Role of PARP1 on DNA damage induced by mineral silicate chrysotile in bronchial epithelial and pleural mesothelial cells

Our plain-English summary of Role of PARP1 on DNA damage induced by mineral silicate chrysotile in bronchial epithelial and pleural mesothelial cells, by M. Zhang, H. Xia, M. Yu, et al (Environmental Science and Pollution Research International, 2021).

The study

• Authors: M. Zhang, H. Xia, M. Yu, L. Ju, Y. Xiao, L. Zhu
• Journal: Environmental Science and Pollution Research International
• Published: 2021;28(30):40871-40878
• Read it: PubMed · Publisher

Abstract

To investigate whether poly (ADP ribose) polymerase-1 (PARP1) is involved in chrysotile-induced DNA damage in pleural mesothelial cells (MeT-5A) and bronchial epithelial cells (BEAS-2B), two PARP1-deficient cell lines were established. Efficiencies of RNA interference on PARP1 were detected by western blot and qPCR. Here, normal cells and PARP1-deficient cells were exposed to chrysotile, and DNA damage and DNA repair were detected by alkaline comet assay. All cells were treated with chrysotile at the indicated concentrations (5, 10, 20, and 40 μg/cm2) for 24 h and then the DNA repair capacity was observed for 12 and 24 h, respectively. The results showed that chrysotile caused DNA damage at an obvious dose-dependent manner in MeT-5A and BEAS-2B cells. In addition, MeT-5A cells had more persistent DNA damage than BEAS-2B. Compared to normal cells, the PARP1-deficient cells were more sensitive to DNA damage caused by chrysotile. In DNA repair experiments, all cell lines recovered from the damage over time. The results of relative repair percentage (RRP) of MeT-5A and BEAS-2B were higher than those of MeT-5A shPARP1 and BEAS-2B shPARP1 cells at all experimental concentrations (except 5 μg/cm2) at 12-h repair. However, RRP of BEAS-2B and BEAS-2B shPARP1 tended to be closer, and RRP of MeT-5A shPARP1 was still lower than that of MeT-5A at 24-h repair. All results suggest that PARP1 plays an important role in early repair of DNA damage in BEAS-2B and MeT-5A cells exposed to chrysotile.

© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

In plain English

Researchers exposed human pleural mesothelial (MeT-5A) and bronchial epithelial (BEAS-2B) cells to chrysotile asbestos at 5, 10, 20 and 40 micrograms per square centimeter for 24 hours. They also tested versions of each line with the DNA-repair protein PARP1 largely switched off. Comet assays measured DNA damage after exposure and after 12 or 24 hours of recovery. Even the lowest dose raised damage in both normal cell types. In MeT-5A cells, damage at the four doses was 3, 5, 6 and 7 times that of unexposed cells. At 20 and 40 micrograms per square centimeter, PARP1-deficient cells showed about 1.4 times (MeT-5A) and 1.2 times (BEAS-2B) normal cells' damage. Damage fell during recovery but had not returned to normal by 24 hours, lasting longer in mesothelial cells. After 12 hours, PARP1-deficient cells had repaired a smaller share of their damage, except at the lowest dose, where differences were not significant. In bronchial cells this gap nearly closed by 24 hours. The authors concluded that PARP1 plays an important role in early repair of chrysotile-induced DNA damage in these cells.

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: Laboratory (in vitro) experiment on human cell lines, using RNA interference to make PARP1-deficient versions of each cell line
• Who was studied: Human pleural mesothelial cells (MeT-5A) and human bronchial epithelial cells (BEAS-2B) obtained from the American Type Culture Collection, plus PARP1-deficient (shPARP1) versions of each; experiments were repeated three times
• Exposure: Chrysotile supplied by the Japan Fibrous Materials Research Association, at 5, 10, 20 and 40 μg/cm2 for 24 hours, followed by 12 or 24 hours of recovery in normal medium
• Main results:
  • In BEAS-2B shPARP1 cells, PARP1 mRNA and protein were 0.24 and 0.1 of the levels in normal BEAS-2B cells, respectively
  • Even the lowest concentration (5 μg/cm2) increased tail DNA percentage in normal BEAS-2B and MeT-5A cells, and the difference from controls was statistically significant
  • In normal MeT-5A cells, tail DNA percentages at 5, 10, 20 and 40 μg/cm2 were 3, 5, 6 and 7 times those of unexposed MeT-5A cells
  • At 20 and 40 μg/cm2, MeT-5A shPARP1 cells had nearly 1.4-fold the tail DNA percentage of normal MeT-5A cells
  • At 20 and 40 μg/cm2, BEAS-2B shPARP1 cells had tail DNA percentages nearly 1.2 times those of normal BEAS-2B cells
  • BEAS-2B and BEAS-2B shPARP1 cells recovered faster than the other cell lines
  • Damage was more persistent in MeT-5A and MeT-5A shPARP1 cells than in the BEAS-2B cell lines
  • DNA damage in both cell types did not return to normal levels after 24 hours of recovery
  • After 12 hours of repair, relative repair percentages of normal MeT-5A and BEAS-2B cells were higher than those of the PARP1-deficient cells at all concentrations except 5 μg/cm2
  • At 5 μg/cm2, relative repair percentages did not differ significantly between normal and PARP1-deficient cells
  • After 24 hours of repair, relative repair percentages of BEAS-2B shPARP1 and normal BEAS-2B cells were very close
• The authors' conclusion: The authors concluded that PARP1 plays an important role in the early repair of chrysotile-induced DNA damage in human bronchial epithelial cells and human mesothelial cells
• Limitations the authors state:
  • The authors noted that PARP1's importance differs between cell types and that repair involves multiple enzymes
  • The authors noted that differences in fiber adhesion and uptake between the two cell lines may matter and need further study

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: Silicate, Chrysotile, Mesothelial Cells, Comet Assay, MeT-5A Cells.

Related studies

• N-acetylcysteine prevents cytotoxic effects induced by man-made mineral fibers in a human bronchial epithelial cell line — M. Zhang, H. Xia, et al. (2018)
• DNA damage in bronchial epithelial and mesothelial cells with and without associated crocidolite asbestos fibers — J. Nygren, S. Suhonen, et al. (2004)
• Chrysotile Causes Human Bronchial Epithelial Cell Apoptosis in Response to the Fas-Mediated Apoptosis Pathway — M. Zhang, J. Chen, et al. (2017)
• Differentially expressed genes in asbestos-induced tumorigenic human bronchial epithelial cells: implication for mechanism — Y.L. Zhao, C.Q. Piao, et al. (2000)
• Karyotype analysis of tumorigenic human bronchial epithelial cells transformed by chrysolite asbestos using chemically induced premature chromosome condensation technique — M. Suzuki, C.Q. Piao, et al. (2001)
• Mitochondria-targeted Ogg1 and aconitase-2 prevent oxidant-induced mitochondrial DNA damage in alveolar epithelial cells — S.J. Kim, P. Cheresh, et al. (2014)

Browse more research in Environmental Science and Pollution Research International, or return to medical research.