-Won</searchLink><relatesTo>2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Shin%2C+Na-Rae%22">Shin, Na-Rae</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Kim%2C+Jae-Hong%22">Kim, Jae-Hong</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Cho%2C+Young-Kwon%22">Cho, Young-Kwon</searchLink><relatesTo>4</relatesTo><br /><searchLink fieldCode="AR" term="%22Shin%2C+Dong-Ho%22">Shin, Dong-Ho</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Kim%2C+Jong-Choon%22">Kim, Jong-Choon</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Lee%2C+In-Chul%22">Lee, In-Chul</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Oh%2C+Sei-Ryang%22">Oh, Sei-Ryang</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Ahn%2C+Kyung-Seop%22">Ahn, Kyung-Seop</searchLink><relatesTo>2</relatesTo><i> ksahn@kribb.re.kr</i><br /><searchLink fieldCode="AR" term="%22Shin%2C+In-Sik%22">Shin, In-Sik</searchLink><relatesTo>1</relatesTo><i> dvmmk79@gmail.com</i>
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  Data: <searchLink fieldCode="JN" term="%22Environmental+Toxicology+%26+Pharmacology%22">Environmental Toxicology & Pharmacology</searchLink>. Apr2016, Vol. 43, p21-26. 6p.
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  Data: *<searchLink fieldCode="DE" term="%22Physiology%22">Physiology</searchLink><br /><searchLink fieldCode="DE" term="%22Copper+oxide%22">Copper oxide</searchLink><br /><searchLink fieldCode="DE" term="%22Nanomedicine%22">Nanomedicine</searchLink><br /><searchLink fieldCode="DE" term="%22Mucus%22">Mucus</searchLink><br /><searchLink fieldCode="DE" term="%22Mitogen-activated+protein+kinases%22">Mitogen-activated protein kinases</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+signal+transduction%22">Cellular signal transduction</searchLink><br /><searchLink fieldCode="DE" term="%22Epithelial+cells%22">Epithelial cells</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: 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. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/j.etap.2016.02.008
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      – Code: eng
        Text: English
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        PageCount: 6
        StartPage: 21
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      – SubjectFull: Physiology
        Type: general
      – SubjectFull: Copper oxide
        Type: general
      – SubjectFull: Nanomedicine
        Type: general
      – SubjectFull: Mucus
        Type: general
      – SubjectFull: Mitogen-activated protein kinases
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      – SubjectFull: Cellular signal transduction
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      – SubjectFull: Epithelial cells
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      – TitleFull: Copper oxide nanoparticle induces inflammatory response and mucus production via MAPK signaling in human bronchial epithelial cells.
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              Text: Apr2016
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