Academic literature on the topic 'Receptores EP'
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Journal articles on the topic "Receptores EP"
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Cipollone, Francesco, and Donato Santovito. "EP Receptors and Coxibs." Circulation Research 113, no. 2 (2013): 91–93. http://dx.doi.org/10.1161/circresaha.113.301616.
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Sawyer, ST, SB Krantz, and K. Sawada. "Receptors for erythropoietin in mouse and human erythroid cells and placenta." Blood 74, no. 1 (1989): 103–9. http://dx.doi.org/10.1182/blood.v74.1.103.103.
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Abstract High and lower affinity receptors for erythropoietin (EP) were initially identified on a very pure population of EP-responsive erythroblasts obtained from the spleens of mice infected with anemia strain of Friend virus (FVA). The structure of the receptor for EP in these cells was determined to be proteins of 100 and 85 Kd by cross- linking 125I-EP. In this investigation, studies on the receptors for EP were extended to other mouse erythroid cells and human erythroid cells as well as to the placentas of mice and rats. Only lower affinity receptors for EP were detected on erythroblasts purified from the spleens of mice infected with the polycythemia strain of Friend virus and a murine erythroleukemia cell line, both of which are not responsive to EP in culture. Internalization of 125I-EP was observed in both groups of cells. The structure of the receptor determined by cross- linking 125I-EP was two equally labeled proteins of 100 Kd and 85 Kd molecular mass in all these mouse erythroid cells. The structure of the receptor was found to be very similar in human erythroid colony forming cells cultured from normal blood. These cells respond to EP with erythroid maturation and were previously shown to have high and lower affinity receptors. Placentas from mice and rats were found to have only lower affinity receptors for EP, and when placental membranes were cross-linked to 125I-EP, the same 100 Kd and 85 Kd bands were found as seen in mouse and human erythroid cells. The structure of the receptor was similar in cells that have high affinity receptors (FVA-infected and human erythroid colony-forming cells) and nonresponsive erythroid cells and placenta that have lower affinity receptors, but only the cells with the high affinity receptors respond to the addition of EP with erythroid maturation.
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Sawyer, ST, SB Krantz, and K. Sawada. "Receptors for erythropoietin in mouse and human erythroid cells and placenta." Blood 74, no. 1 (1989): 103–9. http://dx.doi.org/10.1182/blood.v74.1.103.bloodjournal741103.
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High and lower affinity receptors for erythropoietin (EP) were initially identified on a very pure population of EP-responsive erythroblasts obtained from the spleens of mice infected with anemia strain of Friend virus (FVA). The structure of the receptor for EP in these cells was determined to be proteins of 100 and 85 Kd by cross- linking 125I-EP. In this investigation, studies on the receptors for EP were extended to other mouse erythroid cells and human erythroid cells as well as to the placentas of mice and rats. Only lower affinity receptors for EP were detected on erythroblasts purified from the spleens of mice infected with the polycythemia strain of Friend virus and a murine erythroleukemia cell line, both of which are not responsive to EP in culture. Internalization of 125I-EP was observed in both groups of cells. The structure of the receptor determined by cross- linking 125I-EP was two equally labeled proteins of 100 Kd and 85 Kd molecular mass in all these mouse erythroid cells. The structure of the receptor was found to be very similar in human erythroid colony forming cells cultured from normal blood. These cells respond to EP with erythroid maturation and were previously shown to have high and lower affinity receptors. Placentas from mice and rats were found to have only lower affinity receptors for EP, and when placental membranes were cross-linked to 125I-EP, the same 100 Kd and 85 Kd bands were found as seen in mouse and human erythroid cells. The structure of the receptor was similar in cells that have high affinity receptors (FVA-infected and human erythroid colony-forming cells) and nonresponsive erythroid cells and placenta that have lower affinity receptors, but only the cells with the high affinity receptors respond to the addition of EP with erythroid maturation.
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Broudy, VC, N. Lin, M. Brice, B. Nakamoto, and T. Papayannopoulou. "Erythropoietin receptor characteristics on primary human erythroid cells." Blood 77, no. 12 (1991): 2583–90. http://dx.doi.org/10.1182/blood.v77.12.2583.2583.
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Abstract Erythropoietin (EP) exerts its effects on erythropoiesis by binding to a cell surface receptor. We examined EP receptor expression during normal human erythroid differentiation and maturation from the burst- forming unit-erythroid (BFU-E) to the reticulocyte level. In contrast to previous studies, we assessed EP receptor number and affinity in erythroid precursors immunologically purified from fresh bone marrow aspirates or fetal liver samples and in reticulocytes purified from peripheral blood. EP receptors were quantitated by equilibrium binding experiments with 125I EP. We found that purified primary erythroblasts from both adult and fetal sources exhibited a single high-affinity (kd 100 pmol/L) binding site for EP under our experimental conditions, and 135 or 250 receptors per cell, respectively. Reticulocytes were devoid of EP receptors. We compared these data to in vitro-derived BFU-E progeny at both early and late stages of maturation. Cultured BFU-E progeny also displayed a single class of receptors of slightly lower affinity (210 to 220 pmol/L). Preparations enriched in colony-forming units-erythroid (CFU-E) and proerythroblasts (day 9 BFU-E progeny) displayed approximately 1,100 receptors per cell, whereas populations containing mature erythroblasts (day 14 BFU-E progeny) exhibited approximately 300 receptors per cell. Furthermore, information from binding experiments was complemented by autoradiography in both enriched BFU-E preparations, cultured BFU-E progeny (days 9 and 14), and marrow mononuclear cells. These studies are consistent with a peak in EP receptor expression at the CFU-E/proerythroblast stage and a decrease with further maturation to undetectable levels at the reticulocyte stage. These data examining EP receptor characteristics on freshly isolated erythroid precursor cells complement previous data on EP receptor biology using culture-derived erythroblasts.
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Broudy, VC, N. Lin, M. Brice, B. Nakamoto, and T. Papayannopoulou. "Erythropoietin receptor characteristics on primary human erythroid cells." Blood 77, no. 12 (1991): 2583–90. http://dx.doi.org/10.1182/blood.v77.12.2583.bloodjournal77122583.
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Erythropoietin (EP) exerts its effects on erythropoiesis by binding to a cell surface receptor. We examined EP receptor expression during normal human erythroid differentiation and maturation from the burst- forming unit-erythroid (BFU-E) to the reticulocyte level. In contrast to previous studies, we assessed EP receptor number and affinity in erythroid precursors immunologically purified from fresh bone marrow aspirates or fetal liver samples and in reticulocytes purified from peripheral blood. EP receptors were quantitated by equilibrium binding experiments with 125I EP. We found that purified primary erythroblasts from both adult and fetal sources exhibited a single high-affinity (kd 100 pmol/L) binding site for EP under our experimental conditions, and 135 or 250 receptors per cell, respectively. Reticulocytes were devoid of EP receptors. We compared these data to in vitro-derived BFU-E progeny at both early and late stages of maturation. Cultured BFU-E progeny also displayed a single class of receptors of slightly lower affinity (210 to 220 pmol/L). Preparations enriched in colony-forming units-erythroid (CFU-E) and proerythroblasts (day 9 BFU-E progeny) displayed approximately 1,100 receptors per cell, whereas populations containing mature erythroblasts (day 14 BFU-E progeny) exhibited approximately 300 receptors per cell. Furthermore, information from binding experiments was complemented by autoradiography in both enriched BFU-E preparations, cultured BFU-E progeny (days 9 and 14), and marrow mononuclear cells. These studies are consistent with a peak in EP receptor expression at the CFU-E/proerythroblast stage and a decrease with further maturation to undetectable levels at the reticulocyte stage. These data examining EP receptor characteristics on freshly isolated erythroid precursor cells complement previous data on EP receptor biology using culture-derived erythroblasts.
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Fang, K. M., W. H. Shu, H. C. Chang, J. J. Wang, and O. T. Mak. "Study of prostaglandin receptors in mitochondria on apoptosis of human lung carcinoma cell line A549." Biochemical Society Transactions 32, no. 6 (2004): 1078–80. http://dx.doi.org/10.1042/bst0321078.
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PGs (prostaglandins) are synthesized through the cyclo-oxygenase (COX-1 and -2) pathway in a variety of cells in response to various physiological stimuli. All cells require at least one pathway for apoptosis, and mitochondrial play a central role in regulation of apoptosis. In a previous study, incubation of A549 cells with NS-398 (a COX-2-specific inhibitor) induced apoptosis and inhibited cell proliferation, and the concentrations of different PGs between various cellular compartments were found to be changed. To determine whether PG receptors are involved in this regulation, Western-blot analyses were performed specific for PGE2 (EP receptors) and PGF2α (FP receptor) receptors, which were expressed in A549 cells. Western-blot analysis revealed that mitochondria that were isolated from A549 cells expressed EP receptors (EP2, EP3 and EP4), whereas FP receptors were undetectable. EP receptors (EP1, EP3 and EP4) and FP receptors were detected from A549 cell membrane. These results suggest that the change of PG production in A549-cells-induced cancer cell apoptosis might be related to the different expressions of EP and FP receptors in cell and mitochondrial membrane.
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Wognum, AW, PM Lansdorp, RK Humphries, and G. Krystal. "Detection and isolation of the erythropoietin receptor using biotinylated erythropoietin." Blood 76, no. 4 (1990): 697–705. http://dx.doi.org/10.1182/blood.v76.4.697.697.
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Abstract Procedures have been developed to label human erythropoietin (Ep) with biotin to detect and isolate the Ep-receptor. The labeling method used the abundant carbohydrate groups on Ep and resulted in biologically active biotin-Ep (b-Ep) containing 8 to 10 biotins per Ep molecule. Specific binding of b-Ep to cells from spleens of mice made anemic by phenylhydrazine injections was demonstrated using 125I-labeled streptavidin. B-Ep, together with fluorescently tagged streptavidin, was found to specifically detect Ep-receptor-bearing cells by flow cytometry. This was demonstrated in several ways. First, approximately 90% of nucleated spleen cells from phenylhydrazine-treated mice were clearly fluorescent after staining with b-Ep and streptavidin- phycoerythrin, whereas only background fluorescence was detected using spleen cells from untreated mice. In addition, Ep-receptors were detected on 5% to 10% of normal mouse bone marrow cells, and these cells could be identified as erythroid in nature by separating the cells into subpopulations based on light-scatter properties. Third, Ep- receptor expression was found to correlate positively with expression of transferrin receptors, confirming the erythroid nature of these cells. B-Ep was also used to isolate Ep-receptors from monkey COS cells transfected with the murine Ep-receptor cDNA. In these experiments a cell-surface-bound protein of approximately 65 Kd and an intracellular protein of approximately 60 Kd were isolated from these cells. The procedures described in this report for detecting Ep-receptor expressing cells and for isolating the Ep-receptor should be valuable for purifying erythroid cells from heterogeneous cell populations, for elucidating the structure of the Ep-receptor, and for studying the biological activities of Ep at the cellular and molecular level.
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Wognum, AW, PM Lansdorp, RK Humphries, and G. Krystal. "Detection and isolation of the erythropoietin receptor using biotinylated erythropoietin." Blood 76, no. 4 (1990): 697–705. http://dx.doi.org/10.1182/blood.v76.4.697.bloodjournal764697.
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Procedures have been developed to label human erythropoietin (Ep) with biotin to detect and isolate the Ep-receptor. The labeling method used the abundant carbohydrate groups on Ep and resulted in biologically active biotin-Ep (b-Ep) containing 8 to 10 biotins per Ep molecule. Specific binding of b-Ep to cells from spleens of mice made anemic by phenylhydrazine injections was demonstrated using 125I-labeled streptavidin. B-Ep, together with fluorescently tagged streptavidin, was found to specifically detect Ep-receptor-bearing cells by flow cytometry. This was demonstrated in several ways. First, approximately 90% of nucleated spleen cells from phenylhydrazine-treated mice were clearly fluorescent after staining with b-Ep and streptavidin- phycoerythrin, whereas only background fluorescence was detected using spleen cells from untreated mice. In addition, Ep-receptors were detected on 5% to 10% of normal mouse bone marrow cells, and these cells could be identified as erythroid in nature by separating the cells into subpopulations based on light-scatter properties. Third, Ep- receptor expression was found to correlate positively with expression of transferrin receptors, confirming the erythroid nature of these cells. B-Ep was also used to isolate Ep-receptors from monkey COS cells transfected with the murine Ep-receptor cDNA. In these experiments a cell-surface-bound protein of approximately 65 Kd and an intracellular protein of approximately 60 Kd were isolated from these cells. The procedures described in this report for detecting Ep-receptor expressing cells and for isolating the Ep-receptor should be valuable for purifying erythroid cells from heterogeneous cell populations, for elucidating the structure of the Ep-receptor, and for studying the biological activities of Ep at the cellular and molecular level.
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Audoly, Laurent P., Stephen L. Tilley, Jennifer Goulet, et al. "Identification of specific EP receptors responsible for the hemodynamic effects of PGE2." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (1999): H924—H930. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h924.
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To identify the E-prostanoid (EP) receptors that mediate the hemodynamic actions of PGE2, we studied acute vascular responses to infusions of PGE2using lines of mice in which each of four EP receptors (EP1 through EP4) have been disrupted by gene targeting. In mixed groups of males and females, vasodepressor responses after infusions of PGE2were significantly diminished in the EP2 −/− and EP4 −/− lines but not in the EP1 −/− or EP3 −/− lines. Because the actions of other hormonal systems that regulate blood pressure differ between sexes, we compared the roles of individual EP receptors in males and females. We found that the relative contribution of each EP-receptor subclass was strikingly different in males from that in females. In females, the EP2 and EP4 receptors, which signal by stimulating adenylate cyclase, mediate the major portion of the vasodepressor response to PGE2. In males, the EP2 receptor has a modest effect, but most of the vasodepressor effect is mediated by the phospholipase C-coupled EP1receptor. Finally, in male mice, the EP3 receptor actively opposes the vasodepressor actions of PGE2. Thus the hemodynamic actions of PGE2 are mediated through complex interactions of several EP-receptor subtypes, and the role of individual EP receptors differs dramatically in males from that in females. These differences may contribute to sexual dimorphism of blood pressure regulation.
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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 events, including follicle rupture, absence of an oocyte, and thickening of the granulosa cell layer. Indomethacin-injected follicles did not rupture and contained oocytes surrounded by unexpanded cumulus; granulosa cell hypertrophy did not occur. Follicles injected with indomethacin plus PGE2 were similar to vehicle-injected ovaries, indicating that PGE2 restored the ovulatory changes inhibited by indomethacin. Additional follicles were injected with indomethacin plus an agonist for each EP receptor. EP1, EP2, and EP4 agonists each promoted aspects of follicle rupture, but no single EP agonist recapitulated normal follicle rupture as seen in follicles injected with either vehicle or indomethacin plus PGE2. Although EP4 agonist-injected follicles contained oocytes in unexpanded cumulus, the absence of oocytes in EP1 agonist- and EP2 agonist-injected follicles suggests that these EP receptors promote cumulus expansion. Surprisingly, the EP3 agonist did not stimulate any of these ovulatory changes, despite the high level of EP3 receptor expression in the monkey follicle. Therefore, agonists and antagonists selective for EP1 and EP2 receptors hold the most promise for control of ovulatory events in women.
Dissertations / Theses on the topic "Receptores EP"
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Gomes, Renata Nascimento. "Análise do perfil dos prostanoides e do seu papel no controle da migração celular em glioblastoma." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-23012017-094918/.
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O glioblastoma (GBM) é o tumor mais frequente do sistema nervoso central com um alto grau de malignidade e um prognóstico desfavorável. Apesar dos avanços nas técnicas cirúrgicas e de radioterapia e/ou quimioterapia, não há tratamento eficiente disponível para o GBM. Os prostanoide são derivados do ácido araquidônico e estão envolvidas com vários processos do desenvolvimento e progressão do câncer. O objetivo deste estudo foi analisar in vitro o perfil de diferentes prostanoides nas linhagens de GBM. Além de analisar o papel dos prostanoides e dos receptores na migração celular de GBM. Os resultados demostraram um perfil dos prostanoides da série 2 diferente entre as linhagens, além da expressão dos genes envolvidos na biossíntese de PGE2. Nos ensaios de migração os dados demostraram que os tratamentos realizados com os prostanoides exógenos aumentaram a migração celular e os tratamentos com os antagonistas de EP2 e EP4 diminuiram a migração. Em conjunto esses resultados, demonstram o papel importante dos prostanoides, especialmente PGE2, no processo de migração das células de GBM.<br>Glioblastoma (GBM) is the most common tumor of the central nervous system with a high degree of malignancy and poor prognosis. Despite advances in surgical techniques and radiation therapy and/or chemotherapy, there is no effective treatment available for GBM. The prostanoid are derived from arachidonic acid and are involved in many processes of development and progression of cancer. The aim of this study was to analyze in vitro profile of different prostanoids in the lines of GBM. In addition to analyzing the role of prostanoids and receptors on the cell migration of GBM. The results showed a profile of series 2 prostanoids the different between the cell lines, in addition to expression of genes involved in the biosynthesis of PGE2. In migration testing data showed that the treatments performed with exogenous prostanoids increased cell migration and treatment with antagonists of EP2 and EP4 decreased migration. Together these results demonstrate the important role of prostanoids, especially PGE2, in the migration process of the GBM cells.
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Reschke, Cristina Ruedell. "RECEPTORES EP1 E EP3 MODULAM AS CRISES EPILÉPTICAS INDUZIDAS POR PENTILENOTETRAZOL E ÁCIDO CAÍNICO EM CAMUNDONGOS." Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/3852.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior<br>Epilepsy is one of the most common neurologic disorders. It has been suggested that
seizures may be facilitaded by inflammation. PGE2 is one of the most important inflammatory
mediators, and facilitates pentylenetetrazol (PTZ)-induced seizures by stimulating EP1 and
EP3 receptors. However, up to the present moment, no study has investigated whether EP1
and EP3 receptors blocking attenuate seizures induced by convulsants other than PTZ. It is
also unknown whether Na+,K+-ATPase activity alterations are involved in such an effect.
Therefore, in the current study we investigated whether EP1 and EP3 ligands (agonists and
antagonists) modulate PTZ- and kainic acid (KA)-induced seizures, and whether alterations
in Na+,K+-ATPase activity mediate such a protective effect, in mice. EP1 and EP3
antagonists (ONO-8713 and ONO-AE3-240, respectively, 10 Og/kg, s.c.) attenuated PTZ (60
mg/kg, i.p.)- and KA (20 mg/kg, i.p.)-induced seizures. The respective agonists (ONO-DI-004
and ONO-AE-248, 10 Og/kg, s.c.) facilitated seizures in both acute models, and at noneffective
doses, prevented the protective effects of the antagonists. Animals injected with
PTZ presented decreased Na+,K+-ATPase activity in the cerebral cortex and hippocampus.
On the other hand, animals injected with KA presented increased Na+,K+-ATPase activity in
the same cerebral structures at the end of the experiment. These divergent findings suggest
that alterations in Na+,K+-ATPase activity in both acute models depends on the convulsant
agent used and make difficult to establish a relationship between Na+,K+-ATPase activity and
seizure development. Moreover, EP1 and EP3 antagonists administration abolished Na+,K+-
ATPase activity alterations induced by PTZ and KA, in such a way that these alterations
seem to be related more to the presence of ictal phenomenon itself than to the seizure
induction mechanisms. Notwithstanding, the currrent results clearly show that EP1 and EP3
receptors might constitute novel targets for anticonvulsants development, since EP1 and
EP3 decreased seizures, regardless of the convulsant agent used.<br>A epilepsia é uma das disfunções neurológicas mais comuns. Tem sido sugerido que as
crises epilépticas podem ser facilitadas pela ocorrência de inflamação. A PGE2 é um dos
mediadores inflamatórios mais importantes que, agindo por meio dos receptores EP1 e EP3,
facilita as convulsões induzidas por pentilenotetrazol (PTZ). Contudo, até a presente data,
nenhum estudo investigou, de maneira sistêmica, se a ativação ou bloqueio de receptores
EP1 e EP3 facilitam as convulsões induzidas por outros agentes; tampouco se alterações na
atividade da Na+,K+-ATPase estão envolvidas nesse efeito. Assim, no presente estudo,
investigamos se ligantes (agonistas e antagonistas) de receptores EP1 e EP3 modificam as
crises induzidas por PTZ e ácido caínico (KA), e se tais efeitos estão associados a
alterações na atividade da enzima Na+,K+-ATPase, em camundongos. Os antagonistas EP1
e EP3 (ONO-8713 e ONO-AE3-240, respectivamente, 10 Og/Kg, s.c.) atenuaram as
convulsões induzidas por PTZ (60 mg/Kg, i.p.) e KA (20 mg/Kg). Os seus respectivos
agonistas (ONO-DI-004 e ONO-AE-248 de 10 Og/Kg, s.c.) facilitaram as convulsões em
ambos modelos agudos de crises epilépticas e, em doses não efetivas para gerar crises,
preveniram os efeitos dos antagonistas. Os animais submetidos à administração de PTZ
apresentaram, ao final do experimento, a atividade Na+,K+-ATPásica diminuída no córtex
cerebral e hipocampo. Por outro lado, animais tratados com KA apresentaram um aumento
na atividade Na+,K+-ATPásica nestas mesmas estruturas, que se correlacionou
positivamente com a vigência de status epilepticus no momento do sacrifício. Os achados
divergentes no que diz respeito à alteração da atividade da Na+,K+-ATPase nos dois
modelos de crises agudas sugere que tais alterações estejam relacionadas ao tipo de
agente convulsivante utilizado, e dificultam estabelecer, de forma inequívoca, uma relação
entre atividade desta ATPase e sensibilidade à crises agudas. Ademais, a administração de
antagonistas EP1 e EP3 aboliu as alterações da atividade da Na+,K+-ATPase induzidas tanto
por PTZ como por KA, de tal forma que estas parecem estar mais associadas com o
fenômeno ictal em si, do que com os mecanismos de indução da crise. Contudo, os
resultados mostram de forma clara que os receptores EP1 e EP3 podem se constituir
possíveis novos alvos para o desenvolvimento de drogas antiepilépticas, pois antagonistas
EP1 e EP3 diminuíram as crises, independente do agente convulsivante utilizado.
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Ratzlaff, Viviane. "Padronização e validação de um novo modelo de febre induzida pela injeção intratecal de prostaglandina e2 em ratos jovens." Universidade Federal de Santa Maria, 2006. http://repositorio.ufsm.br/handle/1/11148.
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The fever response, besides being part of host defense response to infection or inflammation, is associated with discomfort and anxiety and may constitute a risk for febrile seizures in children. Therefore, antipyretic therapy is routinely prescribed for febrile patients. The animal models of fever using the systemic injection of lipopolysaccharide (LPS) and Baker yeast, described in the literature, are suitable for screening of novel antipyretics, but they do not provide information regarding the mechanism of action of these compounds. Therefore, the present study aimed to describe and validate a model of fever induction by prostaglandin (PG) E2, the final mediator of febrile response in the central nervous system, in young male Wistar rats (25-30 days of age). In this protocol, PGE2 was injected intrathecally without implantation of cannula. Rectal temperature (TR) was recorded every thirty minutes for three hours after PGE2 injection (08:00 11:00 h). The intrathecal (i.t.) injection of PGE2 10 ηg in 100 μL/animal induced fever in the animals, which was prevented by administration of EP1 and EP3 receptors antagonists, but did not by antagonist of EP4 receptor. In addition, the classic antipyretics dipyrone and acetaminophen, at doses that had no effect per se on TR of animals, did not revert the fever induced by i.t. injection of PGE2. This model seems suitable to investigate whether the action of antipyretics occurs upstream or downstream the prostaglandin coupling in EP receptors. In addition, this protocol is advantageous from the technical, ethical and economical point of view compared to others PGE2-induced fever protocols described in the literature, because trepanation for cannula implantation is not required, reducing the inflammatory response, animals suffering and experimental costs.<br>A febre, apesar de fazer parte da resposta de defesa do hospedeiro à infecção ou inflamação, está associada com desconforto e ansiedade, além de representar um risco iminente de convulsões febris em crianças. Por isso, terapia antipirética é rotineiramente prescrita a pacientes febris. Os modelos animais de febre empregando a injeção sistêmica de lipopolissacarídeo (LPS) e fermento de padeiro, descritos na literatura, são úteis para a triagem de novos antipiréticos, mas não fornecem informações a respeito do mecanismo de ação desses compostos. Diante disso, o presente estudo objetivou padronizar e validar um modelo de indução de febre por prostaglandina (PG) E2, o mediador final da resposta febril no sistema nervoso central, em ratos machos jovens da raça Wistar (25-30 dias). Neste protocolo, a PGE2 foi injetada pela via intratecal (i.t.), não necessitando a implantação de cânula. A temperatura retal (TR) foi registrada a cada trinta minutos durante três horas após a injeção da PGE2 (08:00-11:00 h). A injeção i.t. de PGE2 10 ηg em 100 μL/animal induziu febre nos animais, a qual foi prevenida pela
administração de antagonistas dos receptores EP1 e EP3, mas não por antagonista do receptor EP4. Além disso, os antipiréticos clássicos dipirona e paracetamol, em doses que não tiveram efeito per se na TR dos animais, não reverteram a febre induzida por PGE2 i.t. Este modelo parece útil para investigar se a ação dos antipiréticos ocorre antes ou depois da ligação da PGE2 em seus receptores EP. Além disso, este protocolo é vantajoso do ponto de vista técnico, ético e econômico em relação aos outros protocolos de indução de febre por PGE2 descritos na literatura, porque a trepanação para implantação de cânula não é necessária, reduzindo a resposta inflamatória, o sofrimento dos animais e os custos
experimentais.
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Milne, Stuart Angus. "Characterisation of the inhibitory EP-receptors present in human monocytes." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22496.
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Rahal, Sherine S. "The role of prostaglandin EP receptors in a model of glomerulonephritis." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26750.
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Prostaglandin E2 (PGE2) interacts with four E-Prostanoid (EP) receptor subtypes---designated EP1--4 . In glomerulonephritis (GN), a renal inflammatory disease, inhibition of enhanced renal PGE2 synthesis by nonsteroidal-anti-inflammatory drugs (NSAIDs), results in both beneficial anti-proteinuric effects and deleterious side effects on renal blood flow (RBF) and Na+ homeostasis, implying that one or more EP subtypes may mediate these actions. We set out to investigate the role of the EP1 receptor in GN since it localizes to the collecting duct, where it may regulate Na+ homeostasis, in podocytes and mesangial cells, where it could alter the permeability of the glomerulus, and in arterioles, where EP, receptors may induce vasoconstriction thereby reducing RBF. A mouse model of GN was induced in wildtype (wt) and EP1-/- mice using an anti-rat-glomerular basement membrane (anti-GBM) antibody. Proteinuria was similar in GN wt and GN EP1-/- groups thereby negating a role for this subtype in modulating filtration barrier permeability. (Abstract shortened by UMI.)
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Slipetz, Deborah M. "The prostaglandin E₂ EP₄ receptor : the elucidation of agonist mediated receptor regulation and a novel therapeutic role for an EP₄ agonist in allergic lung inflammation." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111868.
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Prostaglandin (PG) E2 is involved in a number of physiological and path op hysiologicaI events in many tissues. PGE2 mediates its actions through interaction with specific plasma-membrane G-protein coupled receptors (GPCR's). There are four subtypes of PGE2 receptors: EP1, EP2, EP3 and EP4, classified by their different pharmacological profiles and signal transduction pathways. EP4 agonists have potential therapeutic benefit in diseases such as osteoporosis (EP4 mediates the bone anabolic actions of PGE 2), but possibly in other areas such as asthma. A characteristic feature of GPCR's is their ability to undergo agonist-induced desensitization and this response may limit the therapeutic utility of agonists due to tachyphylaxis.<br>This thesis outlines [1] the agonist-induced regulation of EP4 by PGE2; [2] the development of a novel selective agonist of EP 4 that also mediates EP4 desensitization; and [3] the discovery of a new role for EP4 in mouse models of allergic lung inflammation by employing this selective agonist. PGE2 challenge of EP 4 in human embryonic kidney cells results in desensitization of intracellular signalling responses (cAMP), phosphorylation independent of protein kinase A and sequestration. These events are mediated by sequences in the carboxyl-terminal tail of EP4. EP4 agonists were discovered by preparing analogues of PGE2 by replacing the hydroxycyclopentanone ring by a lactam. Optimized compound (19a) shows high potency at EP4 and is highly selective over the other seven prostaglandin receptors. In vivo stability was increased further by the addition of a gem di-fluro group on carbon 15 of the molecule. The resulting compound, EP 4_Ags, was employed to selectively elucidate the role of EP4 in mouse models of allergic lung inflammation. The EP4 agonist prevents ovalbumin (OVA)-induced inflammation, airways hyperreactivity (AHR) and T helper (Th) 2 cytokine increases. While interleukin (IL)-13-induced inflammation is not inhibited by the EP4 agonist, AHR is attenuated. These results demonstrate that an EP4 agonist has potent anti-inflammatory activity in a mouse model of allergen-induced lung inflammation. Additionally, EP4 may have effects on AHR independent of its anti-inflammatory activity. Interestingly, the rapid desensitization observed in-vitro did not appear to limit efficacy in-vivo. The role of EP4 in mouse models of allergic lung inflammation is a novel finding and the use of an EP4 agonist may have therapeutic benefit in the treatment of asthma.
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Li, Sau Wei. "Pharmacological characterization of human neutrophil prostanoid EP receptors : modulation of neutrophil function." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307121.
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Arulkumaran, Shankari. "The roles of prostanoid EP receptors in the control of contractions of human myometrium." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9305.
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The primary function of the uterus during pregnancy is to harbour the growing fetus in a quiescent environment. Upon maturation of the fetus, the uterus generates forceful contractions during labour. Prostaglandins are central in the parturition process. PGE2 in particular, is produced in large quantities by fetal membranes and possible roles include cervical ripening and the stimulation of uterine contractions. PGE2 exhibits a wide spectrum of physiological actions depending on the distribution and subtypes of EP receptors. EP1 and EP3 mediate contractions, but there is no consensus about their relative importance. Preliminary experiments were undertaken to examine the possible expression patterns of EP1 and EP3. The expression data showed there to be no significant changes between the localisation in upper or lower segment biopsies using both RNA and protein samples. However, there was a labour associated change seen in EP3 isoform expression at mRNA level together with changes in the protein expression of EP3 in the lower segment using immunofluorescence. Given that the expression studies suggest that it is the EP3 receptor, and not the EP1 receptor, that is most important in myometrial contractility, I established an in vitro tissue bath to conduct functional studies examining contractility in upper and lower segment myometrial biopsies. My data demonstrated that stretch of term human myometrium results in spontaneous contractions. There was no difference between upper and lower segment myometrium, so subsequent experiments were conducted on lower segment biopsies. The addition of acetyl salicylic acid (a non-selective COX inhibitor) did not completely stop spontaneous contractility but reduced the total work done significantly. This could be reversed by add back of PGE2. Prostaglandins are therefore significant but not crucial for spontaneous contractility. Both PGE2 and PGF2α increased the total work done significantly compared to spontaneous contractions; E2 more so than F2α. The PGF2α antagonist did not inhibit spontaneous contractions, but did inhibit PGF2α induced contractions. The EP1 antagonist did not inhibit spontaneous contractions but EP3 antagonist did. These results suggest that an EP3 antagonist is a better candidate as a new tocolytic compound compared to FP or EP1 antagonist.
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Akram, Asha. "Examining the potential of PGE₂ receptor EP₄ as a neuroprotective target following ischaemic injury." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28245.
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Ischaemic stroke instigates a series of pathological mechanisms which contribute to injury. Despite significant research in this field successful clinical treatment is limited. This highlights the need to identify novel therapeutic targets in order to assess whether clinical investigation is warranted. The enzyme cyclooxygenase-2 (COX-2) is a key contributor to inflammatory injury following stroke. Upregulation of this enzyme results in increased prostanoid synthesis, which mediate many physiological and pathological functions. Prostaglandin E₂ (PGE₂) is a key mediator in inflammation and activation of its receptor subtypes is both neuroprotective and neurotoxic. COX-2 inhibition in animal models of stroke has demonstrated neuroprotection. However, long term arthritis trials have revealed detrimental effects of COX-2 inhibitors. This highlights the need to identify mediators of the detrimental effects of COX-2 and capitalise those that mediate the beneficial effects. The aim of this study was to investigate the role of the PGE₂ receptor EP₄ following in vitro and in vivo ischaemia. Organotypic hippocampal sliced cultures (OHSCs) were exposed to oxygen and glucose deprivation (OGD). Treatment with a selective EP₄ agonist following OGD significantly reduced cell death, whereas application of the EP₄ receptor antagonist exacerbated injury. C57/BL6 mice were subjected to focal cerebral ischaemia via middle cerebral artery occlusion (MCAO). Administration of the selective EP₄ agonist significantly reduced infarct volume and prevented the decline in neurological function. COX-2 inhibition and EP₄ receptor stimulation resulted in similar levels of protection both in vitro and in vivo ischaemia. EP₄ receptor expression was assessed using immunohistochemistry and real time-PCR. This study provides evidence that selective activation of the EP₄ receptor following ischaemic injury is as neuroprotective as COX-2 inhibition but possibly without the deleterious side effects of COX-2 inhibitors. This supports the concept of targeting protective prostaglandin receptor signalling as a potential therapeutic target for stroke.
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Katsuyama, Masato. "A Study on the Structure and Function of the Prostaglandin E Receptor Subtype EP[2]." 京都大学 (Kyoto University), 1998. http://hdl.handle.net/2433/73162.
Full textBook chapters on the topic "Receptores EP"
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Takeuchi, Koji, Shinichi Kato, Yusaku Komoike, Yoshihiro Ogawa, and Masanori Takeeda. "Gastric Cytoprotection by Prostaglandin E2 — Relation to EP Receptor Subtypes —." In Mechanisms and Consequences of Proton Transport. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0971-4_21.
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Zeng, Li, Songzhu An, and Edward J. Goetzl. "EP Receptor Subtype-Dependence of Regulation of Immune Cellular Functions by Prostaglandin E2." In Frontiers in Bioactive Lipids. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5875-0_23.
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Takeuchi, K., S. Kato, and A. Tanaka. "Gastrointestinal Protective Action of Prostaglandin E2 and EP Receptor Subtypes." In Frontiers of Gastrointestinal Research. KARGER, 2002. http://dx.doi.org/10.1159/000060970.
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Jones, Robert L. "EP Prostanoid Receptors." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60088-1.
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Jones, Robert L. "EP-1 Prostanoid Receptor." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60089-3.
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Jones, Robert L. "EP-2 Prostanoid Receptor." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60090-x.
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Jones, Robert L. "EP-3 Prostanoid Receptor." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60336-8.
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Jones, Robert L. "EP-4 Prostanoid Receptor." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60337-x.
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Takeuchi, Koji. "Prostaglandin EP Receptors and Their Roles in Mucosal Protection and Ulcer Healing in the Gastrointestinal Tract." In Advances in Clinical Chemistry. Elsevier, 2010. http://dx.doi.org/10.1016/s0065-2423(10)51005-9.
Full textConference papers on the topic "Receptores EP"
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Morelli, H., D. Villalba, S. D. Shah, A. P. Nayak, and R. B. Penn. "Airway Smooth Muscle Contraction: Distinct EP Receptors, Different Outcomes." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1253.
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Holt, Dawn M., Xinrong Ma, Namita Kundu, and Amy M. Fulton. "Abstract 5308: Targeting the Cox2 pathway prostaglandin EP receptors to regulate NK cell functions." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5308.
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Nayak, A. P., D. Villalba, J. V. Michael, S. W. Twardus, S. S. An, and R. B. Penn. "Differential Regulation of Airway Smooth Muscle Function by E-Prostanoid (EP) Receptor Subtypes." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4283.
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Van Geffen, Chiel, Sandra Beer-Hammera, Bernd Nürnberg, and Saeed Kolahian. "Generation and activation of myeloid derived suppressor cells using prostaglandin E2 and EP receptor agonists in vitro." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3871.
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