Exclusive expression of the Gs‐linked prostaglandin E<sub>2</sub> receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells

Blaschke, Volker; Jungermann, Kurt; Püschel, Gerhard

doi:10.1016/0014-5793(96)00928-3

Cited by 39 publications

(27 citation statements)

References 30 publications

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“…Butaprost had no effect on [cAMP] i , suggesting EP2 receptors are not present on Jurkat cells. This is in accordance with earlier findings in which the EP2 receptor was undetectable on Jurkat cells by RT-PCR (48). The fact that the EP1/EP3 agonist 17-P-T-PGE 2 raised [cAMP] i at a dose of 1 M confirms the hypothesis that at high doses, this agonist activates the EP4 receptor, because in human cells EP1 and EP3 receptors do not classically couple to increases in [cAMP] i (49,50).…”

Section: Discussionsupporting

confidence: 92%

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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 Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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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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Section: Discussionsupporting

confidence: 92%

“…The EP4 receptor has been previously described on Jurkat cells by RT-PCR (48) and flow cytometric analysis (56). To our knowledge, we are the first to describe PGE 2 effects through EP3 on Jurkat cells.…”

Section: Discussionmentioning

confidence: 83%

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 Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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“…3A). Consistent with these observations, both AH6809 -an antagonist of EP1, EP2 and EP3 (Abramovitz et al, 2000) -and AH23848, which selectively blocks EP4 (Blaschke et al, 1996), alone had no effect on the amount of cells displaying podosomes, whereas they effectively interfered with PGE 2 -induced podosome dissolution (Fig. 3B).…”

Section: Resultssupporting

confidence: 77%

PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA–Rho-kinase axis

Helden

Oud

Joosten

et al. 2008

Journal of Cell Science

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Podosomes are dynamic adhesion structures found in dendritic cells (DCs) and other cells of the myeloid lineage. We previously showed that prostaglandin E2 (PGE 2 ), an important proinflammatory mediator produced during DC maturation, induces podosome disassembly within minutes after stimulation. Here, we demonstrate that this response is mediated by cAMP elevation, occurs downstream of Rho kinase and is dependent on myosin II. Whereas PGE 2 stimulation leads to activation of the small GTPase RhoA, decreased levels of Rac1-GTP and Cdc42-GTP are observed. These results show that PGE 2 stimulation leads to activation of the RhoA-Rho-kinase axis to promote actomyosin-based contraction and subsequent podosome dissolution. Because podosome disassembly is accompanied by de novo formation of focal adhesions, we propose that the disassembly/formation of these two different adhesion structures is oppositely regulated by actomyosin contractility and relative activities of RhoA, Rac1 and Cdc42.Supplementary material available online at

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“…Multiple subtypes of the PGE 2 receptor are expressed in cilary epithelial cells (48), osteoblastic cells (49), kerotinocytes (50), fibroblasts (23), and platelets (51). Furthermore, human Jurkat cells express both EP2 and EP4 receptors; however, the expression of EP2 receptor is ϳ100-fold lower than that of EP4 receptors (52). In these cells, the EP4 receptors are the primary receptor subtype mediating the PGE 2 -induced increase in cAMP, whereas EP2 receptors appear to have little or no functional role in PGE 2 -induced cAMP production (52).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, human Jurkat cells express both EP2 and EP4 receptors; however, the expression of EP2 receptor is ϳ100-fold lower than that of EP4 receptors (52). In these cells, the EP4 receptors are the primary receptor subtype mediating the PGE 2 -induced increase in cAMP, whereas EP2 receptors appear to have little or no functional role in PGE 2 -induced cAMP production (52). An analogous situation might exist in sensory neurons.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin Receptor Subtypes, EP3C and EP4, Mediate the Prostaglandin E2-induced cAMP Production and Sensitization of Sensory Neurons

Southall¹,

Vasko

2001

Journal of Biological Chemistry

167

150

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Although a number of prostaglandin E 2 (PGE 2 ) receptor subtypes have been cloned, limited studies have been performed to elucidate subtypes that subserve specific actions of this eicosanoid, in part because of a paucity of selective receptor antagonists. Using reverse transcription-polymerase chain reaction (PCR) and antisense oligonucleotides, we examined which prostaglandin E 2 receptor (EP receptor) subtypes are expressed in sensory neurons and which mediate the PGE 2 -induced increase in cAMP production and augmentation of peptide release. Reverse transcription-PCR of cDNA isolated from rat sensory neurons grown in culture revealed PCR products for the EP1, EP2, EP3C, and EP4 receptor subtypes but not the EP3A or EP3B. Preexposing neuronal cultures for 48 h to antisense oligonucleotides of EP3C and EP4 mRNA diminished expression of the respective receptors by ϳ80%, abolished the PGE 2 -stimulated production of cAMP, and blocked the ability of PGE 2 to augment release of immunoreactive substance P and calcitonin gene-related peptide. Pretreating with individual antisense against the EP2, EP3C, or EP4 receptors or combinations of missense oligonucleotides had no effect on PGE 2 -induced activity. Treatment with antisense to EP3C and EP4 receptor subtypes did not alter the ability of forskolin to increase cAMP or enhance peptide release. These results demonstrate that sensory neurons are capable of expressing multiple EP receptor subtypes but that only the EP3C and EP4 receptors mediate PGE 2 -induced sensitization of sensory neurons. Prostaglandin E 2 receptors (EP receptors)1 have been classified into four general subtypes, EP1, EP2, EP3, and EP4, based on cloning and pharmacological manipulations (1, 2). These receptors are G-protein-coupled, and binding of agonists results in activation of various transduction cascades depending on the receptor subtype activated and the cells being studied. Activation of the EP1 receptor in kidney tubule cells increases the concentration of intracellular calcium, phosphoinositol turnover, and PKC activity (3, 4). EP2 and EP4 receptors are coupled through G s (1) to increase intracellular cAMP in a number of preparations (5-8). The EP3 receptor undergoes post-transcriptional RNA splicing to produce multiple EP3 isoforms, and activation of these splice variants can increase calcium mobilization or either stimulate or inhibit cAMP production (9 -11). Because subtypes of the EP receptor can be linked to different transduction cascades in different types of cells, it is critical to determine which receptors and receptorassociated signal transduction pathways are responsible for specific physiological actions of E-series prostaglandins.Although PGE 2 has a number of diverse physiological actions (12), its role in pain and inflammation is of primary importance. Indeed, both the analgesic and the anti-inflammatory actions of the nonsteroidal anti-inflammatory drugs are attributed to their ability to inhibit prostaglandin synthesis (13). In addition, PGE 2 is produced at sites of ...

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Exclusive expression of the Gs‐linked prostaglandin E₂ receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells

Cited by 39 publications

References 30 publications

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 Pathways

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 Pathways

PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA–Rho-kinase axis

Prostaglandin Receptor Subtypes, EP3C and EP4, Mediate the Prostaglandin E2-induced cAMP Production and Sensitization of Sensory Neurons

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Exclusive expression of the Gs‐linked prostaglandin E2 receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells

Cited by 39 publications

References 30 publications

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 Pathways

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 Pathways

PGE2-mediated podosome loss in dendritic cells is dependent on actomyosin contraction downstream of the RhoA–Rho-kinase axis

Prostaglandin Receptor Subtypes, EP3C and EP4, Mediate the Prostaglandin E2-induced cAMP Production and Sensitization of Sensory Neurons

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Exclusive expression of the Gs‐linked prostaglandin E₂ receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells