Molecular cloning and characterization of the four rat prostaglandin E2 prostanoid receptor subtypes

Boie, Yves; Stocco, Rino; Sawyer, Nicole; Slipetz, Deborah; Ungrin, Mark; Neuschäfer-Rube, Frank; Püschel, Gerhard; Metters, Kathleen M.; Abramovitz, Mark

doi:10.1016/s0014-2999(97)01383-6

Cited by 273 publications

(254 citation statements)

References 30 publications

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“…Four subtypes of PGE 2 receptors (EP 1-4 ) have been classified (Boie et al, 1997;Narumiya et al, 1999). EP 1 receptors couple with the Gq-phospholipase C-IP 3 pathway.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Xing

2007

Brain Research

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The purpose of this study was to determine the role of prostaglandin E 2 (PGE 2 ) in modulating neuronal activity of the dorsolateral periaqueductal gray (dl-PAG) through excitatory and inhibitory synaptic inputs. First, whole cell voltage-clamp recording was performed to obtain excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) of the dl-PAG neurons. Our results show that PGE 2 significantly decreased the frequency of miniature EPSCs and amplitude of evoked EPSCs. The effects were mimicked by sulprostone, an agonist to PGE 2 EP 3 receptors. In contrast, PGE 2 had no distinct effect on IPSCs. In addition, spontaneous action potential of the dl-PAG neurons was recorded using whole cell current-clamp methods. PGE 2 significantly attenuated the discharge rate of the dl-PAG neurons. The decreased firing activity was abolished in the presence of glutamate NMDA and non-NMDA receptors antagonists. The results from the current study provide the first evidence indicating that PGE 2 inhibits the neuronal activity of the dl-PAG via selective attenuation of glutamatergic synaptic inputs, likely due to activation of presynaptic EP 3 receptors.

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“…Four subtypes of PGE 2 receptors (EP 1-4 ) have been classified (Boie et al, 1997;Narumiya et al, 1999). EP 1 receptors couple with the Gq-phospholipase C-IP 3 pathway.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Xing

2007

Brain Research

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“…In the epidermis, PGE 2 is the main prostaglandin produced by keratinocytes in response to ultraviolet irradiation (UVR), and mediates multiple cellular functions including immune regulation, cell growth and differentiation, and carcinogenesis [1][2][3][4]. PGE 2 mediates its effects through 4 G-protein coupled receptors (EP 1 -EP 4 ) that are expressed in a cell-type specific fashion and activate diverse signaling intermediates [5,6]. Melanocytes are pigment-producing cells that provide photoprotection to the skin through the production and distribution of melanin to keratinocytes.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Scott

Fricke

Fender

et al. 2007

Experimental Cell Research

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Prostaglandins are lipid signaling intermediates released by keratinocytes in response to ultraviolet irradiation (UVR) in the skin. The main prostaglandin released following UVR is PGE 2 , a ligand for 4 related G-protein coupled receptors (EP 1 , EP 2 , EP 3 and EP 4 ). Our previous work established that PGE 2 stimulates melanocyte dendrite formation through activation of the EP 1 and EP 3 receptors. The purpose of the present report is to define the signaling intermediates involved in EP 1 and EP 3 -dependent dendrite formation in human melanocytes. We recently showed that activation of the atypical PKCζ isoform stimulates melanocyte dendricity in response to treatment with lysophosphatidylcholine. We therefore examined the potential contribution of PKCζ activation on EP 1 and EP 3 -dependent dendrite formation in melanocytes. Stimulation of the EP 1 and EP 3 receptors by selective agonists activated PKCζ, and inhibition of PKCζ activation abrogated EP 1 and EP 3 -receptor mediated melanocyte dendricity. Because of the importance of Rho-GTP binding proteins in the regulation of melanocyte dendricity, we also examined the effect of EP 1 and EP 3 receptor activation on Rac and Rho activity. Neither Rac nor Rho was activated upon treatment with EP 1,3 -receptor agonists. We show that melanocytes express only the EP 3A1 isoform, but not the EP 3B receptor isoform, previously associated with Rho activation, consistent with a lack of Rho stimulation by EP 3 agonists. Our data suggest that PKCζ activation plays a predominant role in regulation of PGE 2 -dependent melanocyte dendricity.

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“…Four PGE 2 subtype receptors (EP receptors) have been cloned and characterized [6][7][8][9]. They are members of the family of G protein-coupled receptors and appear to be differentially expressed among inflammatory cells.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E₂ modulates the functional responsiveness of human monocytes to chemokines

Panzer¹,

Uguccioni²

2004

Eur J Immunol

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Prostaglandin E 2 (PGE 2 ) plays an important role in the immune response by modulating the complex interactions between leukocytes and tissue cells under inflammatory conditions. PGE 2 may possibly influence pro-inflammatory effects of chemokines and chemokine receptors that are among the main regulators of directional leukocyte migration. We analyzed whether PGE 2 affects chemokine receptor expression on human monocytes and their functional responsiveness to inflammatory chemokines. Expression of CCR5 on monocytes was significantly reduced, whereas CCR2 and CXCR4 expression were not affected by PGE 2 . However, PGE 2 treatment significantly increased the chemotactic response of monocytes to monocyte-chemoattractant protein-1 (MCP-1), RANTES and stromal cell-derived factor-1 (SDF-1). In addition, PGE 2 induced a higher calcium mobilization and actin polymerization upon chemokine stimulation. To better characterize PGE 2 effects, we used specific agonists for the PGE 2 receptors (EP 1 -EP 4 ) characterized so far. The 11-deoxy PGE 1 , an EP 2 /EP 4 ligand, could mimic the effects observed using PGE 2 . In contrast, the EP 1 agonist, sulprostone, had not effects on monocytes, indicating that the effects of PGE 2 are mediated by EP 2 /EP 4 receptors. Monocytes acquire a higher functional responsiveness to MCP-1, RANTES and SDF-1 after exposure to PGE 2 , independently of the level of chemokine receptor expression. This mechanism might enhance the local monocyte recruitment under inflammatory conditions, and suggests specific PGE 2 receptor EP 2 /EP 4 antagonists as novel agents for the treatment of inflammatory diseases.

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Molecular cloning and characterization of the four rat prostaglandin E2 prostanoid receptor subtypes

Cited by 273 publications

References 30 publications

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Prostaglandin E₂ modulates the functional responsiveness of human monocytes to chemokines

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Molecular cloning and characterization of the four rat prostaglandin E2 prostanoid receptor subtypes

Cited by 273 publications

References 30 publications

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Prostaglandin E2 modulates the functional responsiveness of human monocytes to chemokines

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Prostaglandin E₂ modulates the functional responsiveness of human monocytes to chemokines