Base de dados : MEDLINE
Pesquisa : D12.644.276.400.245 [Categoria DeCS]
Referências encontradas : 519 [refinar]
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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


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[PMID]:28379963
[Au] Autor:Dharmayanthi AB; Terai Y; Sulandari S; Zein MS; Akiyama T; Satta Y
[Ad] Endereço:Department of Evolutionary Studies of Biosystems, SOKENDAI (The Graduate University for Advanced Studies), Kanagawa, Japan.
[Ti] Título:The origin and evolution of fibromelanosis in domesticated chickens: Genomic comparison of Indonesian Cemani and Chinese Silkie breeds.
[So] Source:PLoS One;12(4):e0173147, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Like Chinese Silkie, Indonesian Ayam Cemani exhibits fibromelanosis or dermal hyperpigmentation and possesses complex segmental duplications on chromosome 20 that involve the endothelin 3 gene, EDN3. A genomic region, DR1 of 127 kb, together with another region, DR2 of 171 kb, was duplicated by unequal crossing over, accompanied by inversion of one DR2. Quantitative PCR and copy number variation analyses on the Cemani genome sequence confirmed the duplication of EDN3. These genetic arrangements are identical in Cemani and Silkie, indicating a single origin of the genetic cause of Fm. The two DR1s harbor two distinct EDN3 haplotypes in a form of permanent heterozygosity, although they remain allelic in the ancestral Red Jungle Fowl population and some domesticated chicken breeds, with their allelic divergence time being as recent as 0.3 million years ago. In Cemani and Silkie breeds, artificial selection favoring the Fm phenotype has left an unambiguous record for selective sweep that extends in both directions from tandemly duplicated EDN3 loci. This highly homozygous tract is different in length between Cemani and Silkie, reflecting their distinct breeding histories. It is estimated that the Fm phenotype came into existence at least 6600-9100 years ago, prior to domestication of Cemani and Silkie, and that throughout domestication there has been intense artificial selection with strength s > 50% in each breed.
[Mh] Termos MeSH primário: Galinhas/genética
Hiperpigmentação/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Evolução Biológica
Cruzamento/métodos
China
Mapeamento Cromossômico/métodos
Cruzamentos Genéticos
Variações do Número de Cópias de DNA/genética
Endotelina-3/genética
Genômica/métodos
Haplótipos/genética
Indonésia
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173147


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[PMID]:28179472
[Au] Autor:Fouda MA; Abdel-Rahman AA
[Ad] Endereço:Department of Pharmacology, Brody School of Medicine, East Carolina University, North Carolina.
[Ti] Título:Endothelin Confers Protection against High Glucose-Induced Neurotoxicity via Alleviation of Oxidative Stress.
[So] Source:J Pharmacol Exp Ther;361(1):130-139, 2017 Apr.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent findings linked the inhibition in the neuromodulator peptide endothelin-1 (ET-1) level to the high glucose-evoked neurotoxicity. However, definitive neuroprotective role for ET-1 and the major neuronal ET (ET-3) against high glucose-evoked toxicity and the implicated neurochemical responses triggered by their ET-A and ET-B receptors remain unknown. Here, we tested the hypothesis that ET-B activation alleviates high glucose-evoked oxidative stress and cell death. High glucose (100 mM for 48 hours)-evoked cell death was associated with elevation in reactive oxygen species, inhibition of catalase activity, and a paradoxical upregulation of hemeoxygenase-1 expression along with ET-A and ET-B receptors were downregulated and upregulated, respectively. ET-1 or ET-3, in concentrations that had no effect on PC12 cell viability in normal glucose medium, alleviated all high glucose-evoked neurochemical responses, except for the reduction in ET-A receptor expression. Prior (4 hours) incubation with a selective ET-A (BQ123) or ET-B (BQ788) receptor blocker abrogated the neuroprotection conferred by ET-1 or ET-3. However, the ET-B receptor played a greater role because BQ788 abrogated the favorable ET-1- or ET-3-mediated reversal of the ERK1/2 phosphorylation and the inhibition in catalase activity caused by high glucose. These findings suggest that endothelin exerts ET-B receptor-dependent favorable redox and neuroprotective effects against high glucose-evoked oxidative damage and neurotoxicity.
[Mh] Termos MeSH primário: Endotelina-1/farmacologia
Endotelina-3/farmacologia
Glucose/toxicidade
Fármacos Neuroprotetores/farmacologia
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Relação Dose-Resposta a Droga
Estresse Oxidativo/fisiologia
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Endothelin-3); 0 (Neuroprotective Agents); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.238659


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[PMID]:28063956
[Au] Autor:Watanabe Y; Stanchina L; Lecerf L; Gacem N; Conidi A; Baral V; Pingault V; Huylebroeck D; Bondurand N
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale, Créteil, France; Université Paris-Est, Faculté de Médecine, Créteil, France.
[Ti] Título:Differentiation of Mouse Enteric Nervous System Progenitor Cells Is Controlled by Endothelin 3 and Requires Regulation of Ednrb by SOX10 and ZEB2.
[So] Source:Gastroenterology;152(5):1139-1150.e4, 2017 Apr.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Maintenance and differentiation of progenitor cells in the developing enteric nervous system are controlled by molecules such as the signaling protein endothelin 3 (EDN3), its receptor (the endothelin receptor type B [EDNRB]), and the transcription factors SRY-box 10 (SOX10) and zinc finger E-box binding homeobox 2 (ZEB2). We used enteric progenitor cell (EPC) cultures and mice to study the roles of these proteins in enteric neurogenesis and their cross regulation. METHODS: We performed studies in mice with a Zeb2 loss-of-function mutation (Zeb2 ) and mice carrying a spontaneous recessive mutation that prevents conversion of EDN3 to its active form (Edn3 ). EPC cultures issued from embryos that expressed only wild-type Zeb2 (Zeb2 EPCs) or were heterozygous for the mutation (Zeb2 EPCs) were exposed to EDN3; we analyzed the effects on cell differentiation using immunocytochemistry. In parallel, Edn3 mice were crossed with Zeb2 mice; intestinal tissues were collected from embryos for immunohistochemical analyses. We investigated regulation of the EDNRB gene in transactivation and chromatin immunoprecipitation assays; results were validated in functional rescue experiments using transgenes expression in EPCs from retroviral vectors. RESULTS: Zeb2 EPCs had increased neuronal differentiation compared to Zeb2 cells. When exposed to EDN3, Zeb2 EPCs continued expression of ZEB2 but did not undergo any neuronal differentiation. Incubation of Zeb2 EPCs with EDN3, on the other hand, resulted in only partial inhibition of neuronal differentiation. This indicated that 2 copies of Zeb2 are required for EDN3 to prevent neuronal differentiation. Mice with combined mutations in Zeb2 and Edn3 (double mutants) had more severe enteric anomalies and increased neuronal differentiation compared to mice with mutations in either gene alone. The transcription factors SOX10 and ZEB2 directly activated the EDNRB promoter. Overexpression of EDNRB in Zeb2 EPCs restored inhibition of neuronal differentiation, similar to incubation of Zeb2 EPCs with EDN3. CONCLUSIONS: In studies of cultured EPCs and mice, we found that control of differentiation of mouse enteric nervous system progenitor cells by EDN3 requires regulation of Ednrb expression by SOX10 and ZEB2.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Endotelina-3/genética
Sistema Nervoso Entérico/embriologia
Proteínas de Homeodomínio/genética
Células-Tronco Neurais/metabolismo
Neurogênese/genética
Receptor de Endotelina B/metabolismo
Proteínas Repressoras/genética
Fatores de Transcrição SOXE/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Imunoprecipitação da Cromatina
Endotelina-3/metabolismo
Sistema Nervoso Entérico/citologia
Sistema Nervoso Entérico/metabolismo
Citometria de Fluxo
Regulação da Expressão Gênica no Desenvolvimento
Heterozigoto
Doença de Hirschsprung
Proteínas de Homeodomínio/metabolismo
Imunoquímica
Camundongos
Mutação
Células-Tronco Neurais/citologia
Reação em Cadeia da Polimerase
Proteínas Repressoras/metabolismo
Células-Tronco
Homeobox 2 de Ligação a E-box com Dedos de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDNRB protein, mouse); 0 (Endothelin-3); 0 (Homeodomain Proteins); 0 (Receptor, Endothelin B); 0 (Repressor Proteins); 0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse); 0 (ZEB2 protein, mouse); 0 (Zinc Finger E-box Binding Homeobox 2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170109
[St] Status:MEDLINE


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[PMID]:27863272
[Au] Autor:Lin H; Ma Y; Wei Y; Shang H
[Ad] Endereço:Department of Gynaecology and Obstetrics, Shandong University Affiliated Jinan Center Hospital, Jinan 250013, Shandong, China.
[Ti] Título:Genome-wide analysis of aberrant gene expression and methylation profiles reveals susceptibility genes and underlying mechanism of cervical cancer.
[So] Source:Eur J Obstet Gynecol Reprod Biol;207:147-152, 2016 Dec.
[Is] ISSN:1872-7654
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study aimed to explore the molecular mechanism of cervical cancer (CC) by integrated bioinformatic analyses of gene expression and methylation profiles. METHODS: The gene expression and methylation microarrays in CC samples and normal controls were respectively downloaded from the GEO database. After screening the differentially expressed genes (DEGs) with Limma package and the CC-related methylation sites with CpGassoc package in R language, DEGs with CC-related methylation sites were identified from the intersection of the above two groups of results with 50kb upstream and downstream of a gene as the gene region. Then GO enrichment was performed by GenCLIP2.0 software. Sequentially, analysis of metabolic sub-pathways with pathogenic risk was predicted by iSubpathwayMiner package in R language. RESULTS: A total of 1357 DEGs including 721 up-regulated and 636 down-regulated, as well as 666 CC-related methylation sites were screened out. After being analyzed, 26 DEGs with 35 CC-related methylation sites were identified. EDN3 and EDNRB were significantly involved in a function cluster in GO terms of vein smooth muscle contraction, vascular smooth muscle contraction and phasic smooth muscle contraction. LHX2 and PAX6 were significantly involved in a function cluster in GO terms of telencephalon regionalization and forebrain regionalization. ACOX3, CYP39A1 and DPYS were significantly enriched in 25 sub-pathways of 6 major pathways. CONCLUSIONS: EDN3 and EDNRB might play important roles in the molecular mechanism of CC, and LHX2, ACOX3, CYP39A1 and DPYS might be susceptibility genes and potential risk markers in CC.
[Mh] Termos MeSH primário: Colo do Útero/metabolismo
Metilação de DNA
Endotelina-3/metabolismo
Regulação Neoplásica da Expressão Gênica
Proteínas de Neoplasias/metabolismo
Receptor de Endotelina B/metabolismo
Neoplasias do Colo do Útero/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
China/epidemiologia
Biologia Computacional
Bases de Dados Genéticas
Endotelina-3/genética
Epigênese Genética
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Proteínas com Homeodomínio LIM/genética
Proteínas com Homeodomínio LIM/metabolismo
Proteínas de Neoplasias/genética
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Fator de Transcrição PAX6/genética
Fator de Transcrição PAX6/metabolismo
Prosencéfalo/metabolismo
Receptor de Endotelina B/genética
Risco
Telencéfalo/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Neoplasias do Colo do Útero/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (EDN3 protein, human); 0 (EDNRB protein, human); 0 (Endothelin-3); 0 (LHX2 protein, human); 0 (LIM-Homeodomain Proteins); 0 (Neoplasm Proteins); 0 (Nerve Tissue Proteins); 0 (PAX6 Transcription Factor); 0 (PAX6 protein, human); 0 (Receptor, Endothelin B); 0 (Transcription Factors)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170414
[Lr] Data última revisão:
170414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE


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[PMID]:27595334
[Au] Autor:Shihoya W; Nishizawa T; Okuta A; Tani K; Dohmae N; Fujiyoshi Y; Nureki O; Doi T
[Ad] Endereço:Department of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan.
[Ti] Título:Activation mechanism of endothelin ET receptor by endothelin-1.
[So] Source:Nature;537(7620):363-368, 2016 09 15.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Endothelin, a 21-amino-acid peptide, participates in various physiological processes, such as regulation of vascular tone, humoral homeostasis, neural crest cell development and neurotransmission. Endothelin and its G-protein-coupled receptor are involved in the development of various diseases, such as pulmonary arterial hypertension, and thus are important therapeutic targets. Here we report crystal structures of human endothelin type B receptor in the ligand-free form and in complex with the endogenous agonist endothelin-1. The structures and mutation analysis reveal the mechanism for the isopeptide selectivity between endothelin-1 and -3. Transmembrane helices 1, 2, 6 and 7 move and envelop the entire endothelin peptide, in a virtually irreversible manner. The agonist-induced conformational changes are propagated to the receptor core and the cytoplasmic G-protein coupling interface, and probably induce conformational flexibility in TM6. A comparison with the M2 muscarinic receptor suggests a shared mechanism for signal transduction in class A G-protein-coupled receptors.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Receptor de Endotelina B/química
Receptor de Endotelina B/metabolismo
[Mh] Termos MeSH secundário: Regulação Alostérica
Sítio Alostérico
Membrana Celular/metabolismo
Cristalografia por Raios X
Endotelina-1/química
Endotelina-1/farmacologia
Endotelina-3/química
Endotelina-3/metabolismo
Seres Humanos
Ligantes
Modelos Moleculares
Conformação Proteica
Receptor de Endotelina B/agonistas
Receptor de Endotelina B/genética
Receptor Muscarínico M2/química
Receptor Muscarínico M2/metabolismo
Transdução de Sinais
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Endothelin-3); 0 (Ligands); 0 (Receptor, Endothelin B); 0 (Receptor, Muscarinic M2)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160906
[St] Status:MEDLINE
[do] DOI:10.1038/nature19319


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[PMID]:27534650
[Au] Autor:Nehra S; Bhardwaj V; Bansal A; Saraswat D
[Ad] Endereço:Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, New Delhi-54, India.
[Ti] Título:Nanocurcumin accords protection against acute hypobaric hypoxia induced lung injury in rats.
[So] Source:J Physiol Biochem;72(4):763-779, 2016 Dec.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Decline in oxygen availability experienced under hypobaric hypoxia (HH) mediates imbalance in lung fluid clearance and is a causative agent of acute lung injury. Here, we investigate the pathological events behind acute HH mediated lung injury and assess the therapeutic efficacy of nanocurcumin in its amelioration. We assess the protective efficacy of nanotized curcumin (nanocurcumin) in ameliorating HH induced lung injury and compare to curcumin. Rats exposed to acute HH (6, 12, 24, 48 and 72 h) were subjected to histopathology, blood-gas analysis and clinical biochemistry, cytokine response and redox damage. HH induced lung injury was analysed using markers of lung injury due to pulmonary vasoconstriction (ET-1/2/3 and endothelin receptors A and B) and trans-vascular fluid balance mediator (Na+/K+ ATPase). The protective efficacy of nanocurcumin was analysed by examination of Akt/Erk signalling cascade by western blot. HH induced lung injury was associated with discrete changes in blood analytes, differential circulatory cytokine response and severe pulmonary redox damages. Up-regulation of ET-1/2/3 and its receptors along with down-regulation of Na+/K+ ATPase confirmed defective pulmonary fluid clearance which promoted edema formation. Nanocurcumin treatment prevented lung edema formation and restored expression levels of ET-1/2/3 and its receptors while restoring the blood analytes, circulatory cytokines and pulmonary redox status better than curcumin. Modulation in Akt/Erk signalling pathway in rat lungs under HH confirmed the protective efficacy of nanocurcumin.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/tratamento farmacológico
Curcumina/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Hipóxia/tratamento farmacológico
Nanoestruturas/uso terapêutico
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/etiologia
Lesão Pulmonar Aguda/genética
Lesão Pulmonar Aguda/patologia
Animais
Biomarcadores/metabolismo
Modelos Animais de Doenças
Endotelina-1/genética
Endotelina-1/metabolismo
Endotelina-2/genética
Endotelina-2/metabolismo
Endotelina-3/genética
Endotelina-3/metabolismo
Hipóxia/complicações
Hipóxia/genética
Hipóxia/patologia
Masculino
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Nanoestruturas/química
Oxirredução/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor de Endotelina A/genética
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/genética
Receptor de Endotelina B/metabolismo
Transdução de Sinais
ATPase Trocadora de Sódio-Potássio/genética
ATPase Trocadora de Sódio-Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Endothelin-1); 0 (Endothelin-2); 0 (Endothelin-3); 0 (Protective Agents); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE


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[PMID]:26684626
[Au] Autor:Olender J; Nowakowska-Zajdel E; Kruszniewska-Rajs C; Orchel J; Mazurek U; Wierzgon A; Kokot T; Muc-Wierzgon M
[Ad] Endereço:School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Department of Molecular Biology, Sosnowiec, Poland.
[Ti] Título:Epigenetic silencing of endothelin-3 in colorectal cancer.
[So] Source:Int J Immunopathol Pharmacol;29(2):333-40, 2016 Jun.
[Is] ISSN:2058-7384
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Endothelins are expressed in a variety of human tissue and are involved in the processes as proliferation, migration and differentiation. The signal transduction pathway is a result of the endothelin-1-3 (ET1-3) binding to their receptors (ETAR, ETBR). ET-3 is a new candidate tumour suppressor gene, which is often downregulated or silenced in human cancer.The aim of the study was to examine DNA methylation of ET-3 genes in colorectal cancer (CRC) tissue samples in relation to the clinical stage (CS) of cancer. The paper is a continuation of our previously published results, which showed a four-fold transcriptional silencing of the ET-3 gene in the samples of colorectal cancer in comparison to normal tissues.A total of 66 paired CRC and normal (surgical margin) tissue samples were used in the study. The tumour tissues were collected from CRC patients in CS I-IV according the 7th edition of UICC TNM Classification of Malignant Tumours (CS I, n = 8; CS II, n = 20; CS III, n = 27; CS IV, n = 11). Assessment of epigenetic silencing of the ET-3 encoding gene was performed in three steps. The silencing of the ET-3 encoding gene was a result from methylation of the promoter sequence using methylation-specific PCR (MS-PCR). Analyses were performed using primers complementary for a CpG island in the first exon of the gene encoding ET-3. An epigenetic silence through methylation of 7.5% (5/66) in comparison to control was observed, including 10% of CS II (2/20), 7% of CS III (2/27) and 9% of CS IV (1/11). The controls and the samples of tumour in CS I showed no epigenetic silencing via methylation. In conclusion, epigenetic silencing of ET-3 in CRC could play a role in the progression than in the induction process. EDN3 would be a future target for epigenetic therapy in colorectal cancer, but further clinical studies are needed.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Endotelina-3/genética
Epigênese Genética/genética
Inativação Gênica/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ilhas de CpG/genética
Metilação de DNA/genética
Endotelina-1/genética
Feminino
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Masculino
Meia-Idade
Regiões Promotoras Genéticas/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Endothelin-3)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1177/0394632015600371


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[PMID]:25370848
[Au] Autor:Yamamoto Y; Kohka M; Kobayashi Y; Woclawek-Potocka I; Okuda K
[Ad] Endereço:Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University, 1-1-1 Tsushimanaka, Kita-ku, Okayama, Okayama, 700-8530, Japan.
[Ti] Título:Endothelin as a local regulating factor in the bovine oviduct.
[So] Source:Reprod Fertil Dev;28(6):673-81, 2016 Apr.
[Is] ISSN:1031-3613
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Endothelin (EDN) is a possible regulating factor of oviductal motility, which is important for the transport of gametes and embryo. To clarify the factors that control the secretion of EDN in the bovine oviduct, the expression of EDNs, EDN-converting enzymes (ECEs) and EDN receptors (EDNRs) were investigated. All isoforms of EDN (EDN1-3), ECE (ECE1 and ECE2) and EDNR (EDNRA and EDNRB) were immunolocalised in the epithelial cells of the ampulla and the isthmus. EDNRs were also immunolocalised in smooth-muscle cells. The mRNA expression of EDN2 and ECE2 was higher in cultured ampullary oviductal epithelial cells than in isthmic cells. The expression of EDN1, EDN2 and ECE2 in the ampullary tissue was highest on the day of ovulation. Oestradiol-17ß increased EDN2 and ECE1 expression, while progesterone increased only ECE1 expression in cultured ampullary epithelial cells. These results indicate that EDNs are produced by epithelial cells and their target site is smooth-muscle and epithelial cells, and suggest that ovarian steroids are regulators of endothelin synthesis in ampullary oviductal epithelial cells.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Endotelina-2/metabolismo
Enzimas Conversoras de Endotelina/metabolismo
Tubas Uterinas/fisiologia
Membrana Mucosa/metabolismo
Músculo Liso/metabolismo
Receptor de Endotelina A/metabolismo
[Mh] Termos MeSH secundário: Matadouros
Animais
Animais Endogâmicos
Bovinos
Células Cultivadas
Endotelina-1/genética
Endotelina-2/genética
Endotelina-3/genética
Endotelina-3/metabolismo
Enzimas Conversoras de Endotelina/genética
Tubas Uterinas/citologia
Tubas Uterinas/enzimologia
Feminino
Regulação da Expressão Gênica
Imuno-Histoquímica/veterinária
Isoenzimas/genética
Isoenzimas/metabolismo
Membrana Mucosa/citologia
Membrana Mucosa/enzimologia
Músculo Liso/citologia
Músculo Liso/enzimologia
Especificidade de Órgãos
Ovulação/metabolismo
RNA Mensageiro/metabolismo
Receptor de Endotelina A/agonistas
Receptor de Endotelina B/agonistas
Receptor de Endotelina B/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Endothelin-2); 0 (Endothelin-3); 0 (Isoenzymes); 0 (RNA, Messenger); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); EC 3.4.24.71 (Endothelin-Converting Enzymes)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170405
[Lr] Data última revisão:
170405
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141106
[St] Status:MEDLINE
[do] DOI:10.1071/RD14076


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[PMID]:26107453
[Au] Autor:Leão SC; Dashwood MR; Andrade MS; Santos NN; Teles OR; Souza WB; Rodrigues TM
[Ad] Endereço:Universidade Federal de São Paulo, São Paulo, SP, Brazil.
[Ti] Título:Analysis of immunostaining and western blotting of endothelin 1 and its receptors in mitral stenosis.
[So] Source:Rev Bras Cir Cardiovasc;30(2):211-8, 2015 Mar-Apr.
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Rheumatic Fever represents a serious public health problem in developing countries, with thousands of new cases each year. It is an autoimmune disease, which occurs in response to infection by streptococcus A. OBJECTIVE: The aim of this study was to evaluate the immunolabeling and protein expression for endothelin-1 and 3 (ET-1, ET-3) and its receptors (ETA, ETB) in rheumatic mitral valves. METHODS: Immunohistochemistry was used to identify ET-1/ET-3 and ETA/ETB receptors in rheumatic and control mitral valves. Quantitative analysis of immunostaining for ET-1/ET-3 and ETA/ETB receptors was performed. In addition, western blot analysis was carried out to assess protein levels in tissue samples. RESULTS: ET-1 and ETA receptor immunostaining predominated in stenotic valves, mainly associated with fibrotic regions, inflammatory areas and neovascularization. Quantitative analysis showed that the average area with positive expression of ET-1 was 18.21 ± 14.96%. For ETA and ETB, the mean expressed areas were respectively 15.06 ± 13.13% and 9.20 ± 11.09%. ET-3 did not have a significant expression. The correlation between the expression of both endothelin receptors were strongly positive (R = 0.74, P = 0.02), but the correlation between ET-1 and its receptor were negative for both ETA (R = -0.37, P = 0.25), and ETB (R = -0.14, P = 0.39). This data was supported by western blot analysis. CONCLUSION: The strong correlation between ET-1 and its receptors suggests that both play a role in the pathophysiology of rheumatic mitral valve stenosis and may potentially act as biomarkers of this disease.
[Mh] Termos MeSH primário: Endotelina-1/análise
Endotelina-3/análise
Estenose da Valva Mitral/patologia
Receptor de Endotelina A/análise
Receptor de Endotelina B/análise
Febre Reumática/patologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/análise
Western Blotting
Cálcio/análise
Estudos de Casos e Controles
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Estenose da Valva Mitral/fisiopatologia
Valores de Referência
Febre Reumática/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Endothelin-1); 0 (Endothelin-3); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150627
[Lr] Data última revisão:
150627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150625
[St] Status:MEDLINE



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