Base de dados : MEDLINE
Pesquisa : D27.505.519.562.625.249 [Categoria DeCS]
Referências encontradas : 29 [refinar]
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  1 / 29 MEDLINE  
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[PMID]:28411035
[Au] Autor:Fedan JS; Thompson JA; Meighan TG; Zeidler-Erdely PC; Antonini JM
[Ad] Endereço:Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA. Electronic address: jsf2@cdc.gov.
[Ti] Título:Altered ion transport in normal human bronchial epithelial cells following exposure to chemically distinct metal welding fume particles.
[So] Source:Toxicol Appl Pharmacol;326:1-6, 2017 Jul 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Welding fume inhalation causes pulmonary toxicity, including susceptibility to infection. We hypothesized that airway epithelial ion transport is a target of fume toxicity, and investigated the effects of fume particulates from manual metal arc-stainless steel (MMA-SS) and gas metal arc-mild steel (GMA-MS) on ion transport in normal human bronchial epithelium (NHBE) cultured in air-interface. MMA-SS particles, more soluble than GMA-MS particles, contain Cr, Ni, Fe and Mn; GMA-MS particles contain Fe and Mn. MMA-SS or GMA-MS particles (0.0167-166.7µg/cm ) were applied apically to NHBEs. After 18h transepithelial potential difference (V ), resistance (R ), and short circuit current (I ) were measured. Particle effects on Na and Cl¯ channels and the Na ,K ,2Cl¯-cotransporter were evaluated using amiloride (apical), 5-nitro-2-[(3-phenylpropyl)amino]benzoic acid (NPPB, apical), and bumetanide (basolateral), respectively. MMA-SS (0.0167-16.7µg/cm ) increased basal V . Only 16.7µg/cm GMA-MS increased basal V significantly. MMA-SS or GMA-MS exposure potentiated I responses (decreases) to amiloride and bumetanide, while not affecting those to NPPB, GMA-MS to a lesser degree than MMA-SS. Variable effects on R were observed in response to amiloride, and bumetanide. Generally, MMA-SS was more potent in altering responses to amiloride and bumetanide than GMA-MS. Hyperpolarization occurred in the absence of LDH release, but decreases in V , R , and I at higher fume particulate doses accompanied LDH release, to a greater extent for MMA-SS. Thus, Na transport and Na ,K ,2Cl¯-cotransport are affected by fume exposure; MMA-MS is more potent than GMA-MS. Enhanced Na absorption and decreased airway surface liquid could compromise defenses against infection.
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar/toxicidade
Brônquios/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Agonistas do Canal de Sódio Epitelial/toxicidade
Canais Epiteliais de Sódio/efeitos dos fármacos
Simportadores de Cloreto de Sódio-Potássio/efeitos dos fármacos
Aço/toxicidade
Soldagem
[Mh] Termos MeSH secundário: Brônquios/metabolismo
Brônquios/patologia
Células Cultivadas
Canais de Cloreto/efeitos dos fármacos
Canais de Cloreto/metabolismo
Relação Dose-Resposta a Droga
Impedância Elétrica
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Canais Epiteliais de Sódio/metabolismo
Gases
Seres Humanos
Exposição por Inalação/efeitos adversos
Transporte de Íons/efeitos dos fármacos
L-Lactato Desidrogenase/metabolismo
Potenciais da Membrana
Exposição Ocupacional/efeitos adversos
Simportadores de Cloreto de Sódio-Potássio/metabolismo
Aço Inoxidável/toxicidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants, Occupational); 0 (Chloride Channels); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (Gases); 0 (Sodium-Potassium-Chloride Symporters); 12597-68-1 (Stainless Steel); 12597-69-2 (Steel); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170416
[St] Status:MEDLINE


  2 / 29 MEDLINE  
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[PMID]:27645999
[Au] Autor:Lucas R; Yue Q; Alli A; Duke BJ; Al-Khalili O; Thai TL; Hamacher J; Sridhar S; Lebedyeva I; Su H; Tzotzos S; Fischer B; Gameiro AF; Loose M; Chakraborty T; Shabbir W; Aufy M; Lemmens-Gruber R; Eaton DC; Czikora I
[Ad] Endereço:From the Vascular Biology Center, rlucas@augusta.edu.
[Ti] Título:The Lectin-like Domain of TNF Increases ENaC Open Probability through a Novel Site at the Interface between the Second Transmembrane and C-terminal Domains of the α-Subunit.
[So] Source:J Biol Chem;291(45):23440-23451, 2016 Nov 04.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of the epithelial sodium channel (ENaC), which regulates fluid homeostasis and blood pressure, is complex and remains incompletely understood. The TIP peptide, a mimic of the lectin-like domain of TNF, activates ENaC by binding to glycosylated residues in the extracellular loop of ENaC-α, as well as to a hitherto uncharacterized internal site. Molecular docking studies suggested three residues, Val , Glu , and Glu , located at the interface between the second transmembrane and C-terminal domains of ENaC-α, as a critical site for binding of the TIP peptide. We generated Ala replacement mutants in this region of ENaC-α and examined its interaction with TIP peptide (3M, V567A/E568A/E571A; 2M, V567A/E568A; and 1M, E571A). 3M and 2M ENaC-α, but not 1M ENaC-α, displayed significantly reduced binding capacity to TIP peptide and to TNF. When overexpressed in H441 cells, 3M mutant ENaC-α formed functional channels with similar gating and density characteristics as the WT subunit and efficiently associated with the ß and γ subunits in the plasma membrane. We subsequently assayed for increased open probability time and membrane expression, both of which define ENaC activity, following addition of TIP peptide. TIP peptide increased open probability time in H441 cells overexpressing wild type and 1M ENaC-α channels, but not 3M or 2M ENaC-α channels. On the other hand, TIP peptide-mediated reduction in ENaC ubiquitination was similar in cells overexpressing either WT or 3M ENaC-α subunits. In summary, this study has identified a novel site in ENaC-α that is crucial for activation of the open probability of the channel, but not membrane expression, by the lectin-like domain of TNF.
[Mh] Termos MeSH primário: Agonistas do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/metabolismo
Peptídeos Cíclicos/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Canais Epiteliais de Sódio/química
Canais Epiteliais de Sódio/genética
Células HEK293
Seres Humanos
Simulação de Acoplamento Molecular
Mutação Puntual
Domínios Proteicos/efeitos dos fármacos
Subunidades Proteicas/química
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
Ubiquitinação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AP301 peptide); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (Peptides, Cyclic); 0 (Protein Subunits)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160921
[St] Status:MEDLINE


  3 / 29 MEDLINE  
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[PMID]:27592201
[Au] Autor:Galiana-Simal A; Olivares-Álvaro E; Klett-Mingo M; Ruiz-Roso MB; Ballesteros S; de Las Heras N; Fuller PJ; Lahera V; Martín-Fernández B
[Ad] Endereço:Department of Physiology, Faculty of Medicine, Universidad Complutense, 28040 Madrid, Spain.
[Ti] Título:Proanthocyanidins block aldosterone-dependent up-regulation of cardiac gamma ENaC and Nedd4-2 inactivation via SGK1.
[So] Source:J Nutr Biochem;37:13-19, 2016 11.
[Is] ISSN:1873-4847
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aldosterone plays a central role in the development of cardiac pathological states involving ion transport imbalances, especially sodium transport. We have previously demonstrated a cardioprotective effect of proanthocyanidins in aldosterone-treated rats. Our objective was to investigate for the first time the effect of proanthocyanidins on serum and glucocorticoid-regulated kinase 1 (SGK1), epithelial Na channel (γ-ENaC), neuronal precursor cells expressed developmentally down-regulated 4-2 (Nedd4-2) and phosphoNedd4-2 protein expression in the hearts of aldosterone-treated rats. Male Wistar rats received aldosterone (1mg kg day )+1% NaCl for 3weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5mg kg day ). Hypertension and diastolic dysfunction induced by aldosterone were abolished by treatment with PRO80. Expression of fibrotic, inflammatory and oxidative mediators were increased by aldosterone-salt administration and blunted by PRO80. Antioxidant capacity was improved by PRO80. The up-regulated aldosterone mediator SGK1, ENaC and p-Nedd4-2/total Nedd4-2 ratio were blocked by PRO80. PRO80 blunted aldosterone-mineralocorticoid-mediated up-regulation of ENaC provides new mechanistic insight of the beneficial effect of proanthocyanidins preventing the cardiac alterations induced by aldosterone excess.
[Mh] Termos MeSH primário: Suplementos Nutricionais
Complexos Endossomais de Distribuição Requeridos para Transporte/antagonistas & inibidores
Canais Epiteliais de Sódio/metabolismo
Ventrículos do Coração/metabolismo
Proteínas Imediatamente Precoces/antagonistas & inibidores
Proantocianidinas/uso terapêutico
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Disfunção Ventricular Esquerda/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Antioxidantes/uso terapêutico
Biomarcadores/metabolismo
Cardiomegalia/etiologia
Cardiomegalia/prevenção & controle
Cardiotônicos/uso terapêutico
Complexos Endossomais de Distribuição Requeridos para Transporte/agonistas
Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Agonistas do Canal de Sódio Epitelial/antagonistas & inibidores
Agonistas do Canal de Sódio Epitelial/metabolismo
Bloqueadores do Canal de Sódio Epitelial/uso terapêutico
Canais Epiteliais de Sódio/química
Fibrose
Ventrículos do Coração/imunologia
Ventrículos do Coração/patologia
Ventrículos do Coração/fisiopatologia
Hipertensão/etiologia
Hipertensão/prevenção & controle
Proteínas Imediatamente Precoces/agonistas
Proteínas Imediatamente Precoces/metabolismo
Masculino
Antagonistas de Receptores de Mineralocorticoides/uso terapêutico
Ubiquitina-Proteína Ligases Nedd4
Estresse Oxidativo
Proteínas Serina-Treonina Quinases/metabolismo
Ratos Wistar
Ubiquitina-Proteína Ligases/metabolismo
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/patologia
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antihypertensive Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Endosomal Sorting Complexes Required for Transport); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Immediate-Early Proteins); 0 (Mineralocorticoid Receptor Antagonists); 0 (Proanthocyanidins); EC 2.3.2.26 (NEDD4L protein, rat); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160905
[St] Status:MEDLINE


  4 / 29 MEDLINE  
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[PMID]:26852863
[Au] Autor:Nie H; Cui Y; Wu S; Ding Y; Li Y
[Ad] Endereço:Institute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang, Liaoning 110122, China. Electronic address: hgnie@mail.cmu.edu.cn.
[Ti] Título:1,25-Dihydroxyvitamin D Enhances Alveolar Fluid Clearance by Upregulating the Expression of Epithelial Sodium Channels.
[So] Source:J Pharm Sci;105(1):333-8, 2016 Jan.
[Is] ISSN:1520-6017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitamin D is implicated in the pathogenesis of asthma, acute lung injury, and other respiratory diseases. 1,25-Dihydroxyvitamin D (1,25(OH)2D3), the hormonal form of vitamin D, has been shown to reduce vascular permeability and ameliorate lung edema. Therefore, we speculate that 1,25(OH)2D3 may regulate alveolar Na(+) transport via targeting epithelial Na(+) channels (ENaC), a crucial pathway for alveolar fluid clearance. In vivo total alveolar fluid clearance was 39.4 ± 3.8% in 1,25(OH)2D3-treated mice, significantly greater than vehicle-treated controls (24.7 ± 1.9 %, n = 10, p < 0.05). 1,25(OH)2D3 increased amiloride-sensitive short-circuit currents in H441 monolayers, and whole-cell patch-clamp data confirmed that ENaC currents in single H441 cell were enhanced in 1,25(OH)2D3-treated cells. Western blot showed that the expression of α-ENaC was significantly elevated in 1,25(OH)2D3-treated mouse lungs and 1,25(OH)2D3-treated H441 cells. These observations suggest that vitamin D augments transalveolar fluid clearance, and vitamin D therapy may potentially be used to ameliorate pulmonary edema.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Agonistas do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/biossíntese
Alvéolos Pulmonares/efeitos dos fármacos
Alvéolos Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Animais
Permeabilidade Capilar/efeitos dos fármacos
Linhagem Celular
Canais Epiteliais de Sódio/genética
Água Extravascular Pulmonar/metabolismo
Pulmão/citologia
Pulmão/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Técnicas de Patch-Clamp
Edema Pulmonar/tratamento farmacológico
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (RNA, Messenger); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160209
[St] Status:MEDLINE


  5 / 29 MEDLINE  
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[PMID]:25278498
[Au] Autor:Chen MX; Gatfield K; Ward E; Downie D; Sneddon HF; Walsh S; Powell AJ; Laine D; Carr M; Trezise D
[Ad] Endereço:Biological Sciences, GlaxoSmithKline R&D, Stevenage, Herts, UK mark.x.chen@gsk.com.
[Ti] Título:Validation and optimization of novel high-throughput assays for human epithelial sodium channels.
[So] Source:J Biomol Screen;20(2):242-53, 2015 Feb.
[Is] ISSN:1552-454X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epithelial sodium channel (ENaC) plays a crucial role in salt and water homeostasis and is primarily involved in sodium reabsorption in the kidney and lung. Modulators of ENaC function, particularly within lung epithelia, could offer potential treatments for a number of diseases. As a constitutively active sodium channel, ENaC expression at the cell membrane is highly regulated through rapid turnover. This short half-life of the channel at the membrane and cytotoxicity from overexpression pose a problem for reagent generation and assay development in drug discovery. We have generated an HEK293 stable cell line expressing ENaC ß and γ subunits containing the PY motif trafficking mutations found in Liddle's syndrome to overcome rapid channel turnover at the membrane. A BacMam virus was used to transiently express the ENaC α subunit to reconstitute channel function to reduce the toxicity associated with long-term overexpression. We have configured a 384-well FLIPR membrane potential antagonist assay for high-throughput screening and an IonWorks Quattro electrophysiology antagonist assay that is predictive of potency values derived from primary lung epithelial cell short-circuit measurements. The triage strategy for compound screening and profiling against this target using these assays has resulted in the discovery of novel chemotypes.
[Mh] Termos MeSH primário: Avaliação Pré-Clínica de Medicamentos
Agonistas do Canal de Sódio Epitelial/farmacologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/metabolismo
Ensaios de Triagem em Larga Escala/métodos
Ensaios de Triagem em Larga Escala/normas
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Canais Epiteliais de Sódio/química
Canais Epiteliais de Sódio/genética
Expressão Gênica
Células HEK293
Seres Humanos
Potenciais da Membrana/efeitos dos fármacos
Técnicas de Patch-Clamp
Mucosa Respiratória/metabolismo
Bibliotecas de Moléculas Pequenas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150123
[Lr] Data última revisão:
150123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141004
[St] Status:MEDLINE
[do] DOI:10.1177/1087057114552399


  6 / 29 MEDLINE  
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[PMID]:25221873
[Au] Autor:Sieck GC; Wylam ME
[Ad] Endereço:1 Department of Physiology and Biomedical Engineering Mayo Clinic Rochester, Minnesota.
[Ti] Título:Paradoxical use of tumor necrosis factor in treating pulmonary edema.
[So] Source:Am J Respir Crit Care Med;190(6):595-6, 2014 Sep 15.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Agonistas do Canal de Sódio Epitelial/metabolismo
Canais Epiteliais de Sódio/metabolismo
Peptídeos Cíclicos/metabolismo
Alvéolos Pulmonares/metabolismo
Edema Pulmonar/metabolismo
Estreptolisinas
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
[Pt] Tipo de publicação:COMMENT; EDITORIAL
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (Peptides, Cyclic); 0 (Streptolysins); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:140916
[Lr] Data última revisão:
140916
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140916
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201407-1364ED


  7 / 29 MEDLINE  
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[PMID]:25029038
[Au] Autor:Czikora I; Alli A; Bao HF; Kaftan D; Sridhar S; Apell HJ; Gorshkov B; White R; Zimmermann A; Wendel A; Pauly-Evers M; Hamacher J; Garcia-Gabay I; Fischer B; Verin A; Bagi Z; Pittet JF; Shabbir W; Lemmens-Gruber R; Chakraborty T; Lazrak A; Matthay MA; Eaton DC; Lucas R
[Ad] Endereço:1 Vascular Biology Center.
[Ti] Título:A novel tumor necrosis factor-mediated mechanism of direct epithelial sodium channel activation.
[So] Source:Am J Respir Crit Care Med;190(5):522-32, 2014 Sep 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Alveolar liquid clearance is regulated by Na(+) uptake through the apically expressed epithelial sodium channel (ENaC) and basolaterally localized Na(+)-K(+)-ATPase in type II alveolar epithelial cells. Dysfunction of these Na(+) transporters during pulmonary inflammation can contribute to pulmonary edema. OBJECTIVES: In this study, we sought to determine the precise mechanism by which the TIP peptide, mimicking the lectin-like domain of tumor necrosis factor (TNF), stimulates Na(+) uptake in a homologous cell system in the presence or absence of the bacterial toxin pneumolysin (PLY). METHODS: We used a combined biochemical, electrophysiological, and molecular biological in vitro approach and assessed the physiological relevance of the lectin-like domain of TNF in alveolar liquid clearance in vivo by generating triple-mutant TNF knock-in mice that express a mutant TNF with deficient Na(+) uptake stimulatory activity. MEASUREMENTS AND MAIN RESULTS: TIP peptide directly activates ENaC, but not the Na(+)-K(+)-ATPase, upon binding to the carboxy-terminal domain of the α subunit of the channel. In the presence of PLY, a mediator of pneumococcal-induced pulmonary edema, this binding stabilizes the ENaC-PIP2-MARCKS complex, which is necessary for the open probability conformation of the channel and preserves ENaC-α protein expression, by means of blunting the protein kinase C-α pathway. Triple-mutant TNF knock-in mice are more prone than wild-type mice to develop edema with low-dose intratracheal PLY, correlating with reduced pulmonary ENaC-α subunit expression. CONCLUSIONS: These results demonstrate a novel TNF-mediated mechanism of direct ENaC activation and indicate a physiological role for the lectin-like domain of TNF in the resolution of alveolar edema during inflammation.
[Mh] Termos MeSH primário: Agonistas do Canal de Sódio Epitelial/metabolismo
Canais Epiteliais de Sódio/metabolismo
Peptídeos Cíclicos/metabolismo
Alvéolos Pulmonares/metabolismo
Edema Pulmonar/metabolismo
Estreptolisinas
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias
Agonistas do Canal de Sódio Epitelial/química
Canais Epiteliais de Sódio/química
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Peptídeos Cíclicos/química
Alvéolos Pulmonares/microbiologia
Edema Pulmonar/microbiologia
Fator de Necrose Tumoral alfa/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AP301 peptide); 0 (Bacterial Proteins); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (Peptides, Cyclic); 0 (Streptolysins); 0 (Tumor Necrosis Factor-alpha); 0 (plY protein, Streptococcus pneumoniae)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:170416
[Lr] Data última revisão:
170416
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140717
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201405-0833OC


  8 / 29 MEDLINE  
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[PMID]:24303840
[Au] Autor:Lazrak A; Jurkuvenaite A; Ness EC; Zhang S; Woodworth BA; Muhlebach MS; Stober VP; Lim YP; Garantziotis S; Matalon S
[Ad] Endereço:Departments of 1 Anesthesiology.
[Ti] Título:Inter-α-inhibitor blocks epithelial sodium channel activation and decreases nasal potential differences in ΔF508 mice.
[So] Source:Am J Respir Cell Mol Biol;50(5):953-62, 2014 May.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased activity of lung epithelial sodium channels (ENaCs) contributes to the pathophysiology of cystic fibrosis (CF) by increasing the rate of epithelial lining fluid reabsorption. Inter-α-inhibitor (IαI), a serum protease inhibitor, may decrease ENaC activity by preventing its cleavage by serine proteases. High concentrations of IαI were detected in the bronchoalveolar lavage fluid (BALF) of children with CF and lower airway diseases. IαI decreased amiloride-sensitive (IENaC) but not cAMP-activated Cl(-) currents across confluent monolayers of rat ATII, and mouse nasal epithelial cells grew in primary culture by 45 and 25%, respectively. Changes in IENaC by IαI in ATII cells were accompanied by increased levels of uncleaved (immature) surface α-ENaC. IαI increased airway surface liquid depth overlying murine nasal epithelial cells to the same extent as amiloride, consistent with ENaC inhibition. Incubation of lung slices from C57BL/6, those lacking phenylalanine at position 508 (∆F508), or CF transmembrane conductance regulator knockout mice with IαI for 3 hours decreased the open probability of their ENaC channels by 50%. ∆F508 mice had considerably higher levels the amiloride-sensitive fractions of ENaC nasal potential difference (ENaC-NPD) than wild-type littermates and only background levels of IαI in their BALF. A single intranasal instillation of IαI decreased their ENaC-NPD 24 hours later by 25%. In conclusion, we show that IαI is present in the BALF of children with CF, is an effective inhibitor of ENaC proteolysis, and decreases ENaC activity in lung epithelial cells of ∆F508 mice.
[Mh] Termos MeSH primário: alfa-Globulinas/metabolismo
Células Epiteliais/metabolismo
Agonistas do Canal de Sódio Epitelial/metabolismo
Canais Epiteliais de Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar
Células Cultivadas
Fibrose Cística/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Seres Humanos
Pulmão/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Oócitos/metabolismo
Ratos
Xenopus laevis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Alpha-Globulins); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 39346-44-6 (inter-alpha-inhibitor)
[Em] Mês de entrada:1408
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131206
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2013-0215OC


  9 / 29 MEDLINE  
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[PMID]:23547933
[Au] Autor:Alvarez de la Rosa D; Navarro-González JF; Giraldez T
[Ad] Endereço:Department of Physiology, Universidad de La Laguna and Instituto de Tecnologías Biomédicas, La Laguna, Tenerife, Spain. diego.alvarez@ull.es
[Ti] Título:ENaC modulators and renal disease.
[So] Source:Curr Mol Pharmacol;6(1):35-43, 2013 Mar.
[Is] ISSN:1874-4702
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:The epithelial sodium channel (ENaC) plays an essential role in transepithelial sodium reabsorption in the renal connecting tubule and collecting duct. Therefore, controlling ENaC activity is an important regulatory event in electrolyte and extracellular volume homeostasis, and thus in the control of blood pressure. Many independent signaling pathways converge on ENaC, although the most important for its physiological role is the enhancement of channel activity by the steroid hormone aldosterone. In this review, we briefly summarize current knowledge about ENaC regulation and the different chemical compounds available to directly or indirectly modify channel function. In addition, current and possible clinical uses of ENaC and aldosterone antagonists are highlighted.
[Mh] Termos MeSH primário: Canais Epiteliais de Sódio/metabolismo
Nefropatias/metabolismo
[Mh] Termos MeSH secundário: Aldosterona/farmacologia
Aldosterona/uso terapêutico
Diuréticos/uso terapêutico
Agonistas do Canal de Sódio Epitelial/farmacologia
Agonistas do Canal de Sódio Epitelial/uso terapêutico
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Bloqueadores do Canal de Sódio Epitelial/uso terapêutico
Canais Epiteliais de Sódio/química
Seres Humanos
Hipertensão/tratamento farmacológico
Nefropatias/tratamento farmacológico
Nefropatias/patologia
Receptores de Mineralocorticoides/química
Receptores de Mineralocorticoides/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Diuretics); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Receptors, Mineralocorticoid); 4964P6T9RB (Aldosterone); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:130610
[Lr] Data última revisão:
130610
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130404
[St] Status:MEDLINE


  10 / 29 MEDLINE  
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Fotocópia
[PMID]:23547931
[Au] Autor:Fronius M
[Ad] Endereço:Institute of Animal Physiology, Justus-Liebig-University Giessen, Germany. martin.fronius@bio.uni-giessen.de
[Ti] Título:Treatment of pulmonary edema by ENaC activators/stimulators.
[So] Source:Curr Mol Pharmacol;6(1):13-27, 2013 Mar.
[Is] ISSN:1874-4702
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:Lungs contain a particular amount of fluid that is crucial for proper lung function. This fluid content is tightly controlled within certain limits. Fluid accumulation in the alveolar airspace impairs gas exchange and represents a lifethreatening condition referred to as pulmonary edema. Ion transport processes by pulmonary epithelia represent a mechanism, responsible for fluid absorption from the airspace. Thus, it is obvious to consider ion transport processes as target for therapeutic interventions in pulmonary edema. The principle mechanism responsible for fluid absorption from the airspace is: Na(+) diffuses through luminal Na(+) channels into epithelial cells and is extruded by Na(+)/K(+)-ATPases at the basolateral side. This process generates an osmotic gradient that represents the driving force for fluid absorption. The rate of Na(+) absorption is limited by the number/activity of Na+ channels in the luminal membrane of alveolar epithelial cells. Although different Na+ channels have been identified, the epithelial Na+ channel (ENaC) is a major player that participates in Na(+)-driven fluid absorption and thus a suitable target for the treatment of pulmonary edema. This article reviews cellular mechanisms by which ENaC activity can be increased in alveolar epithelia (lectins, proteases, ß-adrenoceptors, mineralo-/glucocorticoid-receptors). These mechanisms are involved in regulating ENaC-dependent fluid absorption under physiological conditions. Additionally, pre-clinical as well as some preliminary clinical studies revealed that "ENaC-activators/stimulators" (ß2-adrenoceptor agonists and mineralo-/glucocorticoid-receptor agonists) could be beneficial for therapeutic interventions in patients with pulmonary edema. However, the outcome of subsequently performed multicenter clinical trials with "ENaC-activators/stimulators" for treatment of patients with pulmonary edema was disappointing.
[Mh] Termos MeSH primário: Agonistas do Canal de Sódio Epitelial/uso terapêutico
Canais Epiteliais de Sódio/metabolismo
Edema Pulmonar/tratamento farmacológico
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Agonistas Adrenérgicos beta/uso terapêutico
Agonistas do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/química
Água Extravascular Pulmonar/efeitos dos fármacos
Glucocorticoides/farmacologia
Glucocorticoides/uso terapêutico
Seres Humanos
Lectinas/metabolismo
Peptídeo Hidrolases/metabolismo
Edema Pulmonar/metabolismo
Edema Pulmonar/patologia
Receptores Adrenérgicos beta/química
Receptores Adrenérgicos beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channels); 0 (Glucocorticoids); 0 (Lectins); 0 (Receptors, Adrenergic, beta); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:130610
[Lr] Data última revisão:
130610
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130404
[St] Status:MEDLINE



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