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Actions of calcium influx blockers in human neutrophils support a role for receptor-operated calcium entry

The action of two potent store operated Ca 2+ entry (SOCE) inhibitors, ML-9 and GdCl 3 on Ca 2+ fluxes induced by the pro-inflammatory agonists FMLP, PAF, LTB 4 as well as the receptor-independent stimulus thapsigargin has not been documented in human neutrophils. In this study, ML-9 enhanced both r...

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Published in:Cellular immunology 2010, Vol.262 (1), p.6-10
Main Authors: Salmon, Michael D., Ahluwalia, Jatinder
Format: Article
Language:English
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Summary:The action of two potent store operated Ca 2+ entry (SOCE) inhibitors, ML-9 and GdCl 3 on Ca 2+ fluxes induced by the pro-inflammatory agonists FMLP, PAF, LTB 4 as well as the receptor-independent stimulus thapsigargin has not been documented in human neutrophils. In this study, ML-9 enhanced both release and subsequent Ca 2+ influx in response to agonists whereas it enhanced Ca 2+ release by thapsigargin, but inhibited Ca 2+ influx. In contrast, 1 μM GdCl 3 completely inhibited Ca 2+ influx in response to thapsigargin, but only partially blocked Ca 2+ influx after agonist stimulation. These results strongly suggest a major role for receptor-operated Ca 2+ influx in human neutrophils.
ISSN:0008-8749
1090-2163
DOI:10.1016/j.cellimm.2010.02.001