The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Nrf2 Is a Key Transcription Factor That Regulates Antioxidant Defense in Macrophages and Epithelial Cells: Protecting against the Proinflammatory and Oxidizing Effects of Diesel Exhaust Chemicals
Abstract
The proinflammatory effects of particulate pollutants, including diesel exhaust particles (DEP), are related to their content of redox cycling chemicals and their ability to generate oxidative stress in the respiratory tract. An antioxidant defense pathway, which involves phase II enzyme expression, protects against the pro-oxidative and proinflammatory effects of DEP. The expression of enzymes, including heme oxygenase-1 (HO-1) and GST, is dependent on the activity of a genetic antioxidant response element in their promoters. In this study we investigated the mechanism by which redox cycling organic chemicals, prepared from DEP, induce phase II enzyme expression as a protective response. We demonstrate that aromatic and polar DEP fractions, which are enriched in polycyclic aromatic hydrocarbons and quinones, respectively, induce the expression of HO-1, GST, and other phase II enzymes in macrophages and epithelial cells. We show that HO-1 expression is mediated through accumulation of the bZIP transcription factor, Nrf2, in the nucleus, and that Nrf2 gene targeting significantly weakens this response. Nrf2 accumulation and subsequent activation of the antioxidant response element is regulated by the proteasomal degradation of Nrf2. This pathway is sensitive to pro-oxidative and electrophilic DEP chemicals and is also activated by ambient ultrafine particles. We propose that Nrf2-mediated phase II enzyme expression protects against the proinflammatory effects of particulate pollutants in the setting of allergic inflammation and asthma.
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Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage
Li, N., Sioutas, C., Cho, A., Schmitz, D., Misra, C., Sempf, J., Wang, M., Oberley, T., Froines, J., & Nel, A. (2003) · Environmental Health Perspectives · doi:10.1289/ehp.6000 · Cited by 2,097
Self-citationPassage of inhaled particles into the blood circulation in humans
Nemmar, A., Hoet, P. H. M., Vanquickenborne, B., Dinsdale, D., Thomeer, M., Hoylaerts, M. F., Vanbilloen, H., Mortelmans, L., & Nemery, B. (2002) · Circulation · doi:10.1161/hc0402.104118 · Cited by 1,719
Role of Quinones in Toxicology
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McMahon, M., Itoh, K., Yamamoto, M., & Hayes, J. D. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300931200 · Cited by 1,141 · cited 2×
“Several models have been proposed to explain the escape of Nrf2 from Keap1-mediated repression (34, 36, 38, 56).”
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Self-citationStewart, D., Killeen, E., Naquin, R., Alam, S., & Alam, J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m209195200 · Cited by 463
Self-citationXiao, G. G., Wang, M., Li, N., Loo, J. A., & Nel, A. E. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m306423200 · Cited by 428
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Cited by
Air Pollution-Related Illness: Effects of Particles
Nel, A. (2005) · Science · doi:10.1126/science.1108752 · Cited by 1,544
Self-citationNrf2, a multi‐organ protector?
Lee, J., Li, J., Johnson, D. A., Stein, T. D., Kraft, A. D., Calkins, M. J., Jakel, R. J., & Johnson, J. A. (2005) · The FASEB Journal · doi:10.1096/fj.04-2591hyp · Cited by 532
Particulate matter and atherosclerosis: role of particle size, composition and oxidative stress
Araujo, J. A., & Nel, A. E. (2009) · Particle and Fibre Toxicology · doi:10.1186/1743-8977-6-24 · Cited by 435
Self-citationGilmour, M. I., Jaakkola, M. S., London, S. J., Nel, A. E., & Rogers, C. A. (2006) · Environmental Health Perspectives · doi:10.1289/ehp.8380 · Cited by 364
Self-citationMalhotra, D., Thimmulappa, R., Navas-Acien, A., Sandford, A., Elliott, M., Singh, A., Chen, L., Zhuang, X., Hogg, J., Pare, P., et al. (2008) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200803-380oc · Cited by 357
Retracted
Metadata
- Authors
- Li, N., Alam, J., Venkatesan, M. I., Eiguren-Fernandez, A., Schmitz, D., Di Stefano, E., Slaughter, N., Killeen, E., Wang, X., Huang, A., Wang, M., Miguel, A. H., Cho, A., Sioutas, C., & Nel, A. E.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-09-01
- Volume
- 173
- Issue
- 5
- Pages
- 3467-3481
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2142655750
- Cited by
- 456
- References
- 14
- FWCI
- 6.34
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Nrf2 Is a Key Transcription Factor That Regulates Antioxidant Defense in Macrophages and Epithelial Cells: Protecting against the Proinflammatory and Oxidizing Effects of Diesel Exhaust Chemicals. https://app.cochat.ai/papers/10.4049/jimmunol.173.5.3467
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- Li, N., Alam, J., Venkatesan, M. I., Eiguren-Fernandez, A., Schmitz, D., Di Stefano, E., Slaughter, N., Killeen, E., Wang, X., Huang, A., Wang, M., Miguel, A. H., Cho, A., Sioutas, C., & Nel, A. E. (2004). Nrf2 Is a Key Transcription Factor That Regulates Antioxidant Defense in Macrophages and Epithelial Cells: Protecting against the Proinflammatory and Oxidizing Effects of Diesel Exhaust Chemicals. The Journal of Immunology. https://doi.org/10.4049/jimmunol.173.5.3467
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
