Prostaglandins E1 and E2 enhance the stimulation of superoxide release by 1‐oleoyl‐2‐acetylglycerol from human neutrophils

Superoxide release from human neutrophils was stimulated either by receptor activation (using fMet‐Leu‐Phe) or by activating, independently, each of the two pathways considered to be involved in signal transduction‐calcium mobilization (using the ionophore, A23187) and protein kinase C activation (u...

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Bibliographic Details
Published in:FEBS letters 1985-02, Vol.181 (2), p.335-338
Main Authors: Penfield, Adrienne, Dale, M.Maureen
Format: Article
Language:English
Subjects:
Alprostadil
Biological and medical sciences
Calcimycin - pharmacology
Cell metabolism, cell oxidation
Cell physiology
DAG, diacylglycerol
Diglycerides - pharmacology
Dinoprostone
Enzyme Activation
fMet-Leu-Phe
Fundamental and applied biological sciences. Psychology
Glycerides - pharmacology
Humans
Molecular and cellular biology
N-Formylmethionine Leucyl-Phenylalanine - pharmacology
Neutrophil
Neutrophils - drug effects
Neutrophils - metabolism
OAG, 1-oleoyl-2-acetylglycerol
PGE1, prostaglandin E1
Phorbol ester
Phosphatidylinositol
PMA, phorbol myristate acetate
Prostaglandin E
Prostaglandins E - pharmacology
Protein Kinase C
Protein Kinases - metabolism
Superoxides - blood
Tetradecanoylphorbol Acetate - pharmacology
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Summary:Superoxide release from human neutrophils was stimulated either by receptor activation (using fMet‐Leu‐Phe) or by activating, independently, each of the two pathways considered to be involved in signal transduction‐calcium mobilization (using the ionophore, A23187) and protein kinase C activation (using phorbol myristate acetate or 1‐oleoyl‐2‐acetylglycerol). Prostaglandin E1 (3 × 10−5 M) decreased fMet‐Leu‐Phe‐stimulated superoxide release, had no effect on superoxide release stimulated by A23187, or by phorbol myristate acetate, and markedly enhanced the superoxide release stimulated by 1‐oleoyl‐2‐acetylglycerol. Similar enhancement was obtained with prostaglandin E2.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(85)80287-8