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Evidence for a Common Mechanism of Action of Interleukin‐1β, Tumor Necrosis Factor‐α, and Epidermal Growth Factor on Prostaglandin Production in Human Chorion Cells
Author(s) -
POLLARD J.K.,
THAI D.,
MITCHELL M.D.
Publication year - 1993
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1993.tb00615.x
Subject(s) - cycloheximide , epidermal growth factor , endocrinology , prostaglandin e2 , prostaglandin , medicine , tumor necrosis factor alpha , arachidonic acid , prostaglandin e , stimulation , cytokine , biology , interleukin , mechanism of action , protein biosynthesis , biochemistry , receptor , enzyme , in vitro
PROBLEM: Although chorion produces prostaglandins in response to interleukin‐1β (IL‐1β), tumor necrosis factor alpha (TNFβ), and epidermal growth factor (EGF), little attention has been given to the mechanisms of action of prostaglandin biosynthesis in this tissue. METHODS: IL‐1β, TNFβ, and EGF induced a concentration‐related stimulation of prostaglandin E 2 (PGE 2 ) biosynthesis in human chorion cells, and this stimulation was enhanced by the addition of exogenous arachidonic acid. RESULTS: Protein synthesis inhibition with cycloheximide or actinomycin D resulted in complete abrogation of the stimulation of PGE 2 production by IL‐1β, TNFα, and EGF. Finally, all three stimulants induced a more rapid recovery of PGE 2 production in chorion cells after ace‐tylsalicylic acid pretreatment than controls. CONCLUSIONS: It is suggested that IL‐1β, TNFα, and EGF all act to stimulate human chorion PGE 2 production primarily via induction of prostaglandin endoperoxide synthase activity.