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Transcriptomic Profiling of Toxic Copper Overload Induced by CuO Nanoparticles or Copper Ions in Human Lung Epithelial and Liver Cells.

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Title: Transcriptomic Profiling of Toxic Copper Overload Induced by CuO Nanoparticles or Copper Ions in Human Lung Epithelial and Liver Cells.
Authors: Kuhn, Jana1 (AUTHOR), Gliga, Anda R.2 (AUTHOR), Aissouni, Cheyenne Ines1,3 (AUTHOR), Glowacki, Anna Maria1,2 (AUTHOR), Parsdorfer, Marlene1,2 (AUTHOR), Link, Martin1,3 (AUTHOR), Karlsson, Hanna Lovisa3 (AUTHOR), Hartwig, Andrea1 (AUTHOR)
Source: Nanomaterials (2079-4991). May2026, Vol. 16 Issue 10, p590. 25p.
Subjects: Transcriptomes, Copper oxide, Cell communication, Metallothionein, Liver cells, RNA sequencing, Respiratory mucosa, Copper poisoning
Abstract: The transition metal copper (Cu) is an essential trace element for humans and serves as a cofactor for numerous enzymes. Therefore, intracellular Cu homeostasis must be tightly regulated. Meanwhile, Cu is increasingly used in industrial and biomedical applications, particularly in nanoparticle (NP) form. However, studies have demonstrated that Cu(II) oxide (CuO) NPs are highly toxic. Therefore, understanding the underlying toxic effects of such compounds is of the utmost importance. In this context, transcriptomic profiling is regarded as a valuable tool. Nevertheless, comparative studies addressing organ-relevant models, such as the liver and lungs, are scarce. Furthermore, no transcriptomic studies have been conducted on human bronchial lung epithelial cells exposed to CuO NPs and Cu2+. In this study, we compared the cellular effects of human bronchial lung epithelial cells exposed to both CuO NPs and Cu2+ to the effects in human liver cells exposed to Cu2+ by applying RNA sequencing. Although cytotoxicity was comparable, we showed that Cu uptake was highly dependent on both the cell type and the form of Cu. The most pronounced concentration-dependent transcriptional changes were observed with CuO NP exposure in BEAS-2B cells. The only differentially expressed genes (DEGs) found by all exposures and treatments were metallothioneins (MTs). The most sensitive targets of Cu-induced toxicity were related to nuclear factor erythroid 2-related factor 2 (NRF2), nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), and mitogen-activated protein kinase (MAPK) signaling. Furthermore, the effects observed at the transcriptome level were studied at the functional level, such as cell cycle regulation and cytokine release. Thus, we demonstrated that the two cell types differ in susceptibility, and that complementing transcriptome profiling with functional studies provides important mechanistic insights. [ABSTRACT FROM AUTHOR]
Copyright of Nanomaterials (2079-4991) is the property of MDPI 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: Transcriptomic Profiling of Toxic Copper Overload Induced by CuO Nanoparticles or Copper Ions in Human Lung Epithelial and Liver Cells.
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  Data: <searchLink fieldCode="JN" term="%22Nanomaterials+%282079-4991%29%22">Nanomaterials (2079-4991)</searchLink>. May2026, Vol. 16 Issue 10, p590. 25p.
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  Data: <searchLink fieldCode="DE" term="%22Transcriptomes%22">Transcriptomes</searchLink><br /><searchLink fieldCode="DE" term="%22Copper+oxide%22">Copper oxide</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+communication%22">Cell communication</searchLink><br /><searchLink fieldCode="DE" term="%22Metallothionein%22">Metallothionein</searchLink><br /><searchLink fieldCode="DE" term="%22Liver+cells%22">Liver cells</searchLink><br /><searchLink fieldCode="DE" term="%22RNA+sequencing%22">RNA sequencing</searchLink><br /><searchLink fieldCode="DE" term="%22Respiratory+mucosa%22">Respiratory mucosa</searchLink><br /><searchLink fieldCode="DE" term="%22Copper+poisoning%22">Copper poisoning</searchLink>
– Name: Abstract
  Label: Abstract
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  Data: The transition metal copper (Cu) is an essential trace element for humans and serves as a cofactor for numerous enzymes. Therefore, intracellular Cu homeostasis must be tightly regulated. Meanwhile, Cu is increasingly used in industrial and biomedical applications, particularly in nanoparticle (NP) form. However, studies have demonstrated that Cu(II) oxide (CuO) NPs are highly toxic. Therefore, understanding the underlying toxic effects of such compounds is of the utmost importance. In this context, transcriptomic profiling is regarded as a valuable tool. Nevertheless, comparative studies addressing organ-relevant models, such as the liver and lungs, are scarce. Furthermore, no transcriptomic studies have been conducted on human bronchial lung epithelial cells exposed to CuO NPs and Cu2+. In this study, we compared the cellular effects of human bronchial lung epithelial cells exposed to both CuO NPs and Cu2+ to the effects in human liver cells exposed to Cu2+ by applying RNA sequencing. Although cytotoxicity was comparable, we showed that Cu uptake was highly dependent on both the cell type and the form of Cu. The most pronounced concentration-dependent transcriptional changes were observed with CuO NP exposure in BEAS-2B cells. The only differentially expressed genes (DEGs) found by all exposures and treatments were metallothioneins (MTs). The most sensitive targets of Cu-induced toxicity were related to nuclear factor erythroid 2-related factor 2 (NRF2), nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), and mitogen-activated protein kinase (MAPK) signaling. Furthermore, the effects observed at the transcriptome level were studied at the functional level, such as cell cycle regulation and cytokine release. Thus, we demonstrated that the two cell types differ in susceptibility, and that complementing transcriptome profiling with functional studies provides important mechanistic insights. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Nanomaterials (2079-4991) is the property of MDPI 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: 10.3390/nano16100590
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      – Code: eng
        Text: English
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      Pagination:
        PageCount: 25
        StartPage: 590
    Subjects:
      – SubjectFull: Transcriptomes
        Type: general
      – SubjectFull: Copper oxide
        Type: general
      – SubjectFull: Cell communication
        Type: general
      – SubjectFull: Metallothionein
        Type: general
      – SubjectFull: Liver cells
        Type: general
      – SubjectFull: RNA sequencing
        Type: general
      – SubjectFull: Respiratory mucosa
        Type: general
      – SubjectFull: Copper poisoning
        Type: general
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      – TitleFull: Transcriptomic Profiling of Toxic Copper Overload Induced by CuO Nanoparticles or Copper Ions in Human Lung Epithelial and Liver Cells.
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              Text: May2026
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