HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gerlo, S. Articles by Kooijman, R. Search for Related Content PubMed PubMed Citation Articles by Gerlo, S. Articles by Kooijman, R.

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.

This article has been cited by other articles:

				N. Ben-Jonathan, C. R. LaPensee, and E. W. LaPensee What Can We Learn from Rodents about Prolactin in Humans? Endocr. Rev., February 1, 2008; 29(1): 1 - 41. [Abstract] [Full Text] [PDF]

				G. Elberg, D. Elberg, T. V. Lewis, S. Guruswamy, L. Chen, C. J. Logan, M. D. Chan, and M. A. Turman EP2 receptor mediates PGE2-induced cystogenesis of human renal epithelial cells Am J Physiol Renal Physiol, November 1, 2007; 293(5): F1622 - F1632. [Abstract] [Full Text] [PDF]

				J. M. Chemnitz, J. Driesen, S. Classen, J. L. Riley, S. Debey, M. Beyer, A. Popov, T. Zander, and J. L. Schultze Prostaglandin E2 Impairs CD4+ T Cell Activation by Inhibition of lck: Implications in Hodgkin's Lymphoma Cancer Res., January 15, 2006; 66(2): 1114 - 1122. [Abstract] [Full Text] [PDF]