Base de dados : MEDLINE
Pesquisa : D12.776.543.750.695.220.200 [Categoria DeCS]
Referências encontradas : 2178 [refinar]
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  1 / 2178 MEDLINE  
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[PMID]:28880927
[Au] Autor:Chen LL; Zhu J; Schumacher J; Wei C; Ramdas L; Prieto VG; Jimenez A; Velasco MA; Tripp SR; Andtbacka RHI; Gouw L; Rodgers GM; Zhang L; Chan BK; Cassidy PB; Benjamin RS; Leachman SA; Frazier ML
[Ad] Endereço:Department of Sarcoma, University of Texas M D Anderson Cancer Center, Houston, Texas, United States of America.
[Ti] Título:SCF-KIT signaling induces endothelin-3 synthesis and secretion: Thereby activates and regulates endothelin-B-receptor for generating temporally- and spatially-precise nitric oxide to modulate SCF- and or KIT-expressing cell functions.
[So] Source:PLoS One;12(9):e0184154, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We demonstrate that SCF-KIT signaling induces synthesis and secretion of endothelin-3 (ET3) in human umbilical vein endothelial cells and melanoma cells in vitro, gastrointestinal stromal tumors, human sun-exposed skin, and myenteric plexus of human colon post-fasting in vivo. This is the first report of a physiological mechanism of ET3 induction. Integrating our finding with supporting data from literature leads us to discover a previously unreported pathway of nitric oxide (NO) generation derived from physiological endothelial NO synthase (eNOS) or neuronal NOS (nNOS) activation (referred to as the KIT-ET3-NO pathway). It involves: (1) SCF-expressing cells communicate with neighboring KIT-expressing cells directly or indirectly (cleaved soluble SCF). (2) SCF-KIT signaling induces timely local ET3 synthesis and secretion. (3) ET3 binds to ETBR on both sides of intercellular space. (4) ET3-binding-initiated-ETBR activation increases cytosolic Ca2+, activates cell-specific eNOS or nNOS. (5) Temporally- and spatially-precise NO generation. NO diffuses into neighboring cells, thus acts in both SCF- and KIT-expressing cells. (6) NO modulates diverse cell-specific functions by NO/cGMP pathway, controlling transcriptional factors, or other mechanisms. We demonstrate the critical physiological role of the KIT-ET3-NO pathway in fulfilling high demand (exceeding basal level) of endothelium-dependent NO generation for coping with atherosclerosis, pregnancy, and aging. The KIT-ET3-NO pathway most likely also play critical roles in other cell functions that involve dual requirement of SCF-KIT signaling and NO. New strategies (e.g. enhancing the KIT-ET3-NO pathway) to harness the benefit of endogenous eNOS and nNOS activation and precise NO generation for correcting pathophysiology and restoring functions warrant investigation.
[Mh] Termos MeSH primário: Endotelina-3/secreção
Óxido Nítrico/metabolismo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptor de Endotelina B/metabolismo
Fator de Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/patologia
Linhagem Celular Tumoral
Endotélio Vascular/metabolismo
Ensaio de Imunoadsorção Enzimática
Motilidade Gastrointestinal
Tumores do Estroma Gastrointestinal/metabolismo
Tumores do Estroma Gastrointestinal/patologia
Tumores do Estroma Gastrointestinal/fisiopatologia
Homeostase
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Imuno-Histoquímica
Melanoma/patologia
Plexo Mientérico/metabolismo
Invasividade Neoplásica
Óxido Nítrico Sintase Tipo I/metabolismo
Óxido Nítrico Sintase Tipo III/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Transdução de Sinais
Pele/metabolismo
Luz Solar
Fatores de Tempo
Regulação para Cima/genética
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-3); 0 (Receptor, Endothelin B); 0 (Stem Cell Factor); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184154


  2 / 2178 MEDLINE  
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[PMID]:28805809
[Au] Autor:Shihoya W; Nishizawa T; Yamashita K; Inoue A; Hirata K; Kadji FMN; Okuta A; Tani K; Aoki J; Fujiyoshi Y; Doi T; Nureki O
[Ad] Endereço:Department of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Nagoya University, Nagoya, Japan.
[Ti] Título:X-ray structures of endothelin ET receptor bound to clinical antagonist bosentan and its analog.
[So] Source:Nat Struct Mol Biol;24(9):758-764, 2017 Sep.
[Is] ISSN:1545-9985
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin receptors (ETRs) have crucial roles in vascular control and are targets for drugs designed to treat circulatory-system diseases and cancer progression. The nonpeptide dual-ETR antagonist bosentan is the first oral drug approved to treat pulmonary arterial hypertension. Here we report crystal structures of human endothelin ET receptor bound to bosentan and to the ET -selective analog K-8794, at 3.6-Å and 2.2-Å resolution, respectively. The K-8794-bound structure reveals the detailed water-mediated hydrogen-bonding network at the transmembrane core, which could account for the weak negative allosteric modulation of ET by Na ions. The bosentan-bound structure reveals detailed interactions with ET , which are probably conserved in the ET receptor. A comparison of the two structures shows unexpected similarity between antagonist and agonist binding. Despite this similarity, bosentan sterically prevents the inward movement of transmembrane helix 6 (TM6), and thus exerts its antagonistic activity. These structural insights will facilitate the rational design of new ETR-targeting drugs.
[Mh] Termos MeSH primário: Antagonistas dos Receptores de Endotelina/química
Antagonistas dos Receptores de Endotelina/metabolismo
Receptor de Endotelina B/química
Receptor de Endotelina B/metabolismo
Sulfonamidas/química
Sulfonamidas/metabolismo
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Seres Humanos
Modelos Moleculares
Ligação Proteica
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDNRB protein, human); 0 (Endothelin Receptor Antagonists); 0 (Receptor, Endothelin B); 0 (Sulfonamides); Q326023R30 (bosentan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/nsmb.3450


  3 / 2178 MEDLINE  
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[PMID]:28802097
[Au] Autor:Zhao Y; Dang Z; Xu S; Chong S
[Ad] Endereço:.
[Ti] Título:Heat shock protein 47 effects on hepatic stellate cell-associated receptors in hepatic fibrosis of Schistosoma japonicum-infected mice.
[So] Source:Biol Chem;398(12):1357-1366, 2017 Nov 27.
[Is] ISSN:1437-4315
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The study aimed to explore the regulation of heat shock protein 47 (HSP47) on expressions of receptors associated with hepatic stellate cell (HSC) in liver fibrosis mouse models induced by Schistosoma japonicum (S. japonicum). Mouse fibroblasts (NIH/3T3) were transfected with HSP47 shRNA plasmid by lipofectamine transfection, and experimental fibrosis in HSCs was studied in S. japonicum mouse models treated with HSP47 shRNA in vivo. HSP47 expression was assessed using Western blot and real-time PCR. Flow cytometry was adopted to determine the expression of cell membrane receptors. HSP47-shRNA could markedly down-regulate the expression of collagen (Col1a1 and Col3a1). The expressions of HSP47, endothelin receptor A (ETAR) and endothelin receptor B (ETBR) significantly increased in the liver tissue of infected mice. However, the expressions of ETAR and HSP47 and ETBR remarkably decreased after the administration of HSP47 shRNA in vitro and in vivo. ETAR and ETBR levels were found to be positively correlated with HSP47 expression. HSP47 might exert influence on liver fibrosis via the regulation of ETAR and ETBR.
[Mh] Termos MeSH primário: Proteínas de Choque Térmico HSP47/metabolismo
Células Estreladas do Fígado/metabolismo
Cirrose Hepática/metabolismo
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/metabolismo
Schistosoma japonicum/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Modelos Animais de Doenças
Feminino
Células Estreladas do Fígado/patologia
Cirrose Hepática/patologia
Camundongos
Camundongos Endogâmicos BALB C
Células NIH 3T3
Schistosoma japonicum/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP47 Heat-Shock Proteins); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 0 (Serpinh1 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE


  4 / 2178 MEDLINE  
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[PMID]:28797761
[Au] Autor:Liu Y; Chen XL; Xu CB; Cao L; Lin J; Chen G; Li J
[Ad] Endereço:Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hu'nan, China.
[Ti] Título:Tail vein injection of mmLDL upregulates mouse mesenteric artery ET receptors via activation of the ERK1/2 pathway.
[So] Source:Vascul Pharmacol;96-98:33-39, 2017 Sep.
[Is] ISSN:1879-3649
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Minimally modified low density lipoprotein (mmLDL) is a risk factor for cardiovascular disease. This study investigated the effect of mmLDL on mouse mesenteric artery endothelin type B (ET ) receptors and its molecular mechanism. Mice were injected with normal saline (NS group), mmLDL in the tail vein (mmLDL group), or with both mmLDL and an intraperitoneal injection of the ERK1/2 pathway-specific inhibitor U0126 (mmLDL+U0126 group). The dose-response curve of mesenteric artery contraction induced by sarafotoxin 6c (S6c), the ET receptor agonist, was measured using a sensitive myograph system. ELISAs, RT-PCR and Western blot were used to determine the serum concentrations of mouse oxidized low density lipoprotein (oxLDL), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) as well as the expression of ET receptors, ICAM-1, VCAM-1 and phosphorylated-extracellular signal-regulated kinase 1/2 (p-ERK1/2). The S6c-induced contraction dose-response curve was significantly enhanced by mmLDL treatment and showed a significantly higher E value than in the NS group (P<0.001), and the ET receptor mRNA and protein expression in the vascular wall was significantly higher than in the NS group. The serum concentration and expression of ICAM-1 and VCAM-1 were also increased by mmLDL treatment, but intraperitoneal injection of U0126 inhibited these changes as well as the increase in p-ERK1/2 protein in the vessel wall caused by mmLDL. ICAM-1 and VCAM-1 serum concentrations were positively correlated with the S6c-induced maximum contraction of blood vessels. Increased in vivo levels of mmLDL increased the serum concentrations and expression of ICAM-1 and VCAM-1 by activating the ERK1/2 pathway, resulting in the expression of ET receptors and the enhancement of contractile function in vascular smooth muscle. Understanding the effect of mmLDL on ET receptors and its mechanism can provide ideas for cardiovascular disease prevention and treatment.
[Mh] Termos MeSH primário: Lipoproteínas LDL/administração & dosagem
Artérias Mesentéricas/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Receptor de Endotelina B/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Vasoconstrição/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Butadienos/farmacologia
Relação Dose-Resposta a Droga
Ativação Enzimática
Feminino
Técnicas In Vitro
Injeções Intravenosas
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Artérias Mesentéricas/enzimologia
Camundongos Endogâmicos ICR
Nitrilos/farmacologia
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Receptor de Endotelina B/metabolismo
Molécula 1 de Adesão de Célula Vascular/metabolismo
Vasoconstritores/farmacologia
Venenos de Víboras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butadienes); 0 (EDNRB protein, mouse); 0 (Icam1 protein, mouse); 0 (Lipoproteins, LDL); 0 (Nitriles); 0 (Protein Kinase Inhibitors); 0 (Receptor, Endothelin B); 0 (U 0126); 0 (Vascular Cell Adhesion Molecule-1); 0 (Vasoconstrictor Agents); 0 (Viper Venoms); 0 (oxidized low density lipoprotein); 0 (sarafotoxins s6); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 2.7.11.24 (Mapk1 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


  5 / 2178 MEDLINE  
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[PMID]:28758529
[Au] Autor:Rosanò L; Cianfrocca R; Sestito R; Tocci P; Di Castro V; Bagnato A
[Ad] Endereço:a Preclinical Models and New Therapeutic Agents Unit, Translational Research Functional Departmental Area , Regina Elena National Cancer Institute , Rome , Italy.
[Ti] Título:Targeting endothelin-1 receptor/ß-arrestin1 network for the treatment of ovarian cancer.
[So] Source:Expert Opin Ther Targets;21(10):925-932, 2017 Oct.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Endothelin-1 receptor (ET-1R)/ß-arrestin1 (ß-arr1) signaling is dysregulated in ovarian cancer. This signaling circuit enables cancer cells to engage several signaling and transcriptional networks that are pervasively intertwined, and represent a potential therapeutic target for developing novel agents for ovarian cancer treatment. Areas covered: In this article, we discuss the role of the signaling network between ET-1R and key pathways mediated by the scaffold protein ß-arr1, as part of signaling complex, or as a transcription co-activator, promoting precise control of transcription of different genes, including ET-1. Therefore ET-1R/ß-arr1 is an actionable node involved in the activation of a persistent feedback loop that contributes to bypass signaling. Targeting ET-1R empowering this circuit can represent a necessary measure to reach clinical efficacy. Preclinical studies demonstrate that blocking ET-1R by FDA approved dual ET R/ET R antagonist prevents ß-arr1 network formation, offering a novel therapeutic strategy in ovarian cancer patients. Expert opinion: The information provided in this review about the ET-1R/ß-arr1 hub represents an invaluable tool for both identifying the interconnected pathways involved in ovarian cancer and targeting them more effectively. The new perspective arising from ET-1R therapeutics will likely prompt a valuable frame for the design of new promising combinatorial therapy, blocking compensatory networks.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Terapia de Alvo Molecular
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Desenho de Drogas
Feminino
Seres Humanos
Neoplasias Ovarianas/patologia
Receptor de Endotelina A/efeitos dos fármacos
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/efeitos dos fármacos
Receptor de Endotelina B/metabolismo
Transdução de Sinais
beta-Arrestina 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 0 (beta-Arrestin 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1080/14728222.2017.1361930


  6 / 2178 MEDLINE  
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[PMID]:28720331
[Au] Autor:Park BG; Shin WS; Oh S; Park GM; Kim NI; Lee S
[Ad] Endereço:Department of Physiology, Catholic Kwandong University College of Medicine, Gangneung 25601, Republic of Korea; Institute for Clinical and Translational Research, Catholic Kwandong University College of Medicine, Gangneung 25601, Republic of Korea.
[Ti] Título:A novel antihypertension agent, sargachromenol D from marine brown algae, Sargassum siliquastrum, exerts dual action as an L-type Ca channel blocker and endothelin A/B receptor antagonist.
[So] Source:Bioorg Med Chem;25(17):4649-4655, 2017 Sep 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We isolated the novel vasoactive marine natural products, (5E,10E)-14-hydroxy-2,6,10-trimethylpentadeca-5,10-dien-4-one (4) and sargachromenol D (5), from Sargassum siliquastrum collected from the coast of the East Sea in South Korea by using activity-guided HPLC purification. The compounds effectively dilated depolarization (50mMK )-induced basilar artery contraction with EC values of 3.52±0.42 and 1.62±0.63µM, respectively, but only sargachromenol D (5) showed a vasodilatory effect on endothelin-1 (ET-1)-induced basilar artery contraction (EC =9.8±0.6µM). These results indicated that sargachromenol D (5) could act as a dual antagonist of l-type Ca channel and endothelin A/B receptors. Moreover, sargachromenol D (5) lowered blood pressure in spontaneous hypertensive rats (SHRs) 2h after oral treatment at a dose of 80mg/kg dose and the effect was maintained for 24h. Based on our ex vivo and in vivo experiments, we propose that sargachromenol D (5) is a strong candidate for the treatment of hypertension that is not controlled by conventional drugs, in particular, severe-, type II diabetes-, salt-sensitive, and metabolic disease-induced hypertension.
[Mh] Termos MeSH primário: Anti-Hipertensivos/química
Benzopiranos/química
Bloqueadores dos Canais de Cálcio/química
Antagonistas do Receptor de Endotelina A/química
Antagonistas do Receptor de Endotelina B/química
Feófitas/química
[Mh] Termos MeSH secundário: Administração Oral
Animais
Anti-Hipertensivos/isolamento & purificação
Anti-Hipertensivos/farmacologia
Artéria Basilar/efeitos dos fármacos
Artéria Basilar/fisiologia
Benzopiranos/isolamento & purificação
Benzopiranos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/isolamento & purificação
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo L/química
Canais de Cálcio Tipo L/metabolismo
Antagonistas do Receptor de Endotelina A/isolamento & purificação
Antagonistas do Receptor de Endotelina A/farmacologia
Antagonistas do Receptor de Endotelina B/isolamento & purificação
Antagonistas do Receptor de Endotelina B/farmacologia
Masculino
Feófitas/metabolismo
Coelhos
Ratos
Ratos Endogâmicos SHR
Receptor de Endotelina A/química
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/química
Receptor de Endotelina B/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Benzopyrans); 0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Endothelin A Receptor Antagonists); 0 (Endothelin B Receptor Antagonists); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 0 (sargachromenol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


  7 / 2178 MEDLINE  
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[PMID]:28701323
[Au] Autor:Becker BK; Feagans AC; Chen D; Kasztan M; Jin C; Speed JS; Pollock JS; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Renal denervation attenuates hypertension but not salt sensitivity in ET receptor-deficient rats.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R425-R437, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypertension is a prevalent pathology that increases risk for numerous cardiovascular diseases. Because the etiology of hypertension varies across patients, specific and effective therapeutic approaches are needed. The role of renal sympathetic nerves is established in numerous forms of hypertension, but their contribution to salt sensitivity and interaction with factors such as endothelin-1 are poorly understood. Rats deficient of functional ET receptors (ET -def) on all tissues except sympathetic nerves are hypertensive and exhibit salt-sensitive increases in blood pressure. We hypothesized that renal sympathetic nerves contribute to hypertension and salt sensitivity in ET -def rats. The hypothesis was tested through bilateral renal sympathetic nerve denervation and measuring blood pressure during normal salt (0.49% NaCl) and high-salt (4.0% NaCl) diets. Denervation reduced mean arterial pressure in ET -def rats compared with sham-operated controls by 12 ± 3 (SE) mmHg; however, denervation did not affect the increase in blood pressure after 2 wk of high-salt diet (+19 ± 3 vs. +16 ± 3 mmHg relative to normal salt diet; denervated vs. sham, respectively). Denervation reduced cardiac sympathetic-to-parasympathetic tone [low frequency-high frequency (LF/HF)] during normal salt diet and vasomotor LF/HF tone during high-salt diet in ET -def rats. We conclude that the renal sympathetic nerves contribute to the hypertension but not to salt sensitivity of ET -def rats.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Denervação
Hipertensão/genética
Hipertensão/cirurgia
Rim/inervação
Receptor de Endotelina B/genética
Cloreto de Sódio na Dieta/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Barorreflexo/efeitos dos fármacos
Barorreflexo/fisiologia
Pressão Sanguínea/efeitos dos fármacos
Hipertensão/fisiopatologia
Rim/fisiopatologia
Rim/cirurgia
Sistema Nervoso Parassimpático/fisiopatologia
Ratos
Ratos Transgênicos
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Endothelin B); 0 (Sodium Chloride, Dietary)
[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/ajpregu.00174.2017


  8 / 2178 MEDLINE  
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[PMID]:28606962
[Au] Autor:Planas-Rigol E; Terrades-Garcia N; Corbera-Bellalta M; Lozano E; Alba MA; Segarra M; Espígol-Frigolé G; Prieto-González S; Hernández-Rodríguez J; Preciado S; Lavilla R; Cid MC
[Ad] Endereço:Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clinic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), CRB-CELLEX, Barcelona, Spain.
[Ti] Título:Endothelin-1 promotes vascular smooth muscle cell migration across the artery wall: a mechanism contributing to vascular remodelling and intimal hyperplasia in giant-cell arteritis.
[So] Source:Ann Rheum Dis;76(9):1624-1634, 2017 Sep.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Giant-cell arteritis (GCA) is an inflammatory disease of large/medium-sized arteries, frequently involving the temporal arteries (TA). Inflammation-induced vascular remodelling leads to vaso-occlusive events. Circulating endothelin-1 (ET-1) is increased in patients with GCA with ischaemic complications suggesting a role for ET-1 in vascular occlusion beyond its vasoactive function. OBJECTIVE: To investigate whether ET-1 induces a migratory myofibroblastic phenotype in human TA-derived vascular smooth muscle cells (VSMC) leading to intimal hyperplasia and vascular occlusion in GCA. METHODS AND RESULTS: Immunofluorescence/confocal microscopy showed increased ET-1 expression in GCA lesions compared with control arteries. In inflamed arteries, ET-1 was predominantly expressed by infiltrating mononuclear cells whereas ET receptors, particularly ET-1 receptor B (ET R), were expressed by both mononuclear cells and VSMC. ET-1 increased TA-derived VSMC migration in vitro and α-smooth muscle actin (αSMA) expression and migration from the media to the intima in cultured TA explants. ET-1 promoted VSMC motility by increasing activation of focal adhesion kinase (FAK), a crucial molecule in the turnover of focal adhesions during cell migration. FAK activation resulted in Y397 autophosphorylation creating binding sites for Src kinases and the p85 subunit of PI3kinases which, upon ET-1 exposure, colocalised with FAK at the focal adhesions of migrating VSMC. Accordingly, FAK or PI3K inhibition abrogated ET-1-induced migration in vitro. Consistently, ET-1 receptor A and ET R antagonists reduced αSMA expression and delayed VSMC outgrowth from cultured GCA-involved artery explants. CONCLUSIONS: ET-1 is upregulated in GCA lesions and, by promoting VSMC migration towards the intimal layer, may contribute to intimal hyperplasia and vascular occlusion in GCA.
[Mh] Termos MeSH primário: Movimento Celular/genética
Endotelina-1/genética
Arterite de Células Gigantes/genética
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Remodelação Vascular/genética
[Mh] Termos MeSH secundário: Actinas/efeitos dos fármacos
Actinas/genética
Actinas/metabolismo
Idoso
Western Blotting
Estudos de Casos e Controles
Movimento Celular/efeitos dos fármacos
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/metabolismo
Endotelina-1/farmacologia
Feminino
Imunofluorescência
Quinase 1 de Adesão Focal/antagonistas & inibidores
Quinase 1 de Adesão Focal/metabolismo
Arterite de Células Gigantes/metabolismo
Arterite de Células Gigantes/patologia
Seres Humanos
Hiperplasia
Técnicas In Vitro
Leucócitos Mononucleares
Masculino
Microscopia Confocal
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Receptor de Endotelina A/efeitos dos fármacos
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Túnica Íntima/patologia
Remodelação Vascular/efeitos dos fármacos
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-210792


  9 / 2178 MEDLINE  
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[PMID]:28438762
[Au] Autor:Wenner MM; Sebzda KN; Kuczmarski AV; Pohlig RT; Edwards DG
[Ad] Endereço:Department of Kinesiology and Applied Physiology, University of Delaware, Newark, Delaware; and mwenner@udel.edu.
[Ti] Título:ET receptor contribution to vascular dysfunction in postmenopausal women.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(1):R51-R57, 2017 Jul 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin-1 (ET-1) contributes to age-related endothelial dysfunction in men via the ET receptor. However, there are sex differences in the ET-1 system, and ET receptors are modulated by sex hormones. The purpose of this study was to test the hypothesis that ET receptors contribute to impaired vasodilatory function in postmenopausal women (PMW). We measured flow-mediated dilation (FMD) using ultrasound, and cutaneous nitric oxide-mediated vasodilation during local heating (42°C) via laser Doppler flowmetry in 18 young women (YW; 22 ± 1 yr) and 16 PMW (56 ± 1 yr). Cutaneous microdialysis perfusions of lactated Ringer (control), an ET receptor antagonist (BQ-788, 300 nM), and an ET receptor antagonist (BQ-123, 500 nM), were done through separate fibers, followed by perfusions of sodium nitroprusside (28 mM) and local heating to 43°C (max). Cutaneous vascular conductance (CVC) was calculated as cutaneous blood flow/mean arterial pressure and expressed as a percent of maximal dilation. FMD (YW: 7.5 ± 0.5 vs. PMW: 5.6 ± 0.6%) and cutaneous vasodilation (YW: 93 ± 2 vs. PMW: 83 ± 4%CVC ) were lower in PMW (both < 0.05). Blockade of ET receptors decreased cutaneous vasodilation in YW (87 ± 2%CVC ; < 0.05 vs. control) but increased vasodilation in PMW (93 ± 1%CVC ; < 0.05 vs. control). ET receptor blockade had minimal effect in YW (92 ± 1%CVC ) but increased cutaneous vasodilation in PMW (91 ± 2%CVC ; < 0.05 vs. control). In conclusion, ET receptors mediate vasodilation in YW, but this effect is lost after menopause. Impaired vasodilatory function in PMW is due in part to a loss of ET -mediated dilation.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Pós-Menopausa/fisiologia
Receptor de Endotelina B/metabolismo
Vasodilatação
[Mh] Termos MeSH secundário: Envelhecimento
Feminino
Seres Humanos
Meia-Idade
Receptor de Endotelina B/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDNRB protein, human); 0 (Receptor, Endothelin B)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00410.2016


  10 / 2178 MEDLINE  
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[PMID]:28356074
[Au] Autor:Yoshihara M; Sato T; Saito D; Ohara O; Kuramoto T; Suyama M
[Ad] Endereço:Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
[Ti] Título:A deletion in the intergenic region upstream of Ednrb causes head spot in the rat strain KFRS4/Kyo.
[So] Source:BMC Genet;18(1):29, 2017 Mar 29.
[Is] ISSN:1471-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Head spot is one of the phenotypes identified in the KFRS4/Kyo rat strain. Although previous linkage analysis suggested that Ednrb, which is frequently involved in coat color variations in various animals, could be the gene responsible for this phenotype, no mutations have been identified in its coding region. RESULTS: To identify mutations causative of this phenotype in KFRS4/Kyo, we analyzed target capture sequencing data that we recently generated. Our target capture method has a unique feature, i.e., it covers not only exonic regions but also conserved non-coding sequences (CNSs) among vertebrates; therefore, it has the potential to detect regulatory mutations. We identified a deletion of approximately 50 kb in length approximately 50 kb upstream of Ednrb. A comparative analysis with the epigenomic data in the corresponding region in humans and mice showed that one of the CNSs might be an enhancer. Further comparison with Hi-C data, which provide information about chromosome conformation, indicated that the putative enhancer is spatially close to the promoter of Ednrb, suggesting that it acts as an enhancer of Ednrb. CONCLUSIONS: These in silico data analyses strongly suggest that the identified deletion in the intergenic region upstream of Ednrb, which might contain a melanocyte-specific enhancer, is the mutation causative of the head spot phenotype in the KFRS4/Kyo rat strain.
[Mh] Termos MeSH primário: Mapeamento Cromossômico/métodos
DNA Intergênico
Receptor de Endotelina B/genética
Deleção de Sequência
[Mh] Termos MeSH secundário: Animais
Simulação por Computador
Epigenômica
Seres Humanos
Camundongos
Fenótipo
Regiões Promotoras Genéticas
Ratos
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Intergenic); 0 (Receptor, Endothelin B); 0 (ednrb protein, rat)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1186/s12863-017-0497-3



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