ArticleBritish journal of pharmacology1995
NPC 15669-modulated human polymorphonuclear neutrophil functional responsiveness: effects on receptor-coupled signal transduction.
Article in British journal of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 13 citations in OpenAlex.
- Age-related changes in membrane lipid composition, fluidity and respiratory burst in rat peritoneal neutrophils.Clinical and experimental immunology · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effect of NPC 15669, N-carboxy-L-leucine, N-[(2,7-dimethylfluoren-9-yl)methyl]ester), an inhibitor of human polymorphonuclear neutrophil (PMN) adhesion, on granule exocytosis and the oxidative burst was investigated in PMN activated with receptor-specific pathophysiological stimuli. 2. NPC 15669 caused a concentration-dependent (1-30 microM) inhibition of the extracellular release of azurophil (myeloperoxidase) and specific (vitamin B12-binding protein) granule constitutents from PMN exposed to N-formyl-methionyl-leucyl-phenylalanine (FMLP), leukotriene B4 (LTB4), platelet activating factor (PAF), C5a and interleukin-8 (IL-8). 3. The receptor agonist-triggered PMN oxidative burst, measured as superoxide anion (O2-) production, was suppressed by NPC 15669. 4. Phorbol myristate acetate (PMA)-stimulated degranulation and O2-) production were unaffected by NPC 15669. 5. NPC 15669 (0.1-10 microM) inhibited receptor-triggered inositol 1,4,5-trisphosphate (IP3) production and the IP3-triggered increase in cytosolic-free calcium ([Ca2+]i) in FMLP-activated PMN, but not in cells exposed to the other receptor agonists. 6. NPC 15669 suppressed FMLP but not PMA-stimulated redistribution of protein kinase C (PKC) in PMN. 7. The specific binding of [3H]-FMLP but not [125I]-C5a to PMN was inhibited by NPC 15669. 8. NPC 15669 suppressed O2- production and the rise in [Ca2+]i in PMN treated with the guanine nucleotide-binding protein (G-protein) activators, sodium fluoride (NaF) and mastoparan, respectively. 9. The results show that NPC 15669 inhibits PMN responsiveness to various receptor agonists, and suggest interference with receptor-coupled signal transduction in this inflammatory cell at both the receptor and post-receptor level in a stimulus-specific manner.
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