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[PMID]:29496867
[Au] Autor:Montell C
[Ad] Endereço:Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, Santa Barbara, CA 93106-9625, USA. cmontell@ucsb.edu.
[Ti] Título:pHirst sour taste channels pHound?
[So] Source:Science;359(6379):991-992, 2018 03 02.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Papilas Gustativas
Paladar
[Mh] Termos MeSH secundário: Canais de Cálcio
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Calcium Channels)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180303
[St] Status:MEDLINE
[do] DOI:10.1126/science.aas9772


  2 / 24724 MEDLINE  
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[PMID]:28460460
[Au] Autor:Valdés-Mora F; Locke WJ; Bandrés E; Gallego-Ortega D; Cejas P; García-Cabezas MA; Colino-Sanguino Y; Feliú J; Del Pulgar TG; Lacal JC
[Ad] Endereço:Histone Variants Group, Epigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
[Ti] Título:Clinical relevance of the transcriptional signature regulated by CDC42 in colorectal cancer.
[So] Source:Oncotarget;8(16):26755-26770, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CDC42 is an oncogenic Rho GTPase overexpressed in colorectal cancer (CRC). Although CDC42 has been shown to regulate gene transcription, the specific molecular mechanisms regulating the oncogenic ability of CDC42 remain unknown. Here, we have characterized the transcriptional networks governed by CDC42 in the CRC SW620 cell line using gene expression analysis. Our results establish that several cancer-related signaling pathways, including cell migration and cell proliferation, are regulated by CDC42. This transcriptional signature was validated in two large cohorts of CRC patients and its clinical relevance was also studied. We demonstrate that three CDC42-regulated genes offered a better prognostic value when combined with CDC42 compared to CDC42 alone. In particular, the concordant overexpression of CDC42 and silencing of the putative tumor suppressor gene CACNA2D2 dramatically improved the prognostic value. The CACNA2D2/CDC42 prognostic classifier was further validated in a third CRC cohort as well as in vitro and in vivo CRC models. Altogether, we show that CDC42 has an active oncogenic role in CRC via the transcriptional regulation of multiple cancer-related pathways and that CDC42-mediated silencing of CACNA2D2 is clinically relevant. Our results further support the use of CDC42 specific inhibitors for the treatment of the most aggressive types of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica
Transcriptoma
Proteína cdc42 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Neoplasias Colorretais/diagnóstico
Neoplasias Colorretais/mortalidade
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Redes Reguladoras de Genes
Genes Supressores de Tumor
Xenoenxertos
Seres Humanos
Camundongos
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Prognóstico
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CACNA2D2 protein, human); 0 (Calcium Channels); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15815


  3 / 24724 MEDLINE  
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[PMID]:29366747
[Au] Autor:Camargo-Silva G; Turones LC; da Cruz KR; Gomes KP; Mendonça MM; Nunes A; de Jesus IG; Colugnati DB; Pansani AP; Pobbe RLH; Santos R; Fontes MAP; Guatimosim S; de Castro CH; Ianzer D; Ferreira RN; Xavier CH
[Ad] Endereço:Laboratory of Cardiovascular Physiology and Therapeutics, Department of Physiological Sciences, Institute of Biological Sciences, Federal University of Goiás, Goiania, GO, Brazil.
[Ti] Título:Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response.
[So] Source:Life Sci;196:84-92, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. AIMS: In the present study, we assessed the role of ghrelin - GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. MAIN METHODS AND KEY FINDINGS: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade. Evaluation of the autonomic balance revealed that the sympathetic branch modulates the ghrelin-evoked positive chronotropy. In isolated hearts, the perfusion with ghrelin potentiated the contractile responses caused by stimulation of the beta-adrenergic receptor, without altering the amplitude of the responses evoked by acetylcholine. Experiments in isolated cardiomyocytes revealed that ghrelin amplified the increases in calcium transient changes evoked by isoproterenol. SIGNIFICANCE: Taken together, our results indicate that the Ghrelin-GHS-R1a axis potentiates the magnitude of stress-evoked tachycardia by modulating the autonomic nervous system and peripheral mechanisms, strongly relying on the activation of cardiac calcium transient and beta-adrenergic receptors.
[Mh] Termos MeSH primário: Grelina/farmacologia
Coração/efeitos dos fármacos
Receptores Adrenérgicos beta/efeitos dos fármacos
Estresse Psicológico/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Animais
Pressão Arterial/efeitos dos fármacos
Canais de Cálcio/efeitos dos fármacos
Coração/inervação
Frequência Cardíaca/efeitos dos fármacos
Técnicas In Vitro
Masculino
Agonistas Muscarínicos/farmacologia
Ratos
Ratos Wistar
Receptores de Grelina/efeitos dos fármacos
Restrição Física
Taquicardia/induzido quimicamente
Taquicardia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Calcium Channels); 0 (Ghrelin); 0 (Muscarinic Agonists); 0 (Receptors, Adrenergic, beta); 0 (Receptors, Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:28493473
[Au] Autor:Tahrir FG; Shanmughapriya S; Ahooyi TM; Knezevic T; Gupta MK; Kontos CD; McClung JM; Madesh M; Gordon J; Feldman AM; Cheung JY; Khalili K
[Ad] Endereço:Department of Neuroscience, Center for Neurovirology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania.
[Ti] Título:Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes.
[So] Source:J Cell Physiol;233(2):748-758, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease remains a leading cause of morbidity and mortality in HIV-positive patients, even in those whose viral loads are well controlled with antiretroviral therapy. However, the underlying molecular events responsible for the development of cardiac disease in the setting of HIV remain unknown. The HIV-encoded Tat protein plays a critical role in the activation of HIV gene expression and profoundly impacts homeostasis in both HIV-infected cells and uninfected cells that have taken up released Tat via a bystander effect. Since cardiomyocyte function, including excitation-contraction coupling, greatly depends on energy provided by the mitochondria, in this study, we performed a series of experiments to assess the impact of Tat on mitochondrial function and bioenergetics pathways in a primary cell culture model derived from neonatal rat ventricular cardiomyocytes (NRVCs). Our results show that the presence of Tat in cardiomyocytes is accompanied by a decrease in oxidative phosphorylation, a decline in the levels of ATP, and an accumulation of reactive oxygen species (ROS). Tat impairs the uptake of mitochondrial Ca ([Ca ] ) and the electrophysiological activity of cardiomyocytes. Tat also affects the protein clearance pathway and autophagy in cardiomyocytes under stress due to hypoxia-reoxygenation conditions. A reduction in the level of ubiquitin along with dysregulated degradation of autophagy proteins including SQSTM1/p62 and a reduction of LC3 II were detected in cardiomyocytes harboring Tat. These results suggest that, by targeting mitochondria and protein quality control, Tat significantly impacts bioenergetics and autophagy resulting in dysregulation of cardiomyocyte health and homeostasis.
[Mh] Termos MeSH primário: Metabolismo Energético
HIV-1/metabolismo
Mitocôndrias Cardíacas/metabolismo
Miócitos Cardíacos/metabolismo
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Apoptose
Autofagia
Cálcio/metabolismo
Canais de Cálcio/metabolismo
Hipóxia Celular
Células Cultivadas
Interações Hospedeiro-Patógeno
Potenciais da Membrana
Proteínas Associadas aos Microtúbulos/metabolismo
Mitocôndrias Cardíacas/virologia
Degradação Mitocondrial
Miócitos Cardíacos/virologia
Fosforilação Oxidativa
Cultura Primária de Células
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (LC3 protein, rat); 0 (Microtubule-Associated Proteins); 0 (Reactive Oxygen Species); 0 (Sequestosome-1 Protein); 0 (Sqstm1 protein, rat); 0 (mitochondrial calcium uniporter); 0 (tat Gene Products, Human Immunodeficiency Virus); 8L70Q75FXE (Adenosine Triphosphate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26002


  5 / 24724 MEDLINE  
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[PMID]:29307826
[Au] Autor:Wu G; Li S; Zong G; Liu X; Fei S; Shen L; Guan X; Yang X; Shen Y
[Ad] Endereço:State Key Laboratory of Medicinal Chemical Biology and College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
[Ti] Título:Single channel recording of a mitochondrial calcium uniporter.
[So] Source:Biochem Biophys Res Commun;496(1):127-132, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial calcium uniporter (MCU) is the pore-forming subunit of the entire uniporter complex and plays an important role in mitochondrial calcium uptake. However, the single channel recording of MCU remains controversial. Here, we expressed and purified different MCU proteins and then reconstituted them into planar lipid bilayers for single channel recording. We showed that MCU alone from Pyronema omphalodes (pMCU) is active with prominent single channel Ca currents. In sharp contrast, MCU alone from Homo sapiens (hMCU) is inactive. The essential MCU regulator (EMRE) activates hMCU, and therefore, the complex (hMCU-hEMRE) shows prominent single channel Ca currents. These single channel currents are sensitive to the specific MCU inhibitor Ruthenium Red. Our results clearly demonstrate that active MCU can conduct large amounts of calcium into the mitochondria.
[Mh] Termos MeSH primário: Canais de Cálcio/química
Sinalização do Cálcio
Cálcio/química
Ativação do Canal Iônico
Bicamadas Lipídicas/química
Potencial da Membrana Mitocondrial
Membranas Mitocondriais/química
[Mh] Termos MeSH secundário: Seres Humanos
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Lipid Bilayers); 0 (mitochondrial calcium uniporter); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  6 / 24724 MEDLINE  
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[PMID]:28448473
[Au] Autor:Pérez-Riesgo E; Gutiérrez LG; Ubierna D; Acedo A; Moyer MP; Núñez L; Villalobos C
[Ad] Endereço:Institute of Molecular Biology and Genetics (IBGM), National Research Council (CSIC), 47003 Valladolid, Spain. epercamh@gmail.com.
[Ti] Título:Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) cells undergo the remodeling of intracellular Ca homeostasis, which contributes to cancer hallmarks such as enhanced proliferation, invasion and survival. Ca remodeling includes critical changes in store-operated Ca entry (SOCE) and Ca store content. Some changes have been investigated at the molecular level. However, since nearly 100 genes are involved in intracellular Ca transport, a comprehensive view of Ca remodeling in CRC is lacking. We have used Next Generation Sequencing (NGS) to investigate differences in expression of 77 selected gene transcripts involved in intracellular Ca transport in CRC. To this end, mRNA from normal human colonic NCM460 cells and human colon cancer HT29 cells was isolated and used as a template for transcriptomic sequencing and expression analysis using Ion Torrent technology. After data transformation and filtering, exploratory analysis revealed that both cell types were well segregated. In addition, differential gene expression using R and bioconductor packages show significant differences in expression of selected voltage-operated Ca channels and store-operated Ca entry players, transient receptor potential (TRP) channels, Ca release channels, Ca pumps, Na⁺/Ca exchanger isoforms and genes involved in mitochondrial Ca transport. These data provide the first comprehensive transcriptomic analysis of Ca remodeling in CRC.
[Mh] Termos MeSH primário: Canais de Cálcio/genética
Cálcio/metabolismo
Perfilação da Expressão Gênica
[Mh] Termos MeSH secundário: Canais de Cálcio/metabolismo
Linhagem Celular Tumoral
Análise por Conglomerados
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Regulação da Expressão Gênica
Células HT29
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Análise de Componente Principal
Análise de Sequência de RNA
Trocador de Sódio e Cálcio/genética
Trocador de Sódio e Cálcio/metabolismo
Canais de Receptores Transientes de Potencial/genética
Canais de Receptores Transientes de Potencial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Sodium-Calcium Exchanger); 0 (Transient Receptor Potential Channels); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


  7 / 24724 MEDLINE  
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[PMID]:27771553
[Au] Autor:Kato T; Yamamoto T; Nakamura Y; Nanno T; Fukui G; Sufu Y; Hamada Y; Maeda T; Nishimura S; Ishiguchi H; Murakami W; Fukuda M; Xu X; Hino A; Ono M; Oda T; Okuda S; Kobayashi S; Koseki N; Kyushiki H; Yano M
[Ad] Endereço:Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
[Ti] Título:Correction of impaired calmodulin binding to RyR2 as a novel therapy for lethal arrhythmia in the pressure-overloaded heart failure.
[So] Source:Heart Rhythm;14(1):120-127, 2017 01.
[Is] ISSN:1556-3871
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Calmodulin (CaM) is a key modulator of the channel gating function of the ryanodine receptor (RyR). OBJECTIVE: The purpose of this study was to investigate the pathogenic role of RyR-bound CaM in diastolic Ca leakage from the sarcoplasmic reticulum and arrhythmogenesis in pressure-overloaded heart failure. METHODS: Pressure overload was induced in 12-week-old mice by transverse aortic constriction (TAC) using a 27-gauge needle. RESULTS: TAC operation for 8 weeks produced a significant increase in left ventricular end-diastolic diameter and frequent occurrence of lethal arrhythmias after infusion of epinephrine and caffeine in TAC mice. The amount of RyR-bound CaM decreased significantly in TAC mice compared with sham mice. The apparent affinity of CaM binding to RyR decreased in pressure-overloaded cells compared with sham cells and untreated cells. High-affinity calmodulin (HA-CaM; ie, CaM whose binding affinity to RyR was significantly increased) restored a normal level of CaM-RyR binding properties in pressure-overloaded cells. HA-CaM corrected abnormally increased Ca spark frequency in the pressure-overloaded cells to the level seen in the sham cells. The frequency of spontaneous Ca transients in TAC cells during and after 1-5 Hz of field stimulation was 44%, whereas it was significantly attenuated by HA-CaM but not with CaM. CONCLUSION: Several disorders in the RyR channel function characteristic of pressure-overloaded cells (increased spontaneous Ca leakage, delayed afterdepolarization, triggered activity, Ca spark frequency, spontaneous Ca transients) are caused by deteriorated CaM binding to RyR2. These disorders could be rectified by restoring normal CaM binding to RyR2.
[Mh] Termos MeSH primário: Calmodulina/metabolismo
Insuficiência Cardíaca/diagnóstico por imagem
Insuficiência Cardíaca/terapia
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Taquicardia Ventricular/diagnóstico
[Mh] Termos MeSH secundário: Animais
Mapeamento Potencial de Superfície Corporal/métodos
Canais de Cálcio/metabolismo
Sinalização do Cálcio
Células Cultivadas
Modelos Animais de Doenças
Insuficiência Cardíaca/mortalidade
Camundongos
Camundongos Endogâmicos
Miócitos Cardíacos/metabolismo
Distribuição Aleatória
Valores de Referência
Retículo Sarcoplasmático/metabolismo
Sensibilidade e Especificidade
Taquicardia Ventricular/mortalidade
Taquicardia Ventricular/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Calmodulin); 0 (Ryanodine Receptor Calcium Release Channel)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  8 / 24724 MEDLINE  
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[PMID]:29283238
[Au] Autor:Gusakova SV; Smagliy LV; Birulina YG; Kovalev IV; Nosarev V; Petrova IV; Reutov VP
[Ti] Título:Molecular Mechanisms of Action of Gas Transmitters NO, CO and H2S in Smooth Muscle Cells and Effect of NO-generating Compounds (Nitrates and Nitrites) on Average Life Expectancy.
[So] Source:Usp Fiziol Nauk;48(1):24-52, 2017 Jan-Mar.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Gaseous signaling molecules (gas transmitters) take an especial position among the numerous signaling molecules involved in the regulation of both intracellular processes that occur in different types of cells and cell-cell interactions. At present time, gas transmitters include three molecules whose enzymatic systems of synthesis and degradation, physiological action and intracellular effectors, the change of which under the action of gas transmitters may result in physiological and/or pathophysiological effects are well- determined. These molecules include nitrogen oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S). They are involved in the regulation of functions of various organs and systems of the human body, including the circulatory system. Interaction of NO, CO and H2S with various enzymatic and structural components of endothelial and, especially, smooth muscle cells has a significant impact on vascular tone and blood pressure. Furthermore, the crossing of NO-, CO- and H2S-mediated signaling pathways at common effectors and interaction with each other can determine the end, resulting functional response of the cell. The knowledge of the molecular targets of gas transmitters' action, the structure of the binding centers for gas transmitters and their interaction with each other may be essential in the development of methods of regulation of these signaling systems by targeted, directed action. This review summarizes the molecular mechanisms of the NO, CO and H2S interaction with the main targets, which carry out their regulatory effect on vascular smooth muscle cells. Also we describe here different ways of cross-regulation of NO-, CO- and H2S-dependent signaling pathways. We analyzed NO-synthase and nitrite reductase systems of nitric oxide cycle and discuss the nitrate-nitrite background of the existence of modern man, which can substantially modify the signaling system, the metabolism of virtually all cell ultrastructure of neurons, neuron-neuron and neuron-glial interactions and exerts its influence on socially significant diseases that can affect the quality and the average life expectancy.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Gasotransmissores/metabolismo
Sulfeto de Hidrogênio/metabolismo
Expectativa de Vida/tendências
Miócitos de Músculo Liso/efeitos dos fármacos
Doadores de Óxido Nítrico/toxicidade
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Canais de Cálcio/metabolismo
Comunicação Celular
Regulação da Expressão Gênica
Seres Humanos
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Neuroglia/citologia
Neuroglia/efeitos dos fármacos
Neuroglia/metabolismo
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Óxido Nítrico Sintase Tipo III/genética
Óxido Nítrico Sintase Tipo III/metabolismo
Nitrito Redutases/genética
Nitrito Redutases/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Gasotransmitters); 0 (Nitric Oxide Donors); 31C4KY9ESH (Nitric Oxide); 7U1EE4V452 (Carbon Monoxide); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.7.- (Nitrite Reductases); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  9 / 24724 MEDLINE  
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[PMID]:29235752
[Au] Autor:Nikolaienko TV; Nikulina VV; Shelest DV; Garmanchuk LV
[Ti] Título:The mechanism of VEGF-mediated endothelial cells survival and proliferation in conditions of unfed-culture.
[So] Source:Ukr Biochem J;88(4):12-9, 2016 Jul-Aug.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The mechanisms of VEGF-mediated effects on endothelial cells during cancer development and progression is not clear. In present study the biological effects of VEGF, VEGF-rich culture medium of peritoneal macrophages from mice with Lewis lung carcinoma were studied on MAEC cell line under conditions of unfed culture. We have shown that VEGF increased cell proliferation by the 5th day of culturing vs control and anti-VEGF-treated cells. This effect was associated with increased consumption of glucose and NO production by the 2nd day while decreased ­ on the 5th day of cell culturing. VEGF-mediated NO production was dependent on Ca2+ ions. Block of Ca2+-channels (LaCl3) had more pronounced inhibitory effect vs chelator of Ca2+ ions (EDTA). It was shown that peritoneal macrophages are the main suppliers of VEGF at tumor angiogenesis, as evidenced by the data obtained on model system of endothelial cells synchronized in G0/G1 phase.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Carcinoma Pulmonar de Lewis/metabolismo
Células Endoteliais/efeitos dos fármacos
Macrófagos Peritoneais/secreção
Neovascularização Patológica/metabolismo
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/metabolismo
Carcinoma Pulmonar de Lewis/patologia
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Transformada
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Técnicas de Cocultura
Meios de Cultivo Condicionados/química
Meios de Cultivo Condicionados/farmacologia
Ácido Edético/farmacologia
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Feminino
Glucose/metabolismo
Lantânio/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Macrófagos Peritoneais/patologia
Camundongos
Neovascularização Patológica/patologia
Óxido Nítrico/biossíntese
Cultura Primária de Células
Fator A de Crescimento do Endotélio Vascular/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Calcium Channel Blockers); 0 (Calcium Channels); 0 (Culture Media, Conditioned); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse); 04M8624OXV (lanthanum chloride); 31C4KY9ESH (Nitric Oxide); 6I3K30563S (Lanthanum); 9G34HU7RV0 (Edetic Acid); IY9XDZ35W2 (Glucose); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.04.012


  10 / 24724 MEDLINE  
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Fotocópia
[PMID]:29176543
[Au] Autor:Annunziata G; Lobo P; Carbuccia C
[Ad] Endereço:Department of Internal Medicine, St. Barnabas Hospital, Affiliated to Albert Einstein College of Medicine, Bronx, NY, USA.
[Ti] Título:A Rare Case of Cerebellar Ataxia Due to Voltage-Gated Calcium Channel and Glutamic Acid Decarboxylase Autoantibodies.
[So] Source:Am J Case Rep;18:1251-1255, 2017 Nov 27.
[Is] ISSN:1941-5923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Autoimmune cerebellar ataxia can be paraneoplastic in nature or can occasionally present without evidence of an ongoing malignancy. The detection of specific autoantibodies has been statistically linked to different etiologies. CASE REPORT A 55-year-old African-American woman with hypertension and a past history of morbid obesity and uncontrolled diabetes status post gastric bypass four years prior to the visit (with significantly improved body mass index and hemoglobin A1c controlled at the time of the clinical encounter) presented to the office complaining of gradual onset of unsteadiness and recurrent falls for the past three years, as well as difficulties coordinating routine daily activities. The neurologic exam showed moderate dysarthria and ataxic gait with bilateral dysmetria and positive Romberg test. Routine laboratory test results were only remarkable for a mild elevation of erythrocyte sedimentation rate, and most laboratory and imaging tests for common causes of ataxia failed to demonstrate an etiology. Upon further workup, evidence of anti-voltage-gated calcium channel and anti-glutamic acid decarboxylase antibody was demonstrated. She was then treated with intravenous immunoglobulins with remarkable clinical improvement. CONCLUSIONS We present a case of antibody-mediated ataxia not associated with malignancy. While ataxia is rarely related to autoantibodies, in such cases it is critical to understand the etiology of this disabling condition in order to treat it correctly. Clinicians should be aware of the possible association with specific autoantibodies and the necessity to rule out an occult malignancy in such cases.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Canais de Cálcio/imunologia
Ataxia Cerebelar/etiologia
Glutamato Descarboxilase/imunologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Calcium Channels); EC 4.1.1.15 (Glutamate Decarboxylase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE



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