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[PMID]:28701311
[Au] Autor:Gonzalez AA; Salinas-Parra N; Leach D; Navar LG; Prieto MC
[Ad] Endereço:Instituto de Química, Pontificia Universidad Católica de Valparaíso, Valparaíso, Chile; alexis.gonzalez@pucv.cl.
[Ti] Título:PGE upregulates renin through E-prostanoid receptor 1 via PKC/cAMP/CREB pathway in M-1 cells.
[So] Source:Am J Physiol Renal Physiol;313(4):F1038-F1049, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During the early phase of ANG II-dependent hypertension, tubular PGE is increased. Renin synthesis and secretion in the collecting duct (CD) are upregulated by ANG II, contributing to further intratubular ANG II formation. However, what happens first and whether the triggering mechanism is independent of tubular ANG II remain unknown. PGE stimulates renin synthesis in juxtaglomerular cells via E-prostanoid (EP) receptors through the cAMP/cAMP-responsive element-binding (CREB) pathway. EP receptors are also expressed in the CD. Here, we tested the hypothesis that renin is upregulated by PGE in CD cells. The M-1 CD cell line expressed EP1, EP3, and EP4 but not EP2. Dose-response experiments, in the presence of ANG II type 1 receptor blockade with candesartan, demonstrated that 10 M PGE maximally increases renin mRNA (approximately 4-fold) and prorenin/renin protein levels (approximately 2-fold). This response was prevented by micromolar doses of SC-19220 (EP1 antagonist), attenuated by the EP4 antagonist, L-161982, and exacerbated by the highly selective EP3 antagonist, L-798106 (~10-fold increase). To evaluate further the signaling pathway involved, we used the PKC inhibitor calphostin C and transfections with PKCα dominant negative. Both strategies blunted the PGE -induced increases in cAMP levels, CREB phosphorylation, and augmentation of renin. Knockdown of the EP1 receptor and CREB also prevented renin upregulation. These results indicate that PGE increases CD renin expression through the EP1 receptor via the PKC/cAMP/CREB pathway. Therefore, we conclude that during the early stages of ANG II-dependent hypertension, there is augmentation of PGE that stimulates renin in the CD, resulting in increased tubular ANG II formation and further stimulation of renin.
[Mh] Termos MeSH primário: Proteína de Ligação a CREB/metabolismo
AMP Cíclico/metabolismo
Dinoprostona/farmacologia
Túbulos Renais Coletores/efeitos dos fármacos
Proteína Quinase C/metabolismo
Receptores de Prostaglandina E Subtipo EP1/agonistas
Sistema Renina-Angiotensina/efeitos dos fármacos
Renina/metabolismo
[Mh] Termos MeSH secundário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Proteína de Ligação a CREB/genética
Linhagem Celular
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Túbulos Renais Coletores/enzimologia
Camundongos
Simulação de Acoplamento Molecular
Fosforilação
Antagonistas de Prostaglandina/farmacologia
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/genética
Inibidores de Proteínas Quinases/farmacologia
Interferência de RNA
Receptores de Prostaglandina E Subtipo EP1/genética
Receptores de Prostaglandina E Subtipo EP1/metabolismo
Receptores de Prostaglandina E Subtipo EP3/metabolismo
Receptores de Prostaglandina E Subtipo EP4/metabolismo
Renina/genética
Transdução de Sinais/efeitos dos fármacos
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Prostaglandin Antagonists); 0 (Protein Kinase Inhibitors); 0 (Ptger1 protein, mouse); 0 (Ptger3 protein, mouse); 0 (Ptger4 protein, mouse); 0 (Receptors, Prostaglandin E, EP1 Subtype); 0 (Receptors, Prostaglandin E, EP3 Subtype); 0 (Receptors, Prostaglandin E, EP4 Subtype); E0399OZS9N (Cyclic AMP); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C); EC 3.4.23.15 (Renin); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00194.2017


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[PMID]:28169162
[Au] Autor:Okumura Y; Yamagishi T; Nukui S; Nakao K
[Ad] Endereço:AskAt Inc., 4F Ito Bldg., 4-11-28 Meieki Nakamura-ku, Nagoya 450-0002, Japan. Electronic address: yoshiyuki.okumura@askat.co.jp.
[Ti] Título:Discovery of AAT-008, a novel, potent, and selective prostaglandin EP4 receptor antagonist.
[So] Source:Bioorg Med Chem Lett;27(5):1186-1192, 2017 Mar 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Starting from acylsufonamide HTS hit 2, a novel series of para-N-acylaminomethylbenzoic acids was identified and developed as selective prostaglandin EP4 receptor antagonists. Structural modifications on lead compound 4a were explored with the aim of improving potency, physicochemical properties, and animal PK predictive of QD (once a day) dosing regimen in human. These efforts led to the discovery of the clinical candidate AAT-008 (4j), which exhibited significantly improved pharmacological profiles over grapiprant (1).
[Mh] Termos MeSH primário: Benzoatos/farmacologia
Niacinamida/análogos & derivados
Antagonistas de Prostaglandina/farmacologia
Receptores de Prostaglandina E Subtipo EP4/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Benzoatos/química
Benzoatos/farmacocinética
Descoberta de Drogas
Seres Humanos
Niacinamida/química
Niacinamida/farmacocinética
Niacinamida/farmacologia
Antagonistas de Prostaglandina/química
Antagonistas de Prostaglandina/farmacocinética
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AAT-008); 0 (Benzoates); 0 (Prostaglandin Antagonists); 0 (Receptors, Prostaglandin E, EP4 Subtype); 25X51I8RD4 (Niacinamide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


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[PMID]:27909962
[Au] Autor:Lavrinenko VA; Babina AV
[Ad] Endereço:Novosibirsk National Research State University, Novosibirsk, Russia. igor@academ.org.
[Ti] Título:Efficiency of Osmotic Concentration after Combined Treatment with Vasopressin and Blockage of Prostaglandin Synthesis.
[So] Source:Bull Exp Biol Med;162(2):187-190, 2016 Dec.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We performed a complex functional study of the effects of prostaglandin synthesis blockage with diclofenac on manifestation of the hydroosmotic effect of vasopressin V -receptor agonist desmopressin in the kidneys of Wistar rats with normal synthesis of endogenous vasopressin and homozygous Brattleboro rats with hereditary impaired synthesis of neurohypophyseal hormone vasopressin. Blockage of prostaglandin synthesis led to more pronounced increase in urine osmolality in Brattleboro rats than in Wistar rats due to elevation of not only urine but also sodium gradient at the expense of elimination of the inhibitory effect of prostaglandins on sodium reabsorption and membrane permeability for urine. During combined treatment, the effects of the hormone predominated: the increase in urine osmolality in Wistar and Brattleboro rats did not differ from that after desmopressin administration.
[Mh] Termos MeSH primário: Antidiuréticos/farmacologia
Diabetes Insípido Nefrogênico/tratamento farmacológico
Diclofenaco/farmacologia
Antagonistas de Prostaglandina/farmacologia
Prostaglandinas/biossíntese
Vasopressinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Desamino Arginina Vasopressina/farmacologia
Diabetes Insípido Nefrogênico/patologia
Diabetes Insípido Nefrogênico/urina
Córtex Renal/efeitos dos fármacos
Córtex Renal/metabolismo
Córtex Renal/patologia
Medula Renal/efeitos dos fármacos
Medula Renal/metabolismo
Medula Renal/patologia
Concentração Osmolar
Ratos
Ratos Brattleboro
Ratos Wistar
Sódio/urina
Vasopressinas/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidiuretic Agents); 0 (Prostaglandin Antagonists); 0 (Prostaglandins); 11000-17-2 (Vasopressins); 144O8QL0L1 (Diclofenac); 9NEZ333N27 (Sodium); ENR1LLB0FP (Deamino Arginine Vasopressin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170210
[Lr] Data última revisão:
170210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE


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[PMID]:27783283
[Au] Autor:Babina AV; Lavrinenko VA
[Ad] Endereço:Novosibirsk National Research State University, Novosibirsk, Russia.
[Ti] Título:Electron Microscopic Study of the Inner Medulla in Rat Kidneys under Conditions of Vasopressin Treatment Combined with Prostaglandin Synthesis Blockade.
[So] Source:Bull Exp Biol Med;161(6):850-852, 2016 Oct.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ultrastructural changes in cells of the renal inner medulla involved in the realization of the antidiuretic effect of vasopressin under conditions of prostaglandin synthesis blockade were studied in the kidneys of Wistar rats and endogenous vasopressin-deficient homozygous Brattleboro rats. The results indicated uniform trend to an increase in the number of clathrincoated vesicles under conditions of hormone treatment combined with prostaglandin synthesis blockade in animals with different neurohypophyseal status. These changes reflected translocation of aquaporins and an increase in the permeability of the collecting tubular epithelium for water. Brattleboro rats, but not Wistar rats, exhibited ultrastructural signs of synthesis activation in the epithelium and widening of the intercellular gaps, which could indicate more intense paracellular water transport.
[Mh] Termos MeSH primário: Antidiuréticos/farmacologia
Diabetes Insípido Neurogênico/tratamento farmacológico
Medula Renal/efeitos dos fármacos
Túbulos Renais Coletores/efeitos dos fármacos
Prostaglandinas/metabolismo
Vasopressinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Aquaporinas/metabolismo
Transporte Biológico
Vesículas Revestidas por Clatrina/efeitos dos fármacos
Vesículas Revestidas por Clatrina/metabolismo
Diabetes Insípido Neurogênico/metabolismo
Diabetes Insípido Neurogênico/patologia
Diclofenaco/farmacologia
Medula Renal/metabolismo
Medula Renal/patologia
Túbulos Renais Coletores/metabolismo
Túbulos Renais Coletores/patologia
Microscopia Eletrônica
Concentração Osmolar
Antagonistas de Prostaglandina/farmacologia
Transporte Proteico
Ratos
Ratos Brattleboro
Ratos Wistar
Vasopressinas/deficiência
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidiuretic Agents); 0 (Aquaporins); 0 (Prostaglandin Antagonists); 0 (Prostaglandins); 059QF0KO0R (Water); 11000-17-2 (Vasopressins); 144O8QL0L1 (Diclofenac)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170209
[Lr] Data última revisão:
170209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161027
[St] Status:MEDLINE


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[PMID]:27030625
[Au] Autor:Dobrek L; Baranowska A; Skowron B; Furgala A; Zurowski D; Thor P
[Ad] Endereço:Department of Pathophysiology, Faculty of Medicine, Jagiellonian University Medical College , Cracow , Poland.
[Ti] Título:Prostaglandin-targeting agents and spectral heart rate variability in experimental partial bladder outlet obstruction in rats.
[So] Source:Physiol Int;103(1):21-34, 2016 Mar.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to determine the activity of the autonomic nervous system (ANS), using spectral analysis of the heart rate variability (HRV) in the model of partial bladder outlet obstruction (PBOO) in rats treated with selected non-steroidal anti-inflammatory drugs (NSAID): piroxicam (PRX) or meloxicam (MLX), and following administration of PGF2a prostaglandin analogue (Enzaprost F5). Neither the use of PGF2a analogue nor of MLX, caused significant changes in the HRV spectrum (except for HRV spectrum total power reduction with MLX). The use of PRX caused reduction of the total power and powers of all components of the HRV spectrum (except for VLF). Moreover, increased nLF and reduced nHF were observed. The obtained results suggest that the total prostaglandin synthesis block with a non-selective cyclooxygenase inhibitor (PRX) results in reduced ANS total activity, with decreased parasympathetic activity and a relative sympathetic predominance. The preferential cyclooxygenase-2 block (MLX) caused reduction of the total ANS activity as well, however with no clear disproportion of any part of the ANS. Therefore, prostaglandin synthesis inhibition and associated decrease of parasympathetic activity may constitute an additional and favourable feature of NSAID pharmacodynamics in the treatment of BPH.
[Mh] Termos MeSH primário: Frequência Cardíaca/efeitos dos fármacos
Terapia de Alvo Molecular/métodos
Antagonistas de Prostaglandina/farmacologia
Prostaglandinas Sintéticas/farmacologia
Obstrução do Colo da Bexiga Urinária/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Inibidores de Ciclo-Oxigenase 2/farmacologia
Inibidores de Ciclo-Oxigenase 2/uso terapêutico
Dinoprosta/farmacologia
Modelos Animais de Doenças
Piroxicam/farmacologia
Piroxicam/uso terapêutico
Antagonistas de Prostaglandina/uso terapêutico
Prostaglandinas/metabolismo
Prostaglandinas Sintéticas/uso terapêutico
Ratos
Ratos Wistar
Tiazinas/farmacologia
Tiazinas/uso terapêutico
Tiazóis/farmacologia
Tiazóis/uso terapêutico
Obstrução do Colo da Bexiga Urinária/tratamento farmacológico
Obstrução do Colo da Bexiga Urinária/patologia
Urodinâmica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cyclooxygenase 2 Inhibitors); 0 (Prostaglandin Antagonists); 0 (Prostaglandins); 0 (Prostaglandins, Synthetic); 0 (Thiazines); 0 (Thiazoles); 13T4O6VMAM (Piroxicam); B7IN85G1HY (Dinoprost); VG2QF83CGL (meloxicam)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170130
[Lr] Data última revisão:
170130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160401
[St] Status:MEDLINE
[do] DOI:10.1556/036.103.2016.1.3


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[PMID]:26945086
[Au] Autor:Nakano Y; Kidani Y; Goto K; Furue S; Tomita Y; Inagaki N; Tanaka H; Shichijo M
[Ad] Endereço:United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu (Y.N., N.I., H.T.), Discovery Research Laboratory for Innovative Frontier Medicines, Shionogi & Co., Ltd., Toyonaka (Y.N., Y.K., K.G., S.F., Y.T., M.S.), and Laboratory of Pharmacology, Department of
[Ti] Título:Role of Prostaglandin D2 and DP1 Receptor on Japanese Cedar Pollen-Induced Allergic Rhinitis in Mice.
[So] Source:J Pharmacol Exp Ther;357(2):258-63, 2016 May.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although we previously demonstrated the contribution of the DP1receptor in nasal obstruction using animals sensitized with ovalbumin in the presence of adjuvant, the contribution of the DP1receptor in sneezing is unclear. Here, we developed a mouse model of Japanese cedar (JC:Cryptomeria japonica) pollinosis to evaluate the symptoms of sneezing. To achieve this, we used JC pollen crude extract in the absence of adjuvant to sensitize mice to develop a model closer to the pathophysiology of human JC pollinosis. The immunologic and pharmacologic features of this model are highly similar to those observed in JC pollinosis in humans. Using this model, we found that DP1receptor antagonists suppressed JC pollen extract-induced sneezing and that a DP1receptor agonist induced sneezing. Moreover, JC pollen extract-induced sneezing was diminished in DP1receptor knockout mice. In conclusion, we developed a novel mouse model of allergic rhinitis that closely mimics human JC pollinosis. A strong contribution of DP1receptor signaling to sneezing was demonstrated using this model, suggesting that DP1receptor antagonists could suppress sneezing and nasal obstruction, and therefore these agents could be a new therapeutic option for allergic rhinitis.
[Mh] Termos MeSH primário: Antialérgicos/farmacologia
Cryptomeria/imunologia
Pólen/imunologia
Antagonistas de Prostaglandina/uso terapêutico
Receptores Imunológicos/antagonistas & inibidores
Receptores de Prostaglandina/antagonistas & inibidores
Rinite Alérgica/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Citocinas/biossíntese
Feminino
Imunoglobulina E/sangue
Linfonodos/efeitos dos fármacos
Linfonodos/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Obstrução Nasal/etiologia
Obstrução Nasal/prevenção & controle
Extratos Vegetais
Receptores Imunológicos/genética
Receptores de Prostaglandina/genética
Espirro
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 0 (Cytokines); 0 (Plant Extracts); 0 (Prostaglandin Antagonists); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (prostaglandin D2 receptor); 0 (prostanoid D receptor 1, mouse); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160402
[Lr] Data última revisão:
160402
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160306
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.115.229799


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[PMID]:26907476
[Au] Autor:Zoccal KF; Sorgi CA; Hori JI; Paula-Silva FW; Arantes EC; Serezani CH; Zamboni DS; Faccioli LH
[Ad] Endereço:Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Universidade de São Paulo (FCFRP/USP), Ribeirao Preto, Sao Paulo 14040-903, Brazil.
[Ti] Título:Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality.
[So] Source:Nat Commun;7:10760, 2016 Feb 23.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tityus serrulatus sting causes thousands of deaths annually worldwide. T. serrulatus-envenomed victims exhibit local or systemic reaction that culminates in pulmonary oedema, potentially leading to death. However, the molecular mechanisms underlying T. serrulatus venom (TsV) activity remain unknown. Here we show that TsV triggers NLRP3 inflammasome activation via K(+) efflux. Mechanistically, TsV triggers lung-resident cells to release PGE2, which induces IL-1ß production via E prostanoid receptor 2/4-cAMP-PKA-NFκB-dependent mechanisms. IL-1ß/IL-1R actions account for oedema and neutrophil recruitment to the lungs, leading to TsV-induced mortality. Inflammasome activation triggers LTB4 production and further PGE2 via IL-1ß/IL-1R signalling. Activation of LTB4-BLT1/2 pathway decreases cAMP generation, controlling TsV-induced inflammation. Exogenous administration confirms LTB4 anti-inflammatory activity and abrogates TsV-induced mortality. These results suggest that the balance between LTB4 and PGE2 determines the amount of IL-1ß inflammasome-dependent release and the outcome of envenomation. We suggest COX1/2 inhibition as an effective therapeutic intervention for scorpion envenomation.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Dinoprostona/farmacologia
Interleucina-1beta/efeitos dos fármacos
Leucotrieno B4/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Picadas de Escorpião/imunologia
Venenos de Escorpião/farmacologia
[Mh] Termos MeSH secundário: Animais
Araquidonato 5-Lipoxigenase/genética
Western Blotting
Proteínas de Transporte/imunologia
Celecoxib/farmacologia
AMP Cíclico/imunologia
Proteínas Quinases Dependentes de AMP Cíclico/efeitos dos fármacos
Proteínas Quinases Dependentes de AMP Cíclico/imunologia
Inibidores de Ciclo-Oxigenase/farmacologia
Dinoprostona/imunologia
Técnicas In Vitro
Indóis/farmacologia
Indometacina/farmacologia
Inflamassomos/imunologia
Interleucina-1beta/imunologia
Leucotrieno B4/imunologia
Inibidores de Lipoxigenase/farmacologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos Peritoneais/imunologia
Camundongos
Camundongos Knockout
NF-kappa B/efeitos dos fármacos
NF-kappa B/imunologia
Proteína 3 que Contém Domínio de Pirina da Família NLR
Fosfoproteínas
Antagonistas de Prostaglandina/farmacologia
Receptores de Prostaglandina E Subtipo EP2/efeitos dos fármacos
Receptores de Prostaglandina E Subtipo EP2/imunologia
Receptores de Prostaglandina E Subtipo EP4/efeitos dos fármacos
Receptores de Prostaglandina E Subtipo EP4/imunologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Picadas de Escorpião/mortalidade
Escorpiões
Xantonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Cyclooxygenase Inhibitors); 0 (IL1B protein, mouse); 0 (Indoles); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (Lipoxygenase Inhibitors); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (Phosphoproteins); 0 (Prostaglandin Antagonists); 0 (Receptors, Prostaglandin E, EP2 Subtype); 0 (Receptors, Prostaglandin E, EP4 Subtype); 0 (Scorpion Venoms); 0 (Xanthones); 080626SQ8C (MK-886); 1HGW4DR56D (Leukotriene B4); 33458-93-4 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid); E0399OZS9N (Cyclic AMP); EC 1.13.11.34 (Arachidonate 5-Lipoxygenase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); JCX84Q7J1L (Celecoxib); K7Q1JQR04M (Dinoprostone); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms10760


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[PMID]:26939228
[Au] Autor:Abdel-Ghany R; Rabia I; El-Ahwany E; Saber S; Gamal R; Nagy F; Mahmoud O; Hamad RS; Barakat W
[Ti] Título:BLOCKADE OF PGE2, PGD2 RECEPTORS CONFERS PROTECTION AGAINST PREPATENT SCHISTOSOMIASIS MANSONI IN MICE.
[So] Source:J Egypt Soc Parasitol;45(3):511-20, 2015 Dec.
[Is] ISSN:1110-0583
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:Schistosomiasis is a chronic disease with considerable social impact. Despite the availability of affordable chemotherapy, drug treatment has not significantly reduced the overall number of disease cases. Among other mechanisms, the parasite produces PGE2 and PGD2 to evade host immune defenses. To investigate the role of PGE2 and PGD2 in schistosomiasis, we evaluated the effects of L-161,982, Ah6809 (PGE2 receptor antagonists alone of combined with each other) and MK-0524 (PGD2 receptor antagonist) during prepatent Schistosoma mansoni infection. Drugs were administered intraperitoneally an hour before and 24 hours after infection of C57BL/6 mice with 100 Schistosoma mansoni cercariae. L-161,982, Ah6809, their combination and MK-0524 caused partial protection against pre-patent S. mansoni infection which was mediated by biasing the immune response towards Th1 phenotype. These results showed that blockade of PGE2 and PGD2 receptors confers partial protection against pre-patent S. mansoni infection in mice and that they may be useful as adjunctive therapy to current anti-schistosomal drugs or vaccines.
[Mh] Termos MeSH primário: Indóis/farmacologia
Receptores Imunológicos/antagonistas & inibidores
Receptores de Prostaglandina E/antagonistas & inibidores
Receptores de Prostaglandina/antagonistas & inibidores
Esquistossomose mansoni/prevenção & controle
Tiofenos/farmacologia
Triazóis/farmacologia
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/metabolismo
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
Antagonistas de Prostaglandina/farmacologia
Linfócitos T Auxiliares-Indutores/efeitos dos fármacos
Linfócitos T Auxiliares-Indutores/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Indoles); 0 (L-161982); 0 (MK-0524); 0 (Prostaglandin Antagonists); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (Receptors, Prostaglandin E); 0 (Thiophenes); 0 (Triazoles); 0 (Xanthones); 0 (prostaglandin D2 receptor); 33458-93-4 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:160304
[Lr] Data última revisão:
160304
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160305
[St] Status:MEDLINE


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[PMID]:26684827
[Au] Autor:Fan Y; Wang Y; Wang K
[Ad] Endereço:Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China. 350177646@qq.com.
[Ti] Título:Prostaglandin E2 stimulates normal bronchial epithelial cell growth through induction of c-Jun and PDK1, a kinase implicated in oncogenesis.
[So] Source:Respir Res;16:149, 2015 Dec 18.
[Is] ISSN:1465-993X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cyclooxygenase-2-derived prostaglandin E2 (PGE2), a bioactive eicosanoid, has been implicated in many biological processes including reproduction, inflammation and tumor growth. We previously showed that PGE2 stimulated lung cancer cell growth and progression through PGE2 receptor EP2/EP4-mediated kinase signaling pathways. However, the role of PGE2 in controlling lung airway epithelial cell phenotype remains unknown. We evaluated the effects of c-Jun and 3-phosphoinositede dependent protein kinase-1 (PDK1) in mediating epithelial cell hyperplasia induced by PGE2. METHOD: The bronchial epithelial cell lines BEAS-2B and HBEc14-KT were cultured and then treated with PGE2. PDK1 small interfering RNA (siRNA) and a PDK1 inhibitor, an antagonist of the PGE2 receptor subtype EP4 and EP4 siRNA, c-Jun siRNA, and overexpressions of c-Jun and PDK1 have been used to evaluate the effects on cell proliferation. RESULTS: We demonstrated that PGE2 increased normal bronchial epithelial cell proliferation through induction of PDK1, an ankyrin repeat-containing Ser/Thr kinase implicated in the induction of apoptosis and the suppression of tumor growth. PDK1 siRNA and a PDK1 inhibitor blocked the effects of PGE2 on normal cell growth. The PGE2-induced PDK1 expression was blocked by an antagonist of the PGE2 receptor subtype EP4 and by EP4 siRNA. In addition, we showed that induction of PDK1 by PGE2 was associated with induction of the transcription factor, c-Jun protein. Silencing of c-Jun using siRNA and point mutations of c-Jun sites in the PDK1 gene promoter resulted in blockade of PDK1 expression and promoter activity induced by PGE2. In contrast, overexpression of c-Jun induced PDK1 gene promoter activity and expression followed increased cell proliferation. CONCLUSION: PGE2 increases normal bronchial epithelial cell proliferation through increased PDK1 gene expression that is dependent on EP4 and induction of c-Jun. Therewith, our data suggest a new role of c-Jun and PDK1 in mediating epithelial cell hyperplasia induced by PGE2.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/metabolismo
Brônquios/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Dinoprostona/farmacologia
Células Epiteliais/efeitos dos fármacos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/antagonistas & inibidores
Proteínas Quinases Dependentes de 3-Fosfoinositídeo/genética
Sítios de Ligação
Brônquios/enzimologia
Brônquios/patologia
Linhagem Celular
Relação Dose-Resposta a Droga
Células Epiteliais/enzimologia
Células Epiteliais/patologia
Seres Humanos
Hiperplasia
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases JNK Ativadas por Mitógeno/genética
Fosforilação
Regiões Promotoras Genéticas
Antagonistas de Prostaglandina/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Interferência de RNA
Receptores de Prostaglandina E Subtipo EP4/efeitos dos fármacos
Receptores de Prostaglandina E Subtipo EP4/genética
Receptores de Prostaglandina E Subtipo EP4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PTGER4 protein, human); 0 (Prostaglandin Antagonists); 0 (Protein Kinase Inhibitors); 0 (Receptors, Prostaglandin E, EP4 Subtype); EC 2.7.11.1 (3-Phosphoinositide-Dependent Protein Kinases); EC 2.7.11.1 (PDPK1 protein, human); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1186/s12931-015-0309-0


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[PMID]:26320551
[Au] Autor:Mizutani Y; Ohi Y; Kimura S; Miyazawa K; Goto S; Haji A
[Ad] Endereço:Laboratory of Neuropharmacology, School of Pharmacy, Aichi Gakuin University, Nagoya 464-8650, Japan; Department of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. Electronic address: ag123d26@dpc.agu.ac.jp.
[Ti] Título:Effects of prostaglandin E2 on synaptic transmission in the rat spinal trigeminal subnucleus caudalis.
[So] Source:Brain Res;1625:29-38, 2015 Nov 02.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The spinal trigeminal subnucleus caudalis (Vc) receives preferentially nociceptive afferent signals from the orofacial area. Nociceptive stimuli to the orofacial area induce cyclooxygenase both peripherally and centrally, which can synthesize a major prostanoid prostaglandin E2 (PGE2) that implicates in diverse physiological functions. To clarify the roles of centrally-synthesized PGE2 in nociception, effects of exogenous PGE2 on synaptic transmission in the Vc neurons were investigated in the rat brainstem slice. Spontaneously occurring excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) were recorded, respectively, under pharmacological blockade of inhibitory and excitatory transmission by whole-cell patch-clamp mode. Perfusion of PGE2 (1-5 µM) increased the frequency of sIPSCs in a concentration-dependent manner but had no significant effect on the amplitude. Similarly to the effects on sIPSCs, PGE2 increased the sEPSC frequency without any effect on the amplitude. These facilitatory effects of PGE2 on spontaneous synaptic transmissions were blocked by an EP1 antagonist SC19220 but not by an EP4 antagonist AH23848. Electrical stimulation of the trigeminal tract evoked short latency EPSCs (eEPSCs) in the Vc neurons. PGE2 (5 µM) was ineffective on the eEPSCs. The present study demonstrated that PGE2 facilitated spontaneous synaptic transmissions in the Vc neurons through activating the presynaptic EP1 receptors but had no effect on the trigeminal tract-mediated excitatory transmission. These results suggest that centrally-synthesized PGE2 modifies the synaptic transmission in the Vc region, thereby contributing to the processing of nociceptive signals originated from the orofacial area.
[Mh] Termos MeSH primário: Dinoprostona/farmacologia
Neurônios/efeitos dos fármacos
Transmissão Sináptica/efeitos dos fármacos
Núcleo Espinal do Trigêmeo/citologia
[Mh] Termos MeSH secundário: Animais
Compostos de Bifenilo/farmacologia
Ácido Dibenzo(b,f)(1,4)oxazepina-10(11H)-carboxílico, 8-cloro-, 2-acetilidrazida/farmacologia
Relação Dose-Resposta a Droga
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Antagonistas GABAérgicos/farmacologia
Técnicas In Vitro
Masculino
Técnicas de Patch-Clamp
Picrotoxina/farmacologia
Antagonistas de Prostaglandina/farmacologia
Quinoxalinas/farmacologia
Ratos
Ratos Wistar
Tempo de Reação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biphenyl Compounds); 0 (Excitatory Amino Acid Antagonists); 0 (GABA Antagonists); 0 (Prostaglandin Antagonists); 0 (Quinoxalines); 124-87-8 (Picrotoxin); 19395-87-0 (Dibenz(b,f)(1,4)oxazepine-10(11H)-carboxylic acid, 8-chloro-, 2-acetylhydrazide); 62T278S1MX (FG 9041); 81443-73-4 (AH 23848); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150901
[St] Status:MEDLINE



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