The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Kinetics and Mechanism of ATP-Dependent IL-1β Release from Microglial Cells
Abstract
Endotoxin-dependent release of IL-1β from mouse microglial cells is a very inefficient process, as it is slow and leads to accumulation of a modest amount of extracellular cytokine. Furthermore, secreted IL-1β is mostly in the procytokine unprocessed form. Addition of extracellular ATP to LPS-primed microglia caused a burst of release of a large amount of processed IL-1β. ATP had no effect on the accumulation of intracellular pro-IL-1β in the absence of LPS. In LPS-treated cells, ATP slightly increased the synthesis of pro-IL-1β. Optimal ATP concentration for IL-1β secretion was between 3 and 5 mM, but significant release could be observed at concentrations as low as 1 mM. At all ATP concentrations IL-1β release could be inhibited by increasing the extracellular K+ concentration. ATP-dependent IL-1β release was also inhibited by 90 and 60% by the caspase inhibitors YVAD and DEVD, respectively. Accordingly, in ATP-stimulated microglia, the p20 proteolytic fragment derived from activation of the IL-1-β-converting enzyme could be detected by immunoblot analysis. These experiments show that in mouse microglial cells extracellular ATP triggers fast maturation and release of intracellularly accumulated IL-β by activating the IL-1-β-converting enzyme/caspase 1.
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Cites
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Cited by
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The P2X7 Receptor: A Key Player in IL-1 Processing and Release
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Metadata
- Authors
- Sanz, J. M., & Virgilio, F. D.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-05-01
- Volume
- 164
- Issue
- 9
- Pages
- 4893-4898
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1886167013
- Cited by
- 273
- References
- 37
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- closed
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- Sanz, J. M., & Virgilio, F. D. (2000). Kinetics and Mechanism of ATP-Dependent IL-1β Release from Microglial Cells. The Journal of Immunology. https://doi.org/10.4049/jimmunol.164.9.4893
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