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Prostaglandins E 1 and E 2 enhance the stimulation of superoxide release by 1‐oleoyl‐2‐acetylglycerol from human neutrophils
Author(s) -
Penfield Adrienne,
Dale M.Maureen
Publication year - 1985
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(85)80287-8
Subject(s) - superoxide , protein kinase c , phorbol , stimulation , chemistry , ionophore , prostaglandin e2 , n formylmethionine leucyl phenylalanine , staurosporine , prostaglandin e , calcium , endocrinology , receptor , signal transduction , medicine , microbiology and biotechnology , biochemistry , biology , enzyme , organic chemistry
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 E 1 (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 E 2 .