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Highly purified, multi-wall carbon nanotubes induce light-chain 3B expression in human lung cells

•HTT2800-treated BEAS-2B cells induced LC3B in a time-dependent manner.•HTT2800-treated BEAS-2B cells showed decreased cell proliferation that was both time- and dose-dependent.•Addition of 3-MA, LC3B-II protein and mRNA levels were significantly decreased.•3-MA and E64-d+pepstatin A, but not brefel...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2013-10, Vol.440 (2), p.348-353
Main Authors: Tsukahara, Tamotsu, Matsuda, Yoshikazu, Usui, Yuki, Haniu, Hisao
Format: Article
Language:English
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Summary:•HTT2800-treated BEAS-2B cells induced LC3B in a time-dependent manner.•HTT2800-treated BEAS-2B cells showed decreased cell proliferation that was both time- and dose-dependent.•Addition of 3-MA, LC3B-II protein and mRNA levels were significantly decreased.•3-MA and E64-d+pepstatin A, but not brefeldin A, provided protection against HTT2800-induced cell death.•These results suggest that HTT2800 predominantly causes autophagy rather than apoptotic cell death in BEAS-2B cells. Bronchial epithelial cells are targets of inhalation and play a critical role in the maintenance of mucosal integrity as mechanical barriers against various particles. Our previous result suggest that vapor-grown carbon fiber, HTT2800, which is one of the most highly purified multi-wall carbon nanotubes (MWCNT) showed cellular uptake of the carbon nanotube, increased cell death, enhanced DNA damage, and induced cytokine release. Increasing evidence suggests that autophagy may critically influence vital cellular processes such as apoptosis, cell proliferation and inflammation and thereby may play a critical role in pulmonary diseases. Autophagy was recently recognized as a critical cell death pathway, and autophagosome accumulation has been found to be associated with the exposure of various nanoparticles. In this study, the authors focus on the autophagic responses of HTT2800 exposure. The HTT2800-exposed cells induced LC3B expression and induced cell growth inhibition.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2013.09.089