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Exclusive expression of the Gs‐linked prostaglandin E 2 receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells
Author(s) -
Blaschke Volker,
Jungermann Kurt,
Püschel Gerhard P.
Publication year - 1996
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(96)00928-3
Subject(s) - jurkat cells , prostaglandin e2 receptor , receptor , microbiology and biotechnology , biology , peripheral blood mononuclear cell , prostaglandin , prostaglandin e2 , cell culture , t cell , immune system , immunology , endocrinology , biochemistry , in vitro , genetics , agonist
Prostaglandin E 2 (PGE 2 ) is regarded as a potent regulator of the immune system. It can regulate apoptosis in monunuclear cells and modulate the cytokine secretion pattern from T‐helper cell subpopulations via an increase in cyclic AMP (cAMP). Of the 4 PGE 2 receptor subtypes (EP1–EP4) that are defined pharmacologically by their affinity to subtype‐specific ligands and their coupling to G proteins, EP2 and EP4 receptors couple to Gs. It is as yet unknown which of these two receptor subtypes mediates the immunomodulatory effects. By quantitative RT‐PCR, the mRNA for EP4 receptors was demonstrated and quantified in the human mononuclear cell lines Jurkat, KM‐3 and U‐937. However, EP2 receptor mRNA was only present in U‐937 cells and was 100‐fold less abundant than EP 4 receptor mRNA. PGE 2 increased cAMP formation with an ED 50 of 50–100 nM in all cell lines. cAMP formation was inhibited by the EP4R‐specific antagonist AH23848. Since AH23848 inhibited PGE 2 ‐induced cAMP formation in U‐937 cells to a similar extent as in Jurkat and KM‐3, EP2 receptors seem to play, if any, only a secondary role for the PGE 2 ‐mediated cAMP formation in U‐937 cells.