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Mechanism of Prostaglandin (PG)E₂-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE₂ Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5'-Monophosphate-Mediated Signaling Pathways¹

Sarah Gerlo^2,*, Peggy Verdood^*, Birgit Gellersen, Elisabeth L. Hooghe-Peters^* and Ron Kooijman^*

^* Laboratory of Neuroendocrine Immunology, Department of Pharmacology, Free University of Brussels, Brussels, Belgium; and Endokrinologikum Hamburg, Hamburg, Germany

We previously reported that prolactin gene expression in the T-leukemic cell line Jurkat is stimulated by PGE₂ and that cAMP acts synergistically with Ca²⁺ or protein kinase C on the activation of the upstream prolactin promoter. Using the transcription inhibitor actinomycin D, we now show that PGE₂-induced prolactin expression requires de novo prolactin mRNA synthesis and that PGE₂ does not influence prolactin mRNA stability. Furthermore, PGE₂-induced prolactin expression was inhibited by protein kinase inhibitor fragment 14–22 and BAPTA-AM, which respectively, inhibit protein kinase A- and Ca²⁺-mediated signaling cascades. Using specific PGE₂ receptor agonists and antagonists, we show that PGE₂ induces prolactin expression through engagement of E-prostanoid (EP) 3 and EP4 receptors. We also found that PGE₂ induces an increase in intracellular cAMP concentration as well as intracellular calcium concentration via EP4 and EP3 receptors, respectively. In transient transfections, 3000 bp flanking the leukocyte prolactin promoter conferred a weak induction of the luciferase reporter gene by PGE₂ and cAMP, whereas cAMP in synergy with ionomycin strongly activated the promoter. Mutation of a C/EBP responsive element at –214 partially abolished the response of the leukocyte prolactin promoter to PGE₂, cAMP, and ionomycin plus cAMP.

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