Different Cellular Response of Human Mesothelial Cell MeT-5A to Short-Term and Long-Term Multiwalled Carbon Nanotubes Exposure

Our plain-English summary of Different Cellular Response of Human Mesothelial Cell MeT-5A to Short-Term and Long-Term Multiwalled Carbon Nanotubes Exposure, by L. Ju, W. Wu, M. Yu, et al (BioMed Research International, 2017).

The study

• Authors: L. Ju, W. Wu, M. Yu, J. Lou, H. Wu, X. Yin, Z. Jia, Y. Xiao, L. Zhu, J. Yang
• Journal: BioMed Research International
• Published: 2017;2017:2747215
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Despite being a commercially important product, multiwalled carbon nanotubes (MWCNTs) continue to raise concerns over human health due to their structural similarity to asbestos. Indeed, exposure to MWCNT has been shown to induce lung cancer and even mesothelioma, but contradictory results also exist. To clarify the potentially carcinogenic effects of rigid and rod-like MWCNT and to elucidate the underlying mechanisms, the effects of MWCNT on human mesothelial cell MeT-5A were examined throughout 3 months of continuous exposure, including cytotoxicity, genotoxicity, and cell motility. It was found that MWCNT did not affect MeT-5A cell proliferation at 10 μg/cm2 within 72 h treatment, but under the same condition, MWCNT induced genotoxicity and perturbed cell motility. In addition, MeT-5A cells demonstrated different cellular responses to MWCNT after short-term and long-term exposure. Taken together, our results indicated a possible carcinogenic potential for MWCNT after long-term treatment, in which Annexin family proteins might be involved.

In plain English

This laboratory study did not test asbestos. It tested multiwalled carbon nanotubes (MWCNTs), which the authors describe as structurally similar to asbestos. Human pleural mesothelial cells (the MeT-5A cell line) were grown with a commercial MWCNT product from Sigma-Aldrich, mostly at 10 micrograms per square centimetre, for periods from hours up to 3 months. In 24-hour tests, cell viability fell significantly only at 20 micrograms per square centimetre and above. At 10 micrograms per square centimetre, no significant differences were found over 72 hours. After 3 months, treated cells became smaller and rounder and grew significantly faster than control cells. A marker of DNA damage (gamma-H2AX foci) increased with longer exposure. Short-term exposure slowed cell migration, and long-term exposure partly reversed this. Invasion through a gel fell to 44% of control at 30 days but rose to almost 2-fold control after 3 months. Levels of several Annexin proteins changed, and lowering Annexin 1 reduced migration of long-term-treated cells. The authors concluded that after long-term exposure the cells showed certain characteristics related to carcinogenic potential, possibly involving Annexin proteins.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: in vitro laboratory (cell culture) experiment comparing short-term and long-term exposure
• Who was studied: human pleural mesothelial MeT-5A cell line obtained from the American Type Culture Collection; no people or animals were studied
• Exposure: multiwalled carbon nanotubes (Sigma-Aldrich 659258), 110 to 170 nm in diameter and 5 to 9 micrometres long, given at 0 to 40 micrograms per square centimetre for 24 h and at 10 micrograms per square centimetre for up to 3 months; no asbestos fibers were tested
• Main results:
  • After 24 h, cell viability was significantly reduced at concentrations of 20 micrograms per square centimetre and above compared with control cells
  • At 10 micrograms per square centimetre for 0 to 72 h, there were no significant differences in cell proliferation
  • Cells exposed for 3 months (M-MeT-5A) became smaller and round, and proliferated significantly faster than passage-matched controls at 48 and 72 hours after seeding
  • Few gamma-H2AX foci (a DNA damage marker) were seen in control cells or cells treated for less than 24 h. With treatment from more than 24 h up to 3 months, foci per cell and the number of cells with foci increased with exposure time
  • Wound-healing migration rates at 24 h and 48 h were: control cells 34.4 ± 2.5% and 100%; 24 h-treated cells 23.6 ± 2.5% and 64.2 ± 1.8%; 48 h-treated cells 2.0 ± 0.3% and 13 ± 1.9%; 30-day-treated cells 36.7 ± 1.6% and 63.9 ± 1.8%; 90-day-treated cells 33.9 ± 2.5% and 66.0 ± 1.4%
  • Cell invasion fell to 44% of control at 30 days of exposure (P less than 0.05), then rose to almost 2-fold that of control cells after 3 months (P less than 0.05)
  • Annexin 1 and Annexin 5 protein levels increased. Annexin 2 and Annexin 6 fell sharply at 30 days and then increased at 90 days
  • In long-term-treated cells, lowering Annexin 1 reduced migration: at 48 h the migration rate was about 50% for Annexin 1-knockdown cells versus 70% for control-transfected cells
• The authors' conclusion: The authors concluded that MeT-5A cells respond differently to short-term and long-term MWCNT treatment. After long-term exposure the cells show certain characteristics related to carcinogenic potential, and Annexin proteins might be involved in the disturbed cell migration and invasion.
• Limitations the authors state:
  • The authors stated that the reasons for the complex changes in Annexin 2 and 6 are not clear
  • The authors noted that Annexin 1 and 5 increased while cell migration was inhibited, which seemed to contradict the known function of these proteins
  • The authors noted that the increased invasion after 3 months was relatively weak, with few cells penetrating

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Mesothelial Cells, Lung Cancer, Mesothelioma, Carcinogenic, Genotoxicity, MeT-5A Cells.

Related studies

• A comparison of acute and long-term effects of industrial multiwalled carbon nanotubes on human lung and immune cells in vitro — T. Thurnherr, C. Brandenberger, et al. (2011)
• Chronic exposure to carbon nanotubes induces invasion of human mesothelial cells through matrix metalloproteinase-2 — W. Lohcharoenkal, L. Wang, et al. (2013)
• The mechanism of pleural inflammation by long carbon nanotubes: interaction of long fibres with macrophages stimulates them to amplify pro-inflammatory responses in mesothelial cells — F.A. Murphy, A. Schinwald, et al. (2012)
• Induction and recovery of CpG site specific methylation changes in human bronchial cells after long-term exposure to carbon nanotubes and asbestos — D. Öner, M. Ghosh, et al. (2020)
• Adverse effects of industrial multiwalled carbon nanotubes on human pulmonary cells — L. Tabet, C. Bussy, et al. (2009)
• The role of iron impurities in the toxic effects exerted by short multiwalled carbon nanotubes (MWCNT) in murine alveolar macrophages — E. Aldieri, I. Fenoglio, et al. (2013)

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