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Journal articles on the topic 'Prostaglandin E receptor EP2'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Breyer, Matthew D., and Richard M. Breyer. "Prostaglandin E receptors and the kidney." American Journal of Physiology-Renal Physiology 279, no. 1 (2000): F12—F23. http://dx.doi.org/10.1152/ajprenal.2000.279.1.f12.

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Prostaglandin E2 is a major renal cyclooxygenase metabolite of arachidonate and interacts with four G protein-coupled E-prostanoid receptors designated EP1, EP2, EP3, and EP4. Through these receptors, PGE2modulates renal hemodynamics and salt and water excretion. The intrarenal distribution and function of EP receptors have been partially characterized, and each receptor has a distinct role. EP1 expression predominates in the collecting duct where it inhibits Na+ absorption, contributing to natriuresis. The EP2 receptor regulates vascular reactivity, and EP2 receptor-knockout mice have salt-se

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2

Patwardhan, A. M., J. Vela, J. Farugia, K. Vela, and K. M. Hargreaves. "Trigeminal Nociceptors Express Prostaglandin Receptors." Journal of Dental Research 87, no. 3 (2008): 262–66. http://dx.doi.org/10.1177/154405910808700306.

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Orofacial inflammation is associated with prostaglandin release and the sensitization of nociceptive receptors such as the transient receptor potential subtype V1 (TRPV1). We hypothesized that certain PGE2 receptor subtypes (EP1–EP4) are co-expressed with TRPV1 in trigeminal nociceptors and sensitize responses to a TRPV1 agonist, capsaicin. Accordingly, combined in situ hybridization was performed with immunohistochemistry on rat trigeminal ganglia. We next evaluated the effects of specific EP2 and EP3 agonists (butaprost and sulprostone) in cultured trigeminal ganglia neurons. The results sho

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Zahner, Gunther, Melanie Schaper, Ulf Panzer, et al. "Prostaglandin EP2 and EP4 receptors modulate expression of the chemokine CCL2 (MCP-1) in response to LPS-induced renal glomerular inflammation." Biochemical Journal 422, no. 3 (2009): 563–70. http://dx.doi.org/10.1042/bj20090420.

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The pro-inflammatory chemokine CCL2 [chemokine (Cys-Cys motif) ligand 2; also known as MCP-1 (monocyte chemotactic protein-1)] is up-regulated in the glomerular compartment during the early phase of LPS (lipopolysaccharide)-induced nephritis. This up-regulation also occurs in cultured MCs (mesangial cells) and is more pronounced in MCs lacking the PGE2 (prostaglandin E2) receptor EP2 or in MCs treated with a prostaglandin EP4 receptor antagonist. To examine a possible feedback mechanism of EP receptor stimulation on CCL2 expression, we used an in vitro model of MCs with down-regulated EP recep

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BEK, MARTIN, ROLF NÜSING, PASCAL KOWARK, ANNA HENGER, PETER MUNDEL, and HERMANN PAVENSTÄDT. "Characterization of Prostanoid Receptors in Podocytes." Journal of the American Society of Nephrology 10, no. 10 (1999): 2084–93. http://dx.doi.org/10.1681/asn.v10102084.

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Abstract. Prostaglandins participate in the regulation of important glomerular functions and are involved in the pathogenesis of glomerular diseases. This study investigates the influence of prostaglandins on membrane voltage, ion conductances, cAMP accumulation, and cytosolic calcium activity ([Ca2+]i) in differentiated podocytes. Prostaglandin E2 (PGE2) caused a concentration-dependent depolarization and an increase of the whole cell conductance in podocytes (EC50 ≈ 50 nM). Compared with PGE2, the EP2/EP3/EP4 receptor agonist 11-deoxy-PGE1 caused an equipotent depolarization, whereas the DP

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Imig, John D., Matthew D. Breyer, and Richard M. Breyer. "Contribution of prostaglandin EP2 receptors to renal microvascular reactivity in mice." American Journal of Physiology-Renal Physiology 283, no. 3 (2002): F415—F422. http://dx.doi.org/10.1152/ajprenal.00351.2001.

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The present studies were performed to determine the contribution of EP2 receptors to renal hemodynamics by examining afferent arteriolar responses to PGE2, butaprost, sulprostone, and endothelin-1 in EP2 receptor-deficient male mice (EP2−/−). Afferent arteriolar diameters averaged 17.8 ± 0.8 μm in wild-type (EP2+/+) mice and 16.7 ± 0.7 μm in EP2−/− mice at a renal perfusion pressure of 100 mmHg. Vessels from both groups of mice responded to norepinephrine (0.5 μM) with similar 17–19% decreases in diameter. Diameters of norepinephrine-preconstricted afferent arterioles increased by 7 ± 2 and 20

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6

Hayashi, Yoshinori, Saori Morinaga, Xia Liu, et al. "An EP2 Agonist Facilitates NMDA-Induced Outward Currents and Inhibits Dendritic Beading through Activation of BK Channels in Mouse Cortical Neurons." Mediators of Inflammation 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/5079597.

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Prostaglandin E2(PGE2), a major metabolite of arachidonic acid produced by cyclooxygenase pathways, exerts its bioactive responses by activating four E-prostanoid receptor subtypes, EP1, EP2, EP3, and EP4. PGE2enables modulatingN-methyl-D-aspartate (NMDA) receptor-mediated responses. However, the effect of E-prostanoid receptor agonists on large-conductance Ca2+-activated K+(BK) channels, which are functionally coupled with NMDA receptors, remains unclear. Here, we showed that EP2 receptor-mediated signaling pathways increased NMDA-induced outward currents (INMDA-OUT), which are associated wit

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Tilley, Stephen L., John M. Hartney, Christopher J. Erikson, et al. "Receptors and pathways mediating the effects of prostaglandin E2 on airway tone." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 4 (2003): L599—L606. http://dx.doi.org/10.1152/ajplung.00324.2002.

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Prostaglandin E2(PGE2) has complex effects on airway tone, and the existence of four PGE2 [E-prostanoid (EP)] receptors, each with distinct signaling characteristics, has provided a possible explanation for the seemingly contradictory actions of this lipid mediator. To identify the receptors mediating the actions of PGE2 on bronchomotor tone, we examined its effects on the airways of wild-type and EP receptor-deficient mice. In conscious mice the administration of PGE2 increased airway responsiveness primarily through the EP1 receptor, although on certain genetic backgrounds a contribution of

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8

Breyer, M. D., L. Davis, H. R. Jacobson, and R. M. Breyer. "Differential localization of prostaglandin E receptor subtypes in human kidney." American Journal of Physiology-Renal Physiology 270, no. 5 (1996): F912—F918. http://dx.doi.org/10.1152/ajprenal.1996.270.5.f912.

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Four prostaglandin E2 (PGE2) receptors designated EP1, EP2, EP3, and EP4 have been pharmacologically identified, cloned, and sequenced. The present studies determined the intrarenal distribution of these EP-receptor subtypes in human kidney using in situ hybridization with riboprobes for the human EP receptors. mRNA for the phosphatidylinositol hydrolysis-coupled EP receptor was highly expressed in cortical, outer medullary, and inner medullary collecting duct. RNA for the Gi-coupled EP3 receptor was primarily expressed in the cortical and outer medullary collecting duct, as well as in the med

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9

Schweda, Frank, Jürgen Klar, Shuh Narumiya, Rolf M. Nüsing, and Armin Kurtz. "Stimulation of renin release by prostaglandin E2 is mediated by EP2 and EP4 receptors in mouse kidneys." American Journal of Physiology-Renal Physiology 287, no. 3 (2004): F427—F433. http://dx.doi.org/10.1152/ajprenal.00072.2004.

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PGE2 is a potent stimulator of renin release. So far, the contribution of each of the four PGE2 receptor subtypes (EP1–EP4) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP1−/−, EP2−/−, EP3−/−, EP4−/−, and wild-type mice. PGE2 concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP1−/−, EP2−/−, EP3−/−, and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP4−/− mice. More

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10

Jadhav, Vikram, Anthony Jabre, Shinn-Zong Lin, and Tony Jer-Fu Lee. "EP1- and EP3-Receptors Mediate Prostaglandin E2–Induced Constriction of Porcine Large Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 24, no. 12 (2004): 1305–16. http://dx.doi.org/10.1097/01.wcb.0000139446.61789.14.

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Prostaglandin E2 (PGE2) has been shown to dilate and constrict the systemic vascular beds, including cerebral vessels. The exact mechanism of PGE2-induced cerebral vasoconstriction, however, is less clarified. The authors' preliminary studies showed that PGE2 exclusively constricted the adult porcine basilar arteries. The present study, therefore, was designed to examine the receptor mechanisms involved in PGE2-induced constriction of large cerebral arteries in the adult pig. Results from an in vitro tissue-bath study indicated that PGE2 and its agonists 17-phenyl trinor PGE2 (17-PGE2), sulpro

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Ye, Yao, Peng Lin, Junyan Zhu, Udo Jeschke, and Viktoria von Schönfeldt. "Multiple Roles of Prostaglandin E2 Receptors in Female Reproduction." Endocrines 1, no. 1 (2020): 22–34. http://dx.doi.org/10.3390/endocrines1010003.

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Among prostaglandins, Prostaglandin E2 (PGE2) (PGE2) is considered especially important for decidualization, ovulation, implantation and pregnancy. Four major PGE2 receptor subtypes, EP1, EP2, EP3, EP4, as well as peroxisome proliferator-activated receptors (PPARs), mediate various PGE2 effects via their coupling to distinct signaling pathways. This review summarizes up-to-date literatures on the role of prostaglandin E2 receptors in female reproduction, which could provide a broad perspective to guide further research in this field. PGE2 plays an indispensable role in decidualization, ovulati

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Jiang, Jianxiong, Thota Ganesh, Yuhong Du, et al. "Neuroprotection by selective allosteric potentiators of the EP2 prostaglandin receptor." Proceedings of the National Academy of Sciences 107, no. 5 (2010): 2307–12. http://dx.doi.org/10.1073/pnas.0909310107.

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Activation of the Gαs-coupled EP2 receptor for prostaglandin E2 (PGE2) promotes cell survival in several models of tissue damage. To advance understanding of EP2 functions, we designed experiments to develop allosteric potentiators of this key prostaglandin receptor. Screens of 292,000 compounds identified 93 that at 20 μM (i) potentiated the cAMP response to a low concentration of PGE2 by > 50%; (ii) had no effect on EP4 or β2 adrenergic receptors, the cAMP assay itself, or the parent cell line; and (iii) increased the potency of PGE2 on EP2 receptors at least 3-fold. In aqueous solution,

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Mukherjee, Subhendu, Wei Sheng, Alexander Michkov, et al. "Prostaglandin E2 inhibits profibrotic function of human pulmonary fibroblasts by disrupting Ca2+ signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 316, no. 5 (2019): L810—L821. http://dx.doi.org/10.1152/ajplung.00403.2018.

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We have shown that calcium (Ca2+) oscillations in human pulmonary fibroblasts (HPFs) contribute to profibrotic effects of transforming growth factor-β (TGF-β) and that disruption of these oscillations blunts features of pulmonary fibrosis. Prostaglandin E2 (PGE2) exerts antifibrotic effects in the lung, but the mechanisms for this action are not well defined. We thus sought to explore interactions between PGE2 and the profibrotic agent TGF-β in pulmonary fibroblasts (PFs) isolated from patients with or without idiopathic pulmonary fibrosis (IPF). PGE2 inhibited TGF-β-promoted [Ca2+] oscillatio

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Li, Xiaodong, Yosuke Okada, Carol C. Pilbeam, et al. "Knockout of the Murine Prostaglandin EP2 Receptor Impairs Osteoclastogenesis in Vitro*." Endocrinology 141, no. 6 (2000): 2054–61. http://dx.doi.org/10.1210/endo.141.6.7518.

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Abstract Prostaglandin E2 (PGE2) stimulates the formation of osteoclast-like tartrate-resistant acid phosphatase-positive multinucleated cells (TRAP + MNC) in vitro. This effect likely results from stimulation of adenylyl cyclase, which is mediated by two PGE2 receptors, designated EP2 and EP4. We used cells from mice in which the EP2 receptor had been disrupted to test its role in the formation of TRAP + MNC. EP2 heterozygous (±) mice in a C57BL/6 x 129/SvEv background were bred to produce homozygous null (EP2 −/−) and wild-type (EP2 +/+) mice. PGE2, PTH, or 1,25 dihydroxyvitamin D increased

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15

Matsuoka, Toshiyuki, and Shuh Narumiya. "Prostaglandin Receptor Signaling in Disease." Scientific World JOURNAL 7 (2007): 1329–47. http://dx.doi.org/10.1100/tsw.2007.182.

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Prostanoids, consisting of the prostaglandins (PGs) and the thromboxanes (TXs), are a group of lipid mediators formed in response to various stimuli. They include PGD2, PGE2, PGF2α, PGI2, and TXA2. They are released outside of the cells immediately after synthesis, and exert their actions by binding to a G-protein coupled rhodopsin-type receptor on the surface of target cells. There are eight types of the prostanoid receptors conserved in mammals from mouse to human. They are the PGD receptor (DP), four subtypes of the PGE receptor (EP1, EP2, EP3, and EP4), the PGF receptor (FP), PGI receptor

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16

Oka, T., and T. Hori. "EP1-receptor mediation of prostaglandin E2-induced hyperthermia in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (1994): R289—R294. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r289.

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To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E2 (PGE2), PGE2 and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (Tco) were observed in a 23 +/- 1 degrees C environment. 17-Phenyl-omega-trinor-PGE2 (an EP1 agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in Tco. Even though the EP1 agonist was 10 times less potent than PGE2 on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE2-induced one. No fever wa

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Breyer, M. D., H. R. Jacobson, and R. M. Breyer. "Functional and molecular aspects of renal prostaglandin receptors." Journal of the American Society of Nephrology 7, no. 1 (1996): 8–17. http://dx.doi.org/10.1681/asn.v718.

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The diverse intrarenal effects of the prostaglandins (PG) are mediated by distinct guanine nucleotide regulatory protein (G-protein)-coupled receptors. The cDNA for these receptors have been cloned, their signal transduction mechanisms determined, and their intrarenal distribution mapped. PGE2, the major intrarenal prostaglandin, interacts with at least three distinct E-prostanoid (EP) receptors that are highly expressed in specific regions of the kidney. Each EP receptor not only selectively binds PGE2, but also preferentially couples to different signal transduction pathways, including: stim

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Blikslager, Anthony T., Susan M. Pell, and Karen M. Young. "PGE2 triggers recovery of transmucosal resistance via EP receptor cross talk in porcine ischemia-injured ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (2001): G375—G381. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g375.

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16,16-Dimethyl-PGE2 (PGE2) may interact with one of four prostaglandin type E (EP) receptors, which signal via cAMP (via EP2 or EP4 receptors) or intracellular Ca2+ (via EP1 receptors). Furthermore, EP3 receptors have several splice variants, which may signal via cAMP or intracellular Ca2+. We sought to determine the PGE2 receptor interactions that mediate recovery of transmucosal resistance ( R) in ischemia-injured porcine ileum. Porcine ileum was subjected to 45 min of ischemia, after which the mucosa was mounted in Ussing chambers. Tissues were pretreated with indomethacin (5 μM). Treatment

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Kim, Soon Ok, Siabhon M. Harris, and Diane M. Duffy. "Prostaglandin E2 (EP) Receptors Mediate PGE2-Specific Events in Ovulation and Luteinization Within Primate Ovarian Follicles." Endocrinology 155, no. 4 (2014): 1466–75. http://dx.doi.org/10.1210/en.2013-2096.

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Prostaglandin E2 (PGE2) is a key mediator of ovulation. All 4 PGE2 receptors (EP receptors) are expressed in the primate follicle, but the specific role of each EP receptor in ovulatory events is poorly understood. To examine the ovulatory events mediated via these EP receptors, preovulatory monkey follicles were injected with vehicle, the PG synthesis inhibitor indomethacin, or indomethacin plus PGE2. An ovulatory dose of human chorionic gonadotropin was administered; the injected ovary was collected 48 hours later and serially sectioned. Vehicle-injected follicles showed normal ovulatory eve

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Kumazawa, T., K. Mizumura, H. Koda, and H. Fukusako. "EP receptor subtypes implicated in the PGE2-induced sensitization of polymodal receptors in response to bradykinin and heat." Journal of Neurophysiology 75, no. 6 (1996): 2361–68. http://dx.doi.org/10.1152/jn.1996.75.6.2361.

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1. Our previous studies, in which we used in vitro canine testispermatic nerve preparations, showed that prostaglandin E2 (PGE2) augments both bradykinin (BK)- and heat-induced discharges of polymodal receptors. However, the PGE2 concentration required to augment the BK responses were 100 times lower than those necessary for the heat responses, suggesting that different receptors are involved in these phenomena. We studied which receptors for E series of prostaglandins (EP receptors) were responsible, using the antagonist and agonists for three subtypes of EP receptors. 2. PGE2-induced augment

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Kopp, Ulla C., Michael Z. Cicha, Kazuhiro Nakamura, Rolf M. Nüsing, Lori A. Smith, and Tomas Hökfelt. "Activation of EP4 receptors contributes to prostaglandin E2-mediated stimulation of renal sensory nerves." American Journal of Physiology-Renal Physiology 287, no. 6 (2004): F1269—F1282. http://dx.doi.org/10.1152/ajprenal.00230.2004.

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Induction of cyclooxygenase-2 (COX-2) in the renal pelvic wall increases prostaglandin E2 (PGE2) leading to stimulation of cAMP production, which results in substance P (SP) release and activation of renal mechanosensory nerves. The subtype of PGE receptors involved, EP2 and/or EP4, was studied by immunohistochemistry and renal pelvic administration of agonists and antagonists of EP2 and EP4 receptors. EP4 receptor-like immunoreactivity (LI) was colocalized with calcitonin gene-related peptide (CGRP)-LI in dorsal root ganglia (DRGs) at Th9-L1 and in nerve terminals in the renal pelvic wall. Th

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Hattori, Youichiro, Takashi Ohno, Takako Ae, et al. "Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 1 (2008): G80—G87. http://dx.doi.org/10.1152/ajpgi.00292.2007.

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Prostaglandin (PG)E derivatives are widely used for treating gastric mucosal injury. PGE receptors are classified into four subtypes, EP1, EP2, EP3, and EP4. We have tested which EP receptor subtypes participate in gastric mucosal protection against ethanol-induced gastric mucosal injury and clarified the mechanisms of such protection. The gastric mucosa of anesthetized rats was perfused at 2 ml/min with physiological saline, agonists for EP1, EP2, EP3, and EP4, or 50% ethanol, using a constant-rate pump connected to a cannula placed in the esophagus. The gastric microcirculation of the mucosa

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Zasłona, Zbigniew, Carlos H. Serezani, Katsuhide Okunishi, David M. Aronoff, and Marc Peters-Golden. "Prostaglandin E2 restrains macrophage maturation via E prostanoid receptor 2/protein kinase A signaling." Blood 119, no. 10 (2012): 2358–67. http://dx.doi.org/10.1182/blood-2011-08-374207.

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Abstract Prostaglandin E2 (PGE2) is a lipid mediator that acts by ligating 4 distinct G protein–coupled receptors, E prostanoid (EP) 1 to 4. Previous studies identified the importance of PGE2 in regulating macrophage functions, but little is known about its effect on macrophage maturation. Macrophage maturation was studied in vitro in bone marrow cell cultures, and in vivo in a model of peritonitis. EP2 was the most abundant PGE2 receptor expressed by bone marrow cells, and its expression further increased during macrophage maturation. EP2-deficient (EP2−/−) macrophages exhibited enhanced in v

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Barclay, J. L., P. Tongnkok, S. T. Anderson, M. J. Waters, and J. D. Curlewis. "283.Effects of prostaglandins on SOCS expression in T-47D breast cancer cells." Reproduction, Fertility and Development 16, no. 9 (2004): 283. http://dx.doi.org/10.1071/srb04abs283.

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There is increasing evidence to suggest that prostaglandins can upregulate suppressor-of-cytokine-signalling (SOCS) expression and so modify cellular responses to cytokines. Here we examined this possibility in two breast cancer cell lines. Initially we characterised prostaglandin receptor expression by reverse transcription-PCR, and found that T-47D cells express EP2, EP3 and EP4 receptors but not FP or EP1 receptors whereas MCF-7 cells expressed EP1 and EP4 receptors. A range of prostaglandin agonists were then used to elucidate whether prostaglandins affect SOCS expression and the receptor

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Jensen, Boye L., Jane Stubbe, Pernille B. Hansen, Ditte Andreasen, and Ole Skøtt. "Localization of prostaglandin E2 EP2 and EP4 receptors in the rat kidney." American Journal of Physiology-Renal Physiology 280, no. 6 (2001): F1001—F1009. http://dx.doi.org/10.1152/ajprenal.2001.280.6.f1001.

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We investigated the localization of cAMP-coupled prostaglandin E2 EP2 and EP4 receptor expression in the rat kidney. EP2 mRNA was restricted to the outer and inner medulla in rat kidney, as determined by RNase protection assay. RT-PCR analysis of microdissected resistance vessels and nephron segments showed EP2 expression in descending thin limb of Henle's loop (DTL) and in vasa recta of the outer medulla. The EP4 receptor was expressed in distal convoluted tubule (DCT) and cortical collecting duct (CCD) in preglomerular vessels, and in outer medullary vasa recta. Butaprost, an EP2 receptor-se

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Take, Ikuko, Yasuhiro Kobayashi, Yohei Yamamoto, et al. "Prostaglandin E2 Strongly Inhibits Human Osteoclast Formation." Endocrinology 146, no. 12 (2005): 5204–14. http://dx.doi.org/10.1210/en.2005-0451.

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Prostaglandin E2 (PGE2) enhances osteoclast formation in mouse macrophage cultures treated with receptor activator of nuclear factor-κB ligand (RANKL). The effects of PGE2 on human osteoclast formation were examined in cultures of CD14+ cells prepared from human peripheral blood mononuclear cells. CD14+ cells differentiated into osteoclasts in the presence of RANKL and macrophage colony-stimulating factor. CD14+ cells expressed EP2 and EP4, but not EP1 or EP3, whereas CD14+ cell-derived osteoclasts expressed none of the PGE2 receptors. PGE2 and PGE1 alcohol (an EP2/4 agonist) stimulated cAMP p

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Kandola, Mandeep K., Lynne Sykes, Yun S. Lee, Mark R. Johnson, Aylin C. Hanyaloglu, and Phillip R. Bennett. "EP2 Receptor Activates Dual G Protein Signaling Pathways that Mediate Contrasting Proinflammatory and Relaxatory Responses in Term Pregnant Human Myometrium." Endocrinology 155, no. 2 (2014): 605–17. http://dx.doi.org/10.1210/en.2013-1761.

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Prostaglandin (PG) E2 (PGE2) plays a central role in the regulation of smooth muscle contractions. Classically, PGE2 stimulates contractions via EP1 and EP3 receptors, whereas EP2 and EP4 maintain quiescence. Labor involves a change from myometrial quiescence to contractions with a shift from anti- to proinflammatory pathways. EP2, a Gαs-coupled receptor, is known to mediate its actions via cAMP signaling. However, we have recently shown that EP2 also activates the proinflammatory PG G/H synthase-2 (PGHS-2). Here, we identify the mechanism underlying the ability of EP2 to maintain uterine quie

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MORATH, RUTA, THOMAS KLEIN, HANNSJÖRG W. SEYBERTH, and ROLF M. NÜSING. "Immunolocalization of the Four Prostaglandin E2 Receptor Proteins EP1, EP2, EP3, and EP4 in Human Kidney." Journal of the American Society of Nephrology 10, no. 9 (1999): 1851–60. http://dx.doi.org/10.1681/asn.v1091851.

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Abstract. Four prostaglandin E2 receptor subtypes designated EP1, EP2, EP3, and EP4 have been shown to mediate a variety of effects of prostaglandin E2 (PGE2) on glomerular hemodynamics, tubular salt and water reabsorption, and on blood vessels in the human kidney. Despite the important role of renal PGE2, the localization of PGE2 receptor proteins in the human kidney is unknown. The present study used antipeptide antibodies to the EP1 to EP4 receptor proteins for immunolocalization in human kidney tissue. Immunoblot studies using these antibodies demonstrated distinct bands in membrane fracti

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Purdy, Kit E., and William J. Arendshorst. "EP1 and EP4receptors mediate prostaglandin E2actions in the microcirculation of rat kidney." American Journal of Physiology-Renal Physiology 279, no. 4 (2000): F755—F764. http://dx.doi.org/10.1152/ajprenal.2000.279.4.f755.

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Vasodilator prostaglandin PGE2 protects the kidney from excessive vasoconstriction during contraction of extracellular fluid volume and pathophysiological states. However, it is not yet clear which of the four known E-prostanoid (EP) receptors is localized to resistance vessels and mediates net vasodilation. In the present study, we assessed the presence, signal transduction, and actions of EP receptor subtypes in preglomerular arterioles of Sprague-Dawley rat kidneys. RNA encoding EP1, an EP1-variant, and EP4 receptors was identified by RT-PCR in freshly isolated preglomerular microvessels; c

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Tsuge, Kyoshiro, Tomoaki Inazumi, Akira Shimamoto, and Yukihiko Sugimoto. "Molecular mechanisms underlying prostaglandin E2-exacerbated inflammation and immune diseases." International Immunology 31, no. 9 (2019): 597–606. http://dx.doi.org/10.1093/intimm/dxz021.

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Abstract Prostaglandins (PGs) are the major lipid mediators in animals and which are biosynthesized from arachidonic acid by the cyclooxygenases (COX-1 or COX-2) as the rate-limiting enzymes. Prostaglandin E2 (PGE2), which is the most abundantly detected PG in various tissues, exerts versatile physiological and pathological actions via four receptor subtypes (EP1–4). Non-steroidal anti-inflammatory drugs, such as aspirin and indomethacin, exert potent anti-inflammatory actions by the inhibition of COX activity and the resulting suppression of PG production. Therefore, PGE2 has been shown to ex

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Endo, Suzu, Akiko Suganami, Keijo Fukushima, et al. "15-Keto-PGE2 acts as a biased/partial agonist to terminate PGE2-evoked signaling." Journal of Biological Chemistry 295, no. 38 (2020): 13338–52. http://dx.doi.org/10.1074/jbc.ra120.013988.

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Prostaglandin E2 (PGE2) is well-known as an endogenous proinflammatory prostanoid synthesized from arachidonic acid by the activation of cyclooxygenase-2. E type prostanoid (EP) receptors are cognates for PGE2 that have four main subtypes: EP1 to EP4. Of these, the EP2 and EP4 prostanoid receptors have been shown to couple to Gαs-protein and can activate adenylyl cyclase to form cAMP. Studies suggest that EP4 receptors are involved in colorectal homeostasis and cancer development, but further work is needed to identify the roles of EP2 receptors in these functions. After sufficient inflammatio

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Mançanares, A. C. F., J. O. Manríquez, J. Cabezas, F. Telleria, L. Rodriguez, and F. O. Castro. "185 Overexpression or CRISPr/Cas9-mediated inhibition of prostaglandin E2 receptors EP2 and EP4 in equine adipose mesenchymal stem cells: implications for cell migration and cellular therapies." Reproduction, Fertility and Development 31, no. 1 (2019): 217. http://dx.doi.org/10.1071/rdv31n1ab185.

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Prostaglandin E2 (PGE2) acts through 4 cellular receptors: EP1, EP2, EP3, and EP4; only EP2 and EP4 are relevant for immunomodulation and migration in immune cells. Besides those, several cells express these receptors on their surface, including mesenchymal stem cells. Pharmacological inhibition of the EP2 receptor prevents migration of immune system cells to inflamed sites, where the concentration of PGE2 is high. Based on this, we hypothesised that overexpression of EP2 or EP4 receptors in equine mesenchymal stem cells (eMSC) will improve their migration to inflammatory sites and subsequent

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Liu, Qingkun, Xibin Liang, Qian Wang, et al. "PGE2 signaling via the neuronal EP2 receptor increases injury in a model of cerebral ischemia." Proceedings of the National Academy of Sciences 116, no. 20 (2019): 10019–24. http://dx.doi.org/10.1073/pnas.1818544116.

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The inflammatory prostaglandin E2 (PGE2) EP2 receptor is a master suppressor of beneficial microglial function, and myeloid EP2 signaling ablation reduces pathology in models of inflammatory neurodegeneration. Here, we investigated the role of PGE2 EP2 signaling in a model of stroke in which the initial cerebral ischemic event is followed by an extended poststroke inflammatory response. Myeloid lineage cell-specific EP2 knockdown in Cd11bCre;EP2lox/lox mice attenuated brain infiltration of Cd11b+CD45hi macrophages and CD45+Ly6Ghi neutrophils, indicating that inflammatory EP2 signaling particip

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Elberg, Gerard, Dorit Elberg, Teresa V. Lewis, et al. "EP2 receptor mediates PGE2-induced cystogenesis of human renal epithelial cells." American Journal of Physiology-Renal Physiology 293, no. 5 (2007): F1622—F1632. http://dx.doi.org/10.1152/ajprenal.00036.2007.

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Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by formation of cysts from tubular epithelial cells. Previous studies indicate that secretion of prostaglandin E2 (PGE2) into cyst fluid and production of cAMP underlie cyst expansion. However, the mechanism by which PGE2 directly stimulates cAMP formation and modulates cystogenesis is still unclear, because the particular E-prostanoid (EP) receptor mediating the PGE2 effect has not been characterized. Our goal is to define the PGE2 receptor subtype involved in ADPKD. We used a three-dimensional cell-culture system of human

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Ruwanpura, S. M. P. M., K. Noguchi та I. Ishikawa. "Prostaglandin E2 Regulates Interleukin-1β-induced Matrix Metalloproteinase-3 Production in Human Gingival Fibroblasts". Journal of Dental Research 83, № 3 (2004): 260–65. http://dx.doi.org/10.1177/154405910408300315.

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Prostaglandin E2 (PGE2) exerts its biological actions via EP receptors (EP1, EP2, EP3, and EP4). In the present study, we investigated whether PGE2 regulated interleukin (IL)-1β-induced matrix metalloproteinase (MMP)-3 production in human gingival fibroblasts (HGF) derived from periodontally healthy subjects and diseased patients. In HGF from healthy gingiva, PGE2 down-regulated IL-1β-induced MMP-3 production, whereas in HGF from periodontitis patients, PGE2 enhanced it. Butaprost (an EP2 agonist) and ONO-AE1-329 (an EP4 agonist) suppressed IL-1β-induced MMP-3 production, and 17-phenyl-ω-trino

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Qu, Changxiu, Chunyou Mao, Peng Xiao, et al. "Ligand recognition, unconventional activation, and G protein coupling of the prostaglandin E2 receptor EP2 subtype." Science Advances 7, no. 14 (2021): eabf1268. http://dx.doi.org/10.1126/sciadv.abf1268.

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Selective modulation of the heterotrimeric G protein α S subunit–coupled prostaglandin E2 (PGE2) receptor EP2 subtype is a promising therapeutic strategy for osteoporosis, ocular hypertension, neurodegenerative diseases, and cardiovascular disorders. Here, we report the cryo–electron microscopy structure of the EP2-Gs complex with its endogenous agonist PGE2 and two synthesized agonists, taprenepag and evatanepag (CP-533536). These structures revealed distinct features of EP2 within the EP receptor family in terms of its unconventional receptor activation and G protein coupling mechanisms, inc

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Sun, Ying, Yue Zhang, Yangyang Zhu, et al. "Inhibition of mitochondrial complex-1 restores the downregulation of aquaporins in obstructive nephropathy." American Journal of Physiology-Renal Physiology 311, no. 4 (2016): F777—F786. http://dx.doi.org/10.1152/ajprenal.00215.2015.

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Obstructive kidney disease is a common complication in the clinic. Downregulation of aquaporins (AQPs) in obstructed kidneys has been thought as a key factor leading to the polyuria and impairment of urine-concentrating capability after the release of kidney obstruction. The present study was to investigate the role of mitochondrial complex-1 in modulating AQPs in obstructive nephropathy. Following 7-day unilateral ureteral obstruction (UUO), AQP1, AQP2, AQP3, and vasopressin 2 (V2) receptor were remarkably reduced as determined by qRT-PCR and/or Western blotting. Notably, inhibition of mitoch

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SILVA, Kumudika I. de, Asif N. DAUD, JiangPing DENG, Stephen B. JONES, Richard L. GAMELLI, and Ravi SHANKAR. "Prostaglandin E2 mediates growth arrest in NFS-60 cells by down-regulating interleukin-6 receptor expression." Biochemical Journal 370, no. 1 (2003): 315–21. http://dx.doi.org/10.1042/bj20021512.

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Interleukin-6 (IL-6), a potent myeloid mitogen, and the immunosuppressive prostanoid prostaglandin E2 (PGE2) are elevated following thermal injury and sepsis. We have previously demonstrated that bone marrow myeloid commitment shifts toward monocytopoiesis and away from granulocytopoiesis during thermal injury and sepsis and that PGE2 plays a central role in this alteration. Here we investigated whether PGE2 can modulate IL-6-stimulated growth in the promyelocytic cell line, NFS-60, by down-regulating IL-6 receptor (IL-6r) expression. Exposure of NFS-60 cells to PGE2 suppressed IL-6-stimulated

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Hashimoto, N., T. Watanabe, Y. Ikeda, et al. "Prostaglandins induce proliferation of rat hepatocytes through a prostaglandin E2 receptor EP3 subtype." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 3 (1997): G597—G604. http://dx.doi.org/10.1152/ajpgi.1997.272.3.g597.

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We characterized the proliferative action of prostaglandins (PGs) in relation to their membrane receptors on rat hepatocytes in primary culture. PGs in the order 16,16-dimethyl PGE2 > PGE2 > PGF2alpha >> PGD2 augmented epidermal growth factor (EGF)/insulin-induced DNA synthesis, assessed by [(3)H]thymidine incorporation, in a concentration-dependent manner, whereas PGs alone did not stimulate basal DNA synthesis without EGF and insulin. The cells exhibited [(3)H]PGE2 binding sites that were displaced by unlabeled PGs in the order PGE1 = PGE2 > PGF2alpha > PGD2. PGE2 inhibited

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Song, Kyoung Seob, Yeon Ho Choi, Jong-Mu Kim, Hyunjae Lee, Tae-Jin Lee, and Joo-Heon Yoon. "Suppression of prostaglandin E2-induced MUC5AC overproduction by RGS4 in the airway." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 4 (2009): L684—L692. http://dx.doi.org/10.1152/ajplung.90396.2008.

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The mechanism by which E-prostanoid (EP) receptor is critically involved in PGE2-induced mucin 5AC ( MUC5AC) gene expression in the airway has been unclear. Furthermore, there have been little reports regarding the negative regulatory mechanism and/or proteins that affect PGE2-induced MUC5AC overproduction. In the present study, we found that PGE2 induced MUC5AC gene expression in a dose-dependent manner (EC50: 73.31 ± 3.13 nM) and that the EP2/4-specific agonist, misoprostol, increased MUC5AC mRNA level, whereas the EP1/3-specific agonist, sulprostone, had no effect. Interestingly, the cAMP c

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Choudhary, Shilpa, Cynthia Alander, Peili Zhan, Qi Gao, Carol Pilbeam, and Lawrence Raisz. "Effect of deletion of the prostaglandin EP2 receptor on the anabolic response to prostaglandin E2 and a selective EP2 receptor agonist." Prostaglandins & Other Lipid Mediators 86, no. 1-4 (2008): 35–40. http://dx.doi.org/10.1016/j.prostaglandins.2008.02.001.

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Friis, Ulla G., Jane Stubbe, Torben R. Uhrenholt, et al. "Prostaglandin E2 EP2 and EP4 receptor activation mediates cAMP-dependent hyperpolarization and exocytosis of renin in juxtaglomerular cells." American Journal of Physiology-Renal Physiology 289, no. 5 (2005): F989—F997. http://dx.doi.org/10.1152/ajprenal.00201.2005.

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PGE2 and PGI2 stimulate renin secretion and cAMP accumulation in juxtaglomerular granular (JG) cells. We addressed, at the single-cell level, the receptor subtypes and intracellular transduction mechanisms involved. Patch clamp was used to determine cell capacitance ( Cm), current, and membrane voltage in response to PGE2, EP2 and EP4 receptor agonists, and an IP receptor agonist. PGE2 (0.1 μmol/l) increased Cm significantly, and the increase was abolished by intracellular application of the protein kinase A antagonist Rp-8-CPT-cAMPS. EP2-selective ligands butaprost (1 μmol/l), AE1–259-01 (1 n

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Pang, Lei, Yin Cai, Eva Hoi Ching Tang, Michael G. Irwin, Haichun Ma, and Zhengyuan Xia. "Prostaglandin E Receptor Subtype 4 Signaling in the Heart: Role in Ischemia/Reperfusion Injury and Cardiac Hypertrophy." Journal of Diabetes Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1324347.

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Prostaglandin E2(PGE2) is an endogenous lipid mediator, produced from the metabolism of arachidonic acids, upon the sequential actions of phospholipase A2, cyclooxygenases, and prostaglandin E synthases. The various biological functions governed by PGE2are mediated through its four distinct prostaglandin E receptors (EPs), designated as EP1, EP2, EP3, and EP4, among which the EP4 receptor is the one most widely distributed in the heart. The availability of global or cardiac-specific EP4 knockout mice and the development of selective EP4 agonists/antagonists have provided substantial evidence t

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Myren, Maja, Michael Baun, Kenneth Beri Ploug, Inger Jansen-Olesen, Jes Olesen, and Saurabh Gupta. "Functional and molecular characterization of prostaglandin E2 dilatory receptors in the rat craniovascular system in relevance to migraine." Cephalalgia 30, no. 9 (2010): 1110–22. http://dx.doi.org/10.1177/0333102409357957.

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Introduction: Migraine pain is thought to involve an increase in trigeminal nerve terminal activity around large cerebral and meningeal arteries, leading to vasodilatation. Because prostaglandin E2 (PGE2) is elevated in cephalic venous blood during migraine attacks, and is also capable of inducing headache in healthy volunteers, we hypothesize that PGE2 dilatory receptors, EP2 and EP4, mediate the response. Materials and methods: By the use of specific agonists and antagonists, the dilatory effect of PGE2 was characterized in rat cranial arteries by use of in vivo and in vitro methods. Further

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Lee, Yeri, Hyun Jin Kim, Donggeon Kim, et al. "707 Discovery of a novel EP2 and EP4 dual antagonist." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A749. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0707.

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BackgroundProstaglandin E2 (PGE2) is one of the most abundant prostaglandins, with crucial roles in normal and pathologic physiology. Especially, PGE2 levels are abnormally elevated in many cancers, and high levels of PGE2 are known to be pro-tumorigenic, likely due to the immune suppressive effect in the tumor microenvironment.1–4 There are four types of PGE2 receptors; EP1, EP2, EP3 and EP4. Among them, EP2 and EP4 activate adenylate cyclase and increase cAMP levels, which induce the cAMP-dependent protein kinase (PKA) signaling pathway. EP2 and EP4 are expressed in various immune cells (e.g

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Olesen, Emma T. B., Hanne B. Moeller, Mette Assentoft, Nanna MacAulay, and Robert A. Fenton. "The vasopressin type 2 receptor and prostaglandin receptors EP2 and EP4 can increase aquaporin-2 plasma membrane targeting through a cAMP-independent pathway." American Journal of Physiology-Renal Physiology 311, no. 5 (2016): F935—F944. http://dx.doi.org/10.1152/ajprenal.00559.2015.

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Apical membrane targeting of the collecting duct water channel aquaporin-2 (AQP2) is essential for body water balance. As this event is regulated by Gs coupled 7-transmembrane receptors such as the vasopressin type 2 receptor (V2R) and the prostanoid receptors EP2 and EP4, it is believed to be cAMP dependent. However, on the basis of recent reports, it was hypothesized in the current study that increased cAMP levels are not necessary for AQP2 membrane targeting. The role and dynamics of cAMP signaling in AQP2 membrane targeting in Madin-Darby canine kidney and mouse cortical collecting duct (m

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Breyer, Richard M., Christopher R. J. Kennedy, Yahua Zhang, and Matthew D. Breyer. "Targeted gene disruption of the prostaglandin E2 EP2 receptor." Prostaglandins & Other Lipid Mediators 59, no. 1-6 (1999): 86. http://dx.doi.org/10.1016/s0090-6980(99)90321-0.

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Bhattacherjee, Parimal, Partha Mukhopadhyay, Stephen L. Tilley, Beverly H. Koller, Thomas Geoghgan, and Christopher A. Paterson. "Blood-aqueous barrier in prostaglandin EP2 receptor knockout mice." Ocular Immunology and Inflammation 10, no. 3 (2002): 187–96. http://dx.doi.org/10.1076/ocii.10.3.187.15601.

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Sugimoto, Y., T. Namba, R. Shigemoto, M. Negishi, A. Ichikawa, and S. Narumiya. "Distinct cellular localization of mRNAs for three subtypes of prostaglandin E receptor in kidney." American Journal of Physiology-Renal Physiology 266, no. 5 (1994): F823—F828. http://dx.doi.org/10.1152/ajprenal.1994.266.5.f823.

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Distribution of the mRNAs for three subtypes of prostaglandin E (PGE) receptors in the mouse kidney was investigated by in situ hybridization. The mRNA for EP1 subtype, which is coupled to Ca2+ mobilization, was specifically localized to the collecting ducts from the cortex to the papilla. The mRNA for EP2 subtype, which is linked to stimulation of adenylate cyclase, was localized to the glomeruli. The mRNA for EP3 subtype, which is coupled to inhibition of adenylate cyclase, was located densely in the tubules in the outer medulla and in the distal tubules in the cortex. These results exhibit

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Sakairi, Y., H. R. Jacobson, T. D. Noland, and M. D. Breyer. "Luminal prostaglandin E receptors regulate salt and water transport in rabbit cortical collecting duct." American Journal of Physiology-Renal Physiology 269, no. 2 (1995): F257—F265. http://dx.doi.org/10.1152/ajprenal.1995.269.2.f257.

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Prostaglandin E2 (PGE2) is the major renal cyclooxygenase metabolite of arachidonic acid. Urinary excretion of PGE2 is increased by dietary salt restriction, as well in cirrhosis and congestive heart failure. To determine whether urinary PGE2 affects transport along the nephron, the actions of luminal PGE2 were studied in the isolated perfused rabbit cortical collecting duct (CCD). Luminal PGE2 transiently hyperpolarized transepithelial voltage (Vt) in a dose-dependent manner (half-maximal effect approximately 10(-8) M) in contrast to a sustained depolarization of Vt produced by basolateral PG

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