ArticleInflammation2000
Activation of human neutrophils with chemotactic peptide, opsonized zymosan and the calcium ionophore A23187, but not with a phorbol ester, is accompanied by efflux and store-operated influx of calcium.
Article in Inflammation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Mitochondria-targeted antioxidant SkQ1 inhibits leukotriene synthesis in human neutrophils.Frontiers in pharmacology · 2022Article
- Studying Neutrophil Function in vitro: Cell Models and Environmental Factors.Journal of inflammation research · 2021Review
- 4C3 Human Monoclonal Antibody: A Proof of Concept for Non-pathogenic Proteinase 3 Anti-neutrophil Cytoplasmic Antibodies in Granulomatosis With Polyangiitis.Frontiers in immunology · 2020Article
- Neutrophil Extracellular Traps: New Aspects.Moscow University biological sciences bulletin · 2020Article
- Article
- A Critical Reappraisal of Neutrophil Extracellular Traps and NETosis Mimics Based on Differential Requirements for Protein Citrullination.Frontiers in immunology · 2016Article
- Regulation of superoxide production in neutrophils: role of calcium influx.Journal of leukocyte biology · 2008Review
- Itraconazole antagonizes store-operated influx of calcium into chemoattractant-activated human neutrophils.Clinical and experimental immunology · 2004Article
- Article
- Dissociation of the PAF-receptor from NADPH oxidase and adenylate cyclase in human neutrophils results in accelerated influx and delayed clearance of cytosolic calcium.British journal of pharmacology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to monitor alterations in cellular Ca2+ metabolism following activation of neutrophils with receptor- (chemotactic peptide, FMLP, 1 microM; opsonized zymosan, OZ, 0.5 mg/ml) and non-receptor (calcium ionophore, A23187, 1 microM; phorbol 12-myristate 13-acetate, PMA, 25 ng/ml)-mediated stimuli of the pro-inflammatory functions of these cells. Ca2+ fluxes in activated neutrophils were measured using a fura-2-based spectrofluorimetric method in combination with radiometric (45Ca) procedures which facilitate distinction between net efflux and net influx of the cation. Exposure of neutrophils to receptor-mediated stimuli and to A23187 was associated with an abrupt increase in cytosolic Ca2+ coincident with a rapid efflux of the cation which terminated at around 30 s. In the case of FMLP and OZ, this was followed by a delayed (30-60 s), store-operated influx of Ca2+, which was complete at around 5 min after addition of the stimulus. With A23187, however, influx of Ca2+ occurred immediately following activation of the cells. There were no detectable alterations in cytosolic Ca2+ or measurable net efflux or influx of the cation above control levels in PMA-activated neutrophils. These data demonstrate that FMLP, OZ- and A23187-mediated alterations in neutrophil cytosolic Ca2+ are due to mobilization of both intracellular and extracellular cation, while activation of neutrophils by PMA is independent of alterations in cytosolic Ca2+.
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