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Pesquisa : D12.776.543.750.695.220 [Categoria DeCS]
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  1 / 3658 MEDLINE  
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[PMID]:28938016
[Au] Autor:Wang J; Ma HY; Krishnamoorthy RR; Yorio T; He S
[Ad] Endereço:Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
[Ti] Título:A feed-forward regulation of endothelin receptors by c-Jun in human non-pigmented ciliary epithelial cells and retinal ganglion cells.
[So] Source:PLoS One;12(9):e0185390, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:c-Jun, c-Jun N-terminal kinase(JNK) and endothelin B (ETB) receptor have been shown to contribute to the pathogenesis of glaucoma. Previously, we reported that an increase of c-Jun and CCAAT/enhancer binding protein ß (C/EBPß) immunohistostaining is associated with upregulation of the ETB receptor within the ganglion cell layer of rats with elevated intraocular pressure (IOP). In addition, both transcription factors regulate the expression of the ETB receptor in human non-pigmented ciliary epithelial cells (HNPE). The current study addressed the mechanisms by which ET-1 produced upregulation of ET receptors in primary rat retinal ganglion cells (RGCs) and HNPE cells. Treatment of ET-1 and ET-3 increased the immunocytochemical staining of c-Jun and C/EBPß in primary rat RGCs and co-localization of both transcription factors was observed. A marked increase in DNA binding activity of AP-1 and C/EBPß as well as elevated protein levels of c-Jun and c-Jun-N-terminal kinase (JNK) were detected following ET-1 treatment in HNPE cells. Overexpression of ETA or ETB receptor promoted the upregulation of c-Jun and also elevated its promoter activity. In addition, upregulation of C/EBPß augmented DNA binding and mRNA expression of c-Jun, and furthermore, the interaction of c-Jun and C/EBPß was confirmed using co-immunoprecipitation. Apoptosis of HNPE cells was identified following ET-1 treatment, and overexpression of the ETA or ETB receptor produced enhanced apoptosis. ET-1 mediated upregulation of c-Jun and C/EBPß and their interaction may represent a novel mechanism contributing to the regulation of endothelin receptor expression. Reciprocally, c-Jun was also found to regulate the ET receptors and C/EBPß appeared to play a regulatory role in promoting expression of c-Jun. Taken together, the data suggests that ET-1 triggers the upregulation of c-Jun through both ETA and ETB receptors, and conversely c-Jun also upregulates endothelin receptor expression, thereby generating a positive feed-forward loop of endothelin receptor activation and expression. This feed-forward regulation may contribute to RGC death and astrocyte proliferation following ET-1 treatment.
[Mh] Termos MeSH primário: Células Epiteliais/enzimologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Receptores de Endotelina/metabolismo
Células Ganglionares da Retina/enzimologia
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
Células Cultivadas
Cílios/enzimologia
Endotelina-1/metabolismo
Seres Humanos
Ligação Proteica
Ratos Sprague-Dawley
Fator de Transcrição AP-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Cebpb protein, rat); 0 (Endothelin-1); 0 (Receptors, Endothelin); 0 (Transcription Factor AP-1); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185390


  2 / 3658 MEDLINE  
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[PMID]:28705795
[Au] Autor:Hubert A; Bochenek ML; Schütz E; Gogiraju R; Münzel T; Schäfer K
[Ad] Endereço:From the Center for Cardiology, Cardiology I (A.H., M.L.B., E.S., R.G., T.M., K.S.) and Center for Thrombosis and Hemostasis (M.L.B.), University Medical Center Mainz, Germany.
[Ti] Título:Selective Deletion of Leptin Signaling in Endothelial Cells Enhances Neointima Formation and Phenocopies the Vascular Effects of Diet-Induced Obesity in Mice.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1683-1697, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Obesity is associated with elevated circulating leptin levels and hypothalamic leptin resistance. Leptin receptors (LepRs) are expressed on endothelial cells, and leptin promotes neointima formation in a receptor-dependent manner. Our aim was to examine the importance of endothelial LepR (End.LepR) signaling during vascular remodeling and to determine whether the cardiovascular consequences of obesity are because of hyperleptinemia or endothelial leptin resistance. APPROACH AND RESULTS: Mice with loxP-flanked LepR alleles were mated with mice expressing Cre recombinase controlled by the inducible endothelial receptor tyrosine kinase promoter. Obesity was induced with high-fat diet. Neointima formation was examined after chemical carotid artery injury. Morphometric quantification revealed significantly greater intimal hyperplasia, neointimal cellularity, and proliferation in End.LepR knockout mice, and similar findings were obtained in obese, hyperleptinemic End.LepR wild-type animals. Analysis of primary endothelial cells confirmed abrogated signal transducer and activator of transcription-3 phosphorylation in response to leptin in LepR knockout and obese LepR wild-type mice. Quantitative PCR, ELISA, and immunofluorescence analyses revealed increased expression and release of endothelin-1 in End.LepR-deficient and LepR-resistant cells, and ET receptor A/B antagonists abrogated their paracrine effects on murine aortic smooth muscle cell proliferation. Reduced expression of peroxisome proliferator-activated receptor-γ and increased nuclear activator protein-1 staining was observed in End.LepR-deficient and LepR-resistant cells, and peroxisome proliferator-activated receptor-γ antagonization increased endothelial endothelin-1 expression. CONCLUSIONS: Our findings suggest that intact endothelial leptin signaling limits neointima formation and that obesity represents a state of endothelial leptin resistance. These observations and the identification of endothelin-1 as soluble mediator of the cardiovascular risk factor obesity may have relevant therapeutic implications.
[Mh] Termos MeSH primário: Lesões das Artérias Carótidas/complicações
Dieta Hiperlipídica
Células Endoteliais/metabolismo
Leptina/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Neointima
Obesidade/complicações
Receptores para Leptina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Artérias Carótidas/metabolismo
Artérias Carótidas/patologia
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/metabolismo
Lesões das Artérias Carótidas/patologia
Movimento Celular
Proliferação Celular
Células Cultivadas
Modelos Animais de Doenças
Células Endoteliais/patologia
Endotelina-1/metabolismo
Feminino
Genótipo
Integrases
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Obesidade/genética
Obesidade/metabolismo
Obesidade/patologia
PPAR gama/metabolismo
Comunicação Parácrina
Fenótipo
Fosforilação
Regiões Promotoras Genéticas
Receptor TIE-2/genética
Receptores de Endotelina/metabolismo
Receptores para Leptina/deficiência
Receptores para Leptina/genética
Fator de Transcrição STAT3/metabolismo
Remodelação Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Leptin); 0 (PPAR gamma); 0 (Receptors, Endothelin); 0 (Receptors, Leptin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (leptin receptor, mouse); EC 2.7.10.1 (Receptor, TIE-2); EC 2.7.10.1 (Tek protein, mouse); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309798


  3 / 3658 MEDLINE  
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[PMID]:28515172
[Au] Autor:Wang L; Song J; Wang S; Buggs J; Chen R; Zhang J; Wang L; Rong S; Li W; Wei J; Liu R
[Ad] Endereço:Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida; leiwang@health.usf.edu.
[Ti] Título:Cross-sex transplantation alters gene expression and enhances inflammatory response in the transplanted kidneys.
[So] Source:Am J Physiol Renal Physiol;313(2):F326-F338, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kidney transplantation (KTX) is a life-saving procedure for patients with end-stage renal disease. Expression levels of many genes in the kidney vary between males and females, which may play an essential role in the sex differences in graft function. However, whether these differences are affected after cross-sex-KTX is unknown. In the present study, we assessed postoperative changes in genotype, function, and inflammatory responses of the grafts in same-sex- and cross-sex-KTX. Single kidney transplants were performed between same and different sex C57BL/6 mice paired into four combination groups: female donor/female recipient (F/F); male donor/male recipient (M/M); female donor/male recipient (F/M); and male donor/female recipient (M/F). The remnant native kidney was removed 4 days posttransplant. Expression levels of genes related to the contractility of the afferent arteriole and tubular sodium reabsorption were assessed. Same-sex-KTX did not significantly alter the magnitude or sex difference pattern of gene expression in male or female grafts. Cross-sex-KTX showed an attenuated sex difference in gene expressions. The measurements of endothelin 1, endothelin ET receptor, Na -K -2Cl cotransporter 2 (NKCC2), and epithelial Na channels (ENaC) subunits exhibited decreases in M/F compared with M/M and increases in F/M compared with F/F. There were no significant differences in hemodynamics or sodium excretion in response to acute volume expansion for any sex combinations. Cross-sex-KTX stimulated more robust inflammatory responses than same-sex-KTX. IL-6 and KC mRNA levels elevated 5- to 20-fold in cross-sex-KTX compared with same-sex-KTX. In conclusion, cross-sex-KTX alters gene expression levels and induces inflammatory responses, which might play an important role in long-term graft function.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Transplante de Rim/efeitos adversos
Rim/metabolismo
Rim/cirurgia
Nefrite/genética
[Mh] Termos MeSH secundário: Animais
Endotelina-1/genética
Endotelina-1/metabolismo
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Feminino
Interação Gene-Ambiente
Genótipo
Hemodinâmica
Mediadores da Inflamação/metabolismo
Rim/irrigação sanguínea
Rim/patologia
Masculino
Camundongos Endogâmicos C57BL
Modelos Animais
Nefrite/metabolismo
Nefrite/patologia
Nefrite/fisiopatologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Angiotensina/genética
Receptores de Angiotensina/metabolismo
Receptores de Endotelina/genética
Receptores de Endotelina/metabolismo
Circulação Renal
Eliminação Renal
Fatores Sexuais
Sódio/metabolismo
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/genética
Trocadores de Sódio-Hidrogênio/metabolismo
Membro 1 da Família 12 de Carreador de Soluto/genética
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Epithelial Sodium Channels); 0 (Inflammation Mediators); 0 (RNA, Messenger); 0 (Receptors, Angiotensin); 0 (Receptors, Endothelin); 0 (Slc12a1 protein, mouse); 0 (Slc12a3 protein, mouse); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (Solute Carrier Family 12, Member 1); 0 (Solute Carrier Family 12, Member 3); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00039.2017


  4 / 3658 MEDLINE  
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[PMID]:28507171
[Au] Autor:Hunter RW; Moorhouse R; Farrah TE; MacIntyre IM; Asai T; Gallacher PJ; Kerr D; Melville V; Czopek A; Morrison EE; Ivy JR; Dear JW; Bailey MA; Goddard J; Webb DJ; Dhaun N
[Ad] Endereço:From the British Heart Foundation Centre of Research Excellence and The Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
[Ti] Título:First-in-Man Demonstration of Direct Endothelin-Mediated Natriuresis and Diuresis.
[So] Source:Hypertension;70(1):192-200, 2017 Jul.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin (ET) receptor antagonists are potentially novel therapeutic agents in chronic kidney disease and resistant hypertension, but their use is complicated by sodium and water retention. In animal studies, this side effect arises from ET receptor blockade in the renal tubule. Previous attempts to determine whether this mechanism operates in humans have been confounded by the hemodynamic consequences of ET receptor stimulation/blockade. We aimed to determine the effects of ET signaling on salt transport in the human nephron by administering subpressor doses of the ET-1 precursor, big ET-1. We conducted a 2-phase randomized, double-blind, placebo-controlled crossover study in 10 healthy volunteers. After sodium restriction, subjects received either intravenous placebo or big ET-1, in escalating dose (≤300 pmol/min). This increased plasma concentration and urinary excretion of ET-1. Big ET-1 reduced heart rate (≈8 beats/min) but did not otherwise affect systemic hemodynamics or glomerular filtration rate. Big ET-1 increased the fractional excretion of sodium (from 0.5 to 1.0%). It also increased free water clearance and tended to increase the abundance of the sodium-potassium-chloride cotransporter (NKCC2) in urinary extracellular vesicles. Our protocol induced modest increases in circulating and urinary ET-1. Sodium and water excretion increased in the absence of significant hemodynamic perturbation, supporting a direct action of ET-1 on the renal tubule. Our data also suggest that sodium reabsorption is stimulated by ET-1 in the thick ascending limb and suppressed in the distal renal tubule. Fluid retention associated with ET receptor antagonist therapy may be circumvented by coprescribing potassium-sparing diuretics.
[Mh] Termos MeSH primário: Endotelina-1
Insuficiência Renal Crônica
Sódio/metabolismo
[Mh] Termos MeSH secundário: Adulto
Animais
Diurese/efeitos dos fármacos
Diurese/fisiologia
Método Duplo-Cego
Antagonistas dos Receptores de Endotelina/administração & dosagem
Antagonistas dos Receptores de Endotelina/efeitos adversos
Antagonistas dos Receptores de Endotelina/farmacocinética
Endotelina-1/administração & dosagem
Endotelina-1/efeitos adversos
Endotelina-1/farmacocinética
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Túbulos Renais/metabolismo
Túbulos Renais/fisiopatologia
Masculino
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Receptores de Endotelina/metabolismo
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/metabolismo
Insuficiência Renal Crônica/fisiopatologia
Resultado do Tratamento
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (Receptors, Endothelin); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.116.08832


  5 / 3658 MEDLINE  
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[PMID]:28302570
[Au] Autor:Chen M; Shu S; Yan HH; Pei L; Wang ZF; Wan Q; Bi LL
[Ad] Endereço:Department of Pathology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China; Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
[Ti] Título:Hippocampal Endothelin-1 decreases excitability of pyramidal neurons and produces anxiolytic effects.
[So] Source:Neuropharmacology;118:242-250, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anxiety disorders contribute to the pathophysiology of psychiatric diseases, including major depression, substance abuse, and schizophrenia. The hippocampus is important for anxiety modulation. However, the mechanisms that control the neuronal activity of the hippocampus in anxiety are still not clear. We found that Endothelin-1 (ET1) mRNA in the hippocampus was down-regulated in high-anxiety mice. Neutralizing endogenous ET1 in the hippocampal CA1 enhanced anxiety-like behaviors. We next revealed that most expression of ET1 and its receptors in the CA1 takes place in pyramidal neurons, and the ET1 signaling pathway directly regulated the excitability of CA1 pyramidal neurons and glutamatergic synaptic neurotransmission. Finally, we proved that neutralizing endogenous CA1 ET1 produces anxiogenic effects on low-anxiety mice, whereas infusing exogenous ET1 into the CA1 alleviates the anxiety susceptibility of high-anxiety mice. Together, these results indicate that ET1 signaling is critical in maintaining the excitability of glutamatergic neurons in the hippocampus and, thus, in modulating anxiety-like behaviors. Because ET1 is a risk factor for ischemic stroke, our findings might also help to explain the potential mechanism of emotional abnormality in stroke.
[Mh] Termos MeSH primário: Ansiedade/patologia
Endotelina-1/metabolismo
Hipocampo/metabolismo
Hipocampo/patologia
Células Piramidais/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/genética
Animais
Biofísica
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo
Modelos Animais de Doenças
Estimulação Elétrica
Endotelina-1/genética
Endotelina-1/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/genética
Comportamento Exploratório/efeitos dos fármacos
Privação de Alimentos
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Aprendizagem em Labirinto/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Patch-Clamp
Células Piramidais/efeitos dos fármacos
Receptores de Endotelina/genética
Receptores de Endotelina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Receptors, Endothelin); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


  6 / 3658 MEDLINE  
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[PMID]:28179257
[Au] Autor:Gohar EY; Kasztan M; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama emangohar@uabmc.edu.
[Ti] Título:Interplay between renal endothelin and purinergic signaling systems.
[So] Source:Am J Physiol Renal Physiol;313(3):F666-F668, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alterations in extracellular fluid volume regulation and sodium balance may result in the development and maintenance of salt-dependent hypertension, a major risk factor for cardiovascular disease. Numerous pathways contribute to the regulation of sodium excretion and blood pressure, including endothelin and purinergic signaling. Increasing evidence suggests a link between purinergic receptor activation and endothelin production within the renal collecting duct as a means of promoting natriuresis. A better understanding of the relationship between these two systems, especially in regard to sodium homeostasis, will fill a significant knowledge gap and may provide novel antihypertensive treatment options. Therefore, this review focuses on the cross talk between endothelin and purinergic signaling as it relates to the renal regulation of sodium and blood pressure homeostasis.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Pressão Sanguínea
Endotelina-1/metabolismo
Túbulos Renais Coletores/metabolismo
Natriurese
Transdução de Sinais
Sódio na Dieta/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Túbulos Renais Coletores/fisiopatologia
Receptores de Endotelina/metabolismo
Receptores Purinérgicos P2/metabolismo
Sódio na Dieta/sangue
Sódio na Dieta/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Receptors, Endothelin); 0 (Receptors, Purinergic P2); 0 (Sodium, Dietary); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00639.2016


  7 / 3658 MEDLINE  
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[PMID]:28095606
[Au] Autor:Lohsiriwat V; Scholefield JH; Wilson VG; Dashwood MR
[Ad] Endereço:Division of Gastrointestinal Surgery, Queen's Medical Centre, University of Nottingham, Nottingham, UK.
[Ti] Título:Endothelin-1 and its receptors on haemorrhoidal tissue: a potential site for therapeutic intervention.
[So] Source:Br J Pharmacol;174(7):569-579, 2017 Apr.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Haemorrhoids is a common anorectal condition affecting millions worldwide. We have studied the effect of endothelin-1 (ET-1) and the role of endothelin ET and ET receptors in haemorrhoid tissue. EXPERIMENTAL APPROACH: Protein expression of ET-1, ET and ET receptors were compared between haemorrhoids and normal rectal submucosa using Western blot analysis, with the localization of proteins determined by autoradiography and immunohistochemistry. Effects of ET-1 and sarafotoxin 6a on human colonic and rectal arteries and veins was assessed by wire myography and the involvement of receptor subtypes established by selective antagonists. KEY RESULTS: Dense binding of [ I]-ET-1 to haemorrhoidal sections was reduced by selective receptor antagonists. A higher density of ET than ET receptors was found in haemorrhoidal, than in control rectal tissue and confirmed by Western blot analysis. ET and ET receptors were localized to smooth muscle of haemorrhoidal arteries and veins, with ET receptors on the endothelium. Human colonic and rectal arteries and veins were similarly sensitive to ET-1 and affected by the ET selective antagonist, but sarafotoxin S6a-induced contractions were more pronounced in veins and antagonized by a selective ET receptor antagonist. CONCLUSIONS AND IMPLICATIONS: ET and ET receptors are present in human haemorrhoids with ET receptors predominating. ET receptors are activated by ET-1 to mediate a contraction in arteries and veins, but the latter are selectively activated by sarafotoxin S6a - a response that involves ET receptors at low concentrations. Selective ET agonists may have therapeutic potential to reduce congestion of the haemorrhoidal venous sinusoids.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Hemorroidas/tratamento farmacológico
Hemorroidas/metabolismo
Receptores de Endotelina/metabolismo
[Mh] Termos MeSH secundário: Autorradiografia
Sítios de Ligação
Western Blotting
Endotelina-1/análise
Hemorroidas/patologia
Seres Humanos
Imuno-Histoquímica
Receptores de Endotelina/agonistas
Receptores de Endotelina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Receptors, Endothelin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13719


  8 / 3658 MEDLINE  
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[PMID]:28057852
[Au] Autor:Wang JW; Li AY; Guo QH; Guo YJ; Weiss JW; Ji ES
[Ad] Endereço:Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
[Ti] Título:Endothelin-1 and ET receptors impair left ventricular function by mediated coronary arteries dysfunction in chronic intermittent hypoxia rats.
[So] Source:Physiol Rep;5(1), 2017 Jan.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obstructive sleep apnea (OSA) results in cardiac dysfunction and vascular endothelium injury. Chronic intermittent hypoxia (CIH), the main characteristic of OSAS, is considered to be mainly responsible for cardiovascular system impairment. This study is aimed to evaluate the role of endothelin-1(ET-1) system in coronary injury and cardiac dysfunction in CIH rats. In our study, Sprague-Dawley rats were exposed to CIH (FiO 9% for 1.5 min, repeated every 3 min for 8 h/d, 7 days/week for 3 weeks). After 3 weeks, the left ventricular developed pressure (LVDP) and coronary resistance (CR) were measured with the langendorff mode in isolated hearts. Meanwhile, expressions of ET-1 and ET receptors were detected by immunohistochemical and western blot, histological changes were also observed to determine effects of CIH on coronary endothelial cells. Results suggested that decreased LVDP level combined with augmented coronary resistance was exist in CIH rats. CIH could induce endothelial injury and endothelium-dependent vasodilatation dysfunction in the coronary arteries. Furthermore, ET-1 and ET receptor expressions in coronary vessels were increased after CIH exposure, whereas ET receptors expression was decreased. Coronary contractile response to ET-1 in both normoxia and CIH rats was inhibited by ET receptor antagonist BQ123. However, ET receptor antagonist BQ788 enhanced ET-1-induced contractile in normoxia group, but had no significant effects on CIH group. These results indicate that CIH-induced cardiac dysfunction may be associated with coronary injury. ET-1 plays an important role in coronary pathogenesis of CIH through ET receptor by mediating a potent vasoconstrictor response. Moreover, decreased ET receptor expression that leads to endothelium-dependent vasodilatation decline, might be also participated in coronary and cardiac dysfunction.
[Mh] Termos MeSH primário: Vasos Coronários/fisiopatologia
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/farmacologia
Ventrículos do Coração/fisiopatologia
Hipóxia/metabolismo
Receptores de Endotelina/metabolismo
Disfunção Ventricular Esquerda/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Vasos Coronários/metabolismo
Vasos Coronários/patologia
Antagonistas dos Receptores de Endotelina/administração & dosagem
Endotelina-1/administração & dosagem
Endotelina-1/metabolismo
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Endotélio Vascular/patologia
Ventrículos do Coração/patologia
Hipóxia/complicações
Hipóxia/fisiopatologia
Hipóxia/veterinária
Masculino
Contração Miocárdica/efeitos dos fármacos
Contração Miocárdica/imunologia
Oligopeptídeos/administração & dosagem
Oligopeptídeos/farmacologia
Peptídeos Cíclicos/administração & dosagem
Peptídeos Cíclicos/farmacologia
Piperidinas/administração & dosagem
Piperidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Apneia Obstrutiva do Sono/complicações
Apneia Obstrutiva do Sono/metabolismo
Apneia Obstrutiva do Sono/fisiopatologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/fisiologia
Disfunção Ventricular Esquerda/patologia
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (Oligopeptides); 0 (Peptides, Cyclic); 0 (Piperidines); 0 (Receptors, Endothelin); 44OLL8XEJ4 (BQ 788); S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE


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[PMID]:27991911
[Au] Autor:Lee TM; Chang NC; Lin SZ
[Ad] Endereço:Department of Medicine, Cardiology Section, China Medical University-An Nan Hospital, Tainan, Taiwan.
[Ti] Título:Inhibition of infarction-induced sympathetic innervation with endothelin receptor antagonism via a PI3K/GSK-3ß-dependent pathway.
[So] Source:Lab Invest;97(3):243-255, 2017 Mar.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although endothelin (ET)-1 has been shown to upregulate nerve growth factor (NGF) expression, the molecular mechanisms are largely unknown. Phosphatidylinositol 3-kinase (PI3K)/Akt/glycogen synthase kinase (GSK)-3ß signal has been implicated in the regulation of NGF. We investigated whether selective ET receptor blockers attenuated cardiac sympathetic reinnervation through restoring PI3K/Akt/GSK-3ß activity. After ligation of the left anterior descending artery, male Wistar rats were randomized to either vehicle, atrasentan (an ET receptor antagonist) or A-192621 (an ET receptor antagonist) for 4 weeks. Sympathetic hyperinnervation after infarction was confirmed by myocardial norepinephrine measurement and immunofluorescent analysis. Post infarction was associated with increased reactive oxygen species (ROS), as measured by myocardial superoxide levels and dihydroethidine fluorescence staining. This was paralleled by a significant upregulation of NGF expression on mRNA and protein levels in the vehicle-treated rats, which reduced after administering atrasentan, not A-192621. Arrhythmic scores in the vehicle-treated rats were significantly higher than those treated with atrasentan. In an in vivo study atrasentan-induced decreased NGF was associated with activation of PI3K/Akt signaling pathway, which was further confirmed by the ex vivo study showing the restoration of NGF levels after coadministration of PI3K inhibitors (wortmannin and LY294002). Lithium chloride, an inhibitor of GSK-3ß, did not provide additional attenuated NGF levels compared with atrasentan alone. Finally, atrasentan-attenuated NGF levels were reversed in the presence of peroxynitrite generator. ET receptor antagonism is a mediator to attenuate sympathetic hyperinnervation probably through restoration of PI3K/Akt/GSK-3ß/ROS signaling pathway, a potential pharmacological target for arrhythmias after infarction.
[Mh] Termos MeSH primário: Antagonistas dos Receptores de Endotelina/farmacologia
Glicogênio Sintase Quinase 3 beta/metabolismo
Infarto do Miocárdio/prevenção & controle
Fosfatidilinositol 3-Quinase/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Arritmias Cardíacas/genética
Arritmias Cardíacas/metabolismo
Arritmias Cardíacas/prevenção & controle
Western Blotting
Inibidores Enzimáticos/farmacologia
Glicogênio Sintase Quinase 3 beta/antagonistas & inibidores
Coração/efeitos dos fármacos
Coração/inervação
Coração/fisiopatologia
Masculino
Infarto do Miocárdio/genética
Infarto do Miocárdio/metabolismo
Miocárdio/metabolismo
Fator de Crescimento Neural/genética
Fator de Crescimento Neural/metabolismo
Norepinefrina/metabolismo
Fosfatidilinositol 3-Quinase/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Pirrolidinas/farmacologia
Distribuição Aleatória
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
Receptores de Endotelina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Sistema Nervoso Simpático/metabolismo
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (A 192621); 0 (Endothelin Receptor Antagonists); 0 (Enzyme Inhibitors); 0 (Pyrrolidines); 0 (Reactive Oxygen Species); 0 (Receptors, Endothelin); 9061-61-4 (Nerve Growth Factor); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); V6D7VK2215 (atrasentan); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.138


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[PMID]:27803435
[Au] Autor:Horinouchi T; Mazaki Y; Terada K; Higashi T; Miwa S
[Ti] Título:Current progress in therapeutic agents for pulmonary arterial hypertension: new insights into their mechanisms of action from endothelin system.
[So] Source:Nihon Yakurigaku Zasshi;148(5):231-238, 2016.
[Is] ISSN:0015-5691
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Endotelinas/metabolismo
Hipertensão Pulmonar/tratamento farmacológico
Hipertensão Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Endotelinas/química
Epoprostenol/metabolismo
Seres Humanos
Óxido Nítrico/metabolismo
Receptores de Endotelina/química
Receptores de Endotelina/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelins); 0 (Receptors, Endothelin); 31C4KY9ESH (Nitric Oxide); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.1254/fpj.148.231



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