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Mitochondrial-Derived Oxidants and Quartz Activation of Chemokine Gene Expression
Abstract
Macrophage inflammatory protein 2 (MIP-2) is a chemotactic cytokine which mediates neutrophil recruitment in the lung and other tissues. Pneumotoxic particles such as quartz increase MIP-2 expression in rat lung and rat alveolar type II epithelial cells. Deletion mutant analysis of the rat MIP-2 promoter demonstrated quartz-induction depended on a single NFkappaB consensus binding site. Quartz activation of NFkappaB and MIP-2 gene expression in RLE-6TN cells was inhibited by anti-oxidants suggesting the responses were dependent on oxidative stress. Consistent with anti-oxidant effects, quartz was demonstrated to increase RLE-6TN cell production of hydrogen peroxide. Rotenone treatment of RLE-6TN cells attenuated hydrogen peroxide production, NFkappaB activation and MIP-2 gene expression induced by quartz indicating that mitochondria-derived oxidants were contributing to these responses. Collectively, these findings indicate that quartz and crocidolite induction of MIP-2 gene expression in rat alveolar type II cells results from stimulation of an intracellular signaling pathway involving increased generation of hydrogen peroxide by mitochondria and subsequent activation of NFkappaB.
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“The decade between 2001 and 2010 was also very productive especially in elucidating the importance of surface properties of particles and fibres and their variability in relation to their biological effects [391–404].”
From Particle toxicology and health - where are we? (2019) · cites this paper as [400]
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Metadata
- Authors
- Driscoll, K. E., Howard, B. W., Carter, J. M., Janssen, Y. M. W., Mossman, B. T., & Isfort, R. J.
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer US
- Published
- 2001
- Pages
- 489-496
- ISSN
- 0065-2598
- Cited by
- 41
- References
- 0
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