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[PMID]:28453575
[Au] Autor:Hodonsky CJ; Jain D; Schick UM; Morrison JV; Brown L; McHugh CP; Schurmann C; Chen DD; Liu YM; Auer PL; Laurie CA; Taylor KD; Browning BL; Li Y; Papanicolaou G; Rotter JI; Kurita R; Nakamura Y; Browning SR; Loos RJF; North KE; Laurie CC; Thornton TA; Pankratz N; Bauer DE; Sofer T; Reiner AP
[Ad] Endereço:Department of Epidemiology, University of North Carolina Gillings School of Public Health, Chapel Hill, NC, United States of America.
[Ti] Título:Genome-wide association study of red blood cell traits in Hispanics/Latinos: The Hispanic Community Health Study/Study of Latinos.
[So] Source:PLoS Genet;13(4):e1006760, 2017 Apr.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prior GWAS have identified loci associated with red blood cell (RBC) traits in populations of European, African, and Asian ancestry. These studies have not included individuals with an Amerindian ancestral background, such as Hispanics/Latinos, nor evaluated the full spectrum of genomic variation beyond single nucleotide variants. Using a custom genotyping array enriched for Amerindian ancestral content and 1000 Genomes imputation, we performed GWAS in 12,502 participants of Hispanic Community Health Study and Study of Latinos (HCHS/SOL) for hematocrit, hemoglobin, RBC count, RBC distribution width (RDW), and RBC indices. Approximately 60% of previously reported RBC trait loci generalized to HCHS/SOL Hispanics/Latinos, including African ancestral alpha- and beta-globin gene variants. In addition to the known 3.8kb alpha-globin copy number variant, we identified an Amerindian ancestral association in an alpha-globin regulatory region on chromosome 16p13.3 for mean corpuscular volume and mean corpuscular hemoglobin. We also discovered and replicated three genome-wide significant variants in previously unreported loci for RDW (SLC12A2 rs17764730, PSMB5 rs941718), and hematocrit (PROX1 rs3754140). Among the proxy variants at the SLC12A2 locus we identified rs3812049, located in a bi-directional promoter between SLC12A2 (which encodes a red cell membrane ion-transport protein) and an upstream anti-sense long-noncoding RNA, LINC01184, as the likely causal variant. We further demonstrate that disruption of the regulatory element harboring rs3812049 affects transcription of SLC12A2 and LINC01184 in human erythroid progenitor cells. Together, these results reinforce the importance of genetic study of diverse ancestral populations, in particular Hispanics/Latinos.
[Mh] Termos MeSH primário: Proteínas de Homeodomínio/genética
Complexo de Endopeptidases do Proteassoma/genética
RNA Longo não Codificante/genética
Membro 2 da Família 12 de Carreador de Soluto/genética
Proteínas Supressoras de Tumor/genética
alfa-Globinas/genética
[Mh] Termos MeSH secundário: Contagem de Eritrócitos
Eritrócitos
Feminino
Estudo de Associação Genômica Ampla
Hemoglobinas/genética
Hispano-Americanos/genética
Seres Humanos
Masculino
Polimorfismo de Nucleotídeo Único
Globinas beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemoglobins); 0 (Homeodomain Proteins); 0 (RNA, Long Noncoding); 0 (SLC12A2 protein, human); 0 (Solute Carrier Family 12, Member 2); 0 (Tumor Suppressor Proteins); 0 (alpha-Globins); 0 (beta-Globins); 0 (long noncoding RNA LINC01186, human); 0 (prospero-related homeobox 1 protein); EC 3.4.25.1 (PSMB5 protein, human); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006760


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[PMID]:28962859
[Au] Autor:Furukawa M; Tsukahara T; Tomita K; Iwai H; Sonomura T; Miyawaki S; Sato T
[Ad] Endereço:Department of Applied Pharmacology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima, 890-8544, Japan; Department of Orthodontics and Dentofacial Orthopedics, Kagoshima University Graduate School of Medical and Dental Sciences,
[Ti] Título:Neonatal maternal separation delays the GABA excitatory-to-inhibitory functional switch by inhibiting KCC2 expression.
[So] Source:Biochem Biophys Res Commun;493(3):1243-1249, 2017 Nov 25.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The excitatory-to-inhibitory functional switch of γ-aminobutyric acid (GABA; GABA switch), which normally occurs in the first to the second postnatal week in the hippocampus, is necessary for the development of appropriate central nervous system function. A deficit in GABAergic inhibitory function could cause excitatory/inhibitory (E/I) neuron imbalance that is found in many neurodegenerative disorders. In the present study, we examined whether neonatal stress can affect the timing of the GABA functional switch and cause disorders during adolescence. Neonatal stress was induced in C57BL/6J male mouse pups by maternal separation (MS) on postnatal days (PND) 1-21. Histological quantification of K -Cl co-transporter (KCC2) and Ca imaging were performed to examine the timing of the GABA switch during the MS period. To evaluate the influence of neonatal MS on adolescent hippocampal function, we quantified KCC2 expression and evaluated hippocampal-related behavioral tasks at PND35-38. We showed that MS delayed the timing of the GABA switch in the hippocampus and inhibited the increase in membrane KCC2 expression, with KCC2 expression inhibition persisting until adolescence. Behavioral tests showed impaired cognition, declined attention, hyperlocomotion, and aggressive character in maternally separated mice. Taken together, our results show that neonatal stress delayed the timing of the GABA switch, which could change the E/I balance and cause neurodegenerative disorders in later life.
[Mh] Termos MeSH primário: Hipocampo/metabolismo
Privação Materna
Estresse Psicológico/metabolismo
Simportadores/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Comportamento Animal/fisiologia
Cálcio/análise
Cálcio/metabolismo
Feminino
Hipocampo/fisiologia
Masculino
Camundongos Endogâmicos C57BL
Neurônios/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Slc12a2 protein, mouse); 0 (Solute Carrier Family 12, Member 2); 0 (Symporters); 0 (potassium-chloride symporters); 56-12-2 (gamma-Aminobutyric Acid); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE


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[PMID]:28692063
[Au] Autor:Karimy JK; Zhang J; Kurland DB; Theriault BC; Duran D; Stokum JA; Furey CG; Zhou X; Mansuri MS; Montejo J; Vera A; DiLuna ML; Delpire E; Alper SL; Gunel M; Gerzanich V; Medzhitov R; Simard JM; Kahle KT
[Ad] Endereço:Department of Neurosurgery, Yale School of Medicine, New Haven, Connecticut, USA.
[Ti] Título:Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus.
[So] Source:Nat Med;23(8):997-1003, 2017 Aug.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The choroid plexus epithelium (CPE) secretes higher volumes of fluid (cerebrospinal fluid, CSF) than any other epithelium and simultaneously functions as the blood-CSF barrier to gate immune cell entry into the central nervous system. Posthemorrhagic hydrocephalus (PHH), an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH), is a common disease usually treated by suboptimal CSF shunting techniques. PHH is classically attributed to primary impairments in CSF reabsorption, but little experimental evidence supports this concept. In contrast, the potential contribution of CSF secretion to PHH has received little attention. In a rat model of PHH, we demonstrate that IVH causes a Toll-like receptor 4 (TLR4)- and NF-κB-dependent inflammatory response in the CPE that is associated with a ∼3-fold increase in bumetanide-sensitive CSF secretion. IVH-induced hypersecretion of CSF is mediated by TLR4-dependent activation of the Ste20-type stress kinase SPAK, which binds, phosphorylates, and stimulates the NKCC1 co-transporter at the CPE apical membrane. Genetic depletion of TLR4 or SPAK normalizes hyperactive CSF secretion rates and reduces PHH symptoms, as does treatment with drugs that antagonize TLR4-NF-κB signaling or the SPAK-NKCC1 co-transporter complex. These data uncover a previously unrecognized contribution of CSF hypersecretion to the pathogenesis of PHH, demonstrate a new role for TLRs in regulation of the internal brain milieu, and identify a kinase-regulated mechanism of CSF secretion that could be targeted by repurposed US Food and Drug Administration (FDA)-approved drugs to treat hydrocephalus.
[Mh] Termos MeSH primário: Hemorragia Cerebral/imunologia
Líquido Cefalorraquidiano/secreção
Plexo Corióideo/secreção
Hidrocefalia/imunologia
NF-kappa B/imunologia
Receptor 4 Toll-Like/imunologia
[Mh] Termos MeSH secundário: Acetazolamida/farmacologia
Animais
Antioxidantes/farmacologia
Western Blotting
Bumetanida/farmacologia
Hemorragia Cerebral/complicações
Ventrículos Cerebrais
Plexo Corióideo/efeitos dos fármacos
Plexo Corióideo/imunologia
Diuréticos/farmacologia
Técnicas de Silenciamento de Genes
Técnicas de Inativação de Genes
Hidrocefalia/etiologia
Hidrocefalia/metabolismo
Immunoblotting
Imuno-Histoquímica
Imunoprecipitação
Inflamação
Prolina/análogos & derivados
Prolina/farmacologia
Proteínas Serina-Treonina Quinases/metabolismo
Ratos
Ratos Wistar
Salicilanilidas/farmacologia
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
Sulfonamidas/farmacologia
Tiocarbamatos/farmacologia
Receptor 4 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Diuretics); 0 (NF-kappa B); 0 (Salicylanilides); 0 (Slc12a2 protein, mouse); 0 (Solute Carrier Family 12, Member 2); 0 (Sulfonamides); 0 (Thiocarbamates); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 0 (ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate); 0Y2S3XUQ5H (Bumetanide); 135467-92-4 (prolinedithiocarbamate); 9DLQ4CIU6V (Proline); EC 2.7.1.- (Stk39 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EUL532EI54 (closantel); O3FX965V0I (Acetazolamide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4361


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[PMID]:28574574
[Au] Autor:Marunaka Y
[Ad] Endereço:Departments of Molecular Cell Physiology and Bio-Ionomics, Kyoto Prefectural University of Medicine, Kyoto, Japan.
[Ti] Título:Actions of quercetin, a flavonoid, on ion transporters: its physiological roles.
[So] Source:Ann N Y Acad Sci;1398(1):142-151, 2017 Jun.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Flavonoids keep us healthy by controlling various body and cellular functions. It is well known that cations, such as Na , K , and Ca , play important roles in the regulation of body and cellular functions, including generation of action potentials and the resting membrane potential of neural and muscle cells and signal transduction as intracellular second messengers. However, we have little information on the physiological roles of anions, particularly Cl , in body and cellular functions. Quercetin, a flavonoid, stimulates Na -K -2Cl cotransporter 1 (NKCC1), which is one of the most important ion transporters regulating the cytosolic Cl concentration ([Cl ] ). Here, we introduce the molecular mechanism by which flavonoids, specifically quercetin, act through elevation of [Cl ] via activation of NKCC1 on important factors controlling various body and cellular functions, such as (1) antihypertensive actions controlling blood volume dependent on the amounts of renal Na reabsorption via expression of the epithelial Na channel, (2) neurite-elongating actions via polymerization of tubulin by inhibiting GTPase activity, and (3) antibacterial and antiviral infective actions through stimulation of epithelial Cl secretion by increasing the driving force for epithelial Cl secretion.
[Mh] Termos MeSH primário: Flavonoides/metabolismo
Transporte de Íons/efeitos dos fármacos
Quercetina/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/biossíntese
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/metabolismo
Anti-Hipertensivos/uso terapêutico
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Flavonoides/uso terapêutico
Seres Humanos
Neuritos/efeitos dos fármacos
Potássio/metabolismo
Quercetina/uso terapêutico
Sódio/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Flavonoids); 0 (SLC12A2 protein, human); 0 (Solute Carrier Family 12, Member 2); 9IKM0I5T1E (Quercetin); 9NEZ333N27 (Sodium); RWP5GA015D (Potassium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13361


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[PMID]:28258579
[Au] Autor:Huang B; Wang H; Yang B
[Ad] Endereço:Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
[Ti] Título:Water Transport Mediated by Other Membrane Proteins.
[So] Source:Adv Exp Med Biol;969:251-261, 2017.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Water transport through membrane is so intricate that there are still some debates. (Aquaporins) AQPs are entirely accepted to allow water transmembrane movement depending on osmotic gradient. Cotransporters and uniporters , however, are also concerned in water homeotatsis. Urea transporter B (UT-B) has a single-channel water permeability that is similar to AQP1. Cystic fibrosis transmembrane conductance regulator (CFTR ) was initially thought as a water channel but now not believed to transport water directly. By cotranporters, water is transported by water osmosis coupling with substrates, which explains how water is transported across the isolated small intestine. This chapter provides information about water transport mediated by other membrane proteins except AQPs .
[Mh] Termos MeSH primário: Células Eucarióticas/metabolismo
Transportador 1 de Aminoácido Excitatório/metabolismo
Transportadores de Ácidos Monocarboxílicos/metabolismo
Simportadores/metabolismo
Água/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Transportadores de Ácidos Dicarboxílicos/genética
Transportadores de Ácidos Dicarboxílicos/metabolismo
Células Eucarióticas/citologia
Transportador 1 de Aminoácido Excitatório/genética
Regulação da Expressão Gênica
Seres Humanos
Proteínas de Membrana Transportadoras/genética
Proteínas de Membrana Transportadoras/metabolismo
Transportadores de Ácidos Monocarboxílicos/genética
Transportadores de Ânions Orgânicos Dependentes de Sódio/genética
Transportadores de Ânions Orgânicos Dependentes de Sódio/metabolismo
Concentração Osmolar
Transportador 1 de Glucose-Sódio/genética
Transportador 1 de Glucose-Sódio/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/genética
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
Simportadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CFTR protein, human); 0 (Dicarboxylic Acid Transporters); 0 (Excitatory Amino Acid Transporter 1); 0 (Membrane Transport Proteins); 0 (Monocarboxylic Acid Transporters); 0 (Organic Anion Transporters, Sodium-Dependent); 0 (SLC12A7 protein, human); 0 (SLC13A2 protein, human); 0 (SLC1A3 protein, human); 0 (SLC5A1 protein, human); 0 (Sodium-Glucose Transporter 1); 0 (Solute Carrier Family 12, Member 2); 0 (Symporters); 0 (monocarboxylate transport protein 1); 0 (urea transporter); 059QF0KO0R (Water); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170305
[St] Status:MEDLINE
[do] DOI:10.1007/978-94-024-1057-0_17


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[PMID]:28158484
[Au] Autor:Miceli S; Nadif Kasri N; Joosten J; Huang C; Kepser L; Proville R; Selten MM; van Eijs F; Azarfar A; Homberg JR; Celikel T; Schubert D
[Ad] Endereço:Department of Cognitive Neuroscience, Radboudumc, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands.
[Ti] Título:Reduced Inhibition within Layer IV of Sert Knockout Rat Barrel Cortex is Associated with Faster Sensory Integration.
[So] Source:Cereb Cortex;27(2):933-949, 2017 Feb 01.
[Is] ISSN:1460-2199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neural activity is essential for the maturation of sensory systems. In the rodent primary somatosensory cortex (S1), high extracellular serotonin (5-HT) levels during development impair neural transmission between the thalamus and cortical input layer IV (LIV). Rodent models of impaired 5-HT transporter (SERT) function show disruption in their topological organization of S1 and in the expression of activity-regulated genes essential for inhibitory cortical network formation. It remains unclear how such alterations affect the sensory information processing within cortical LIV. Using serotonin transporter knockout (Sert-/-) rats, we demonstrate that high extracellular serotonin levels are associated with impaired feedforward inhibition (FFI), fewer perisomatic inhibitory synapses, a depolarized GABA reversal potential and reduced expression of KCC2 transporters in juvenile animals. At the neural population level, reduced FFI increases the excitatory drive originating from LIV, facilitating evoked representations in the supragranular layers II/III. The behavioral consequence of these changes in network excitability is faster integration of the sensory information during whisker-based tactile navigation, as Sert-/- rats require fewer whisker contacts with tactile targets and perform object localization with faster reaction times. These results highlight the association of serotonergic homeostasis with formation and excitability of sensory cortical networks, and consequently with sensory perception.
[Mh] Termos MeSH primário: Inibição Neural/fisiologia
Proteínas de Ligação a RNA/metabolismo
Córtex Somatossensorial/fisiologia
Navegação Espacial/fisiologia
Percepção do Tato/fisiologia
Vibrissas/fisiologia
[Mh] Termos MeSH secundário: Animais
Espaço Extracelular/metabolismo
Masculino
Potenciais da Membrana/fisiologia
Neurônios/patologia
Neurônios/fisiologia
Proteínas de Ligação a RNA/genética
Ratos Transgênicos
Ratos Wistar
Tempo de Reação/fisiologia
Serotonina/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
Córtex Somatossensorial/patologia
Simportadores/metabolismo
Técnicas de Cultura de Tecidos
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA-Binding Proteins); 0 (SERT protein, rat); 0 (Slc12a2 protein, rat); 0 (Solute Carrier Family 12, Member 2); 0 (Symporters); 0 (potassium-chloride symporters); 333DO1RDJY (Serotonin); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1093/cercor/bhx016


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[PMID]:28146071
[Au] Autor:Marunaka Y; Marunaka R; Sun H; Yamamoto T; Kanamura N; Inui T; Taruno A
[Ad] Endereço:Department of Molecular Cell Physiology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. marunaka@koto.kpu-m.ac.jp.
[Ti] Título:Actions of Quercetin, a Polyphenol, on Blood Pressure.
[So] Source:Molecules;22(2), 2017 Jan 29.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Disorder of blood pressure control causes serious diseases in the cardiovascular system. This review focuses on the anti-hypertensive action of quercetin, a flavonoid, which is one of the polyphenols characterized as the compounds containing large multiples of phenol structural units, by varying the values of various blood pressure regulatory factors, such as vascular compliance, peripheral vascular resistance, and total blood volume via anti-inflammatory and anti-oxidant actions. In addition to the anti-inflammatory and anti-oxidant actions of quercetin, we especially describe a novel mechanism of quercetin's action on the cytosolic Cl concentration ([Cl ] ) and novel roles of the cytosolic Cl i.e.: (1) quercetin elevates [Cl ] by activating Na⁺-K⁺-2Cl cotransporter 1 (NKCC1) in renal epithelial cells contributing to Na⁺ reabsorption via the epithelial Na⁺ channel (ENaC); (2) the quercetin-induced elevation of [Cl ] in renal epithelial cells diminishes expression of ENaC leading to a decrease in renal Na⁺ reabsorption; and (3) this reduction of ENaC-mediated Na⁺ reabsorption in renal epithelial cells drops volume-dependent elevated blood pressure. In this review, we introduce novel, unique mechanisms of quercetin's anti-hypertensive action via activation of NKCC1 in detail.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Polifenóis/farmacologia
Quercetina/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios
Anti-Hipertensivos/química
Anti-Hipertensivos/metabolismo
Anti-Hipertensivos/uso terapêutico
Antioxidantes
Cloretos/metabolismo
Ensaios Clínicos como Assunto
Avaliação Pré-Clínica de Medicamentos
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Polifenóis/química
Polifenóis/metabolismo
Polifenóis/uso terapêutico
Quercetina/química
Quercetina/metabolismo
Quercetina/uso terapêutico
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antihypertensive Agents); 0 (Antioxidants); 0 (Chlorides); 0 (Epithelial Sodium Channels); 0 (Polyphenols); 0 (Solute Carrier Family 12, Member 2); 9IKM0I5T1E (Quercetin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE


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[PMID]:28110691
[Au] Autor:Bou Khalil R
[Ad] Endereço:Hotel Dieu de France, Beirut, Lebanon; Saint Joseph University, Beirut, Lebanon. Electronic address: ramiboukhalil@hotmail.com.
[Ti] Título:Is insulin growth factor-1 the future for treating autism spectrum disorder and/or schizophrenia?
[So] Source:Med Hypotheses;99:23-25, 2017 Feb.
[Is] ISSN:1532-2777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To date, no curative psychopharmacologic treatment exists for the core symptoms of autism spectrum disorder (ASD) as well as for schizophrenia. Bumatenide is a specific antagonist of the first isoform of the Na-K-Cl cotransporter (NKCC1). It is usually used as a diuretic but may also promote a decrease in intraneuronal chloride ion concentration leading to hyperpolarization in neuronal membrane and subsequent decrease in neuronal hyperexcitability. This physiologic effect has been considered to be behind the relative efficacy of bumetanide in improving symptoms of ASD and, to a lesser extent, schizophrenia. However, insulin growth factor-1 (IGF-1) shows the same physiologic effect. In addition, it may improve brain network dysconnectivity which is known to be an important neurobiological feature in ASD and schizophrenia. IGF-1 has started to prove its efficacy in improving symptoms of children with Rett syndrome, a genetic disorder that shares several clinical similarities with ASD. IGF-1 may also improve oxytocin secretion through the enhancement of the transient potential receptor V2 channel function. Accordingly, IGF-1 should be studied as a potential treatment of ASD and other mental disorders characterized with brain dysconnectivity such as schizophrenia.
[Mh] Termos MeSH primário: Transtorno do Espectro Autista/terapia
Fator de Crescimento Insulin-Like I/metabolismo
Fator de Crescimento Insulin-Like I/uso terapêutico
Esquizofrenia/terapia
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
[Mh] Termos MeSH secundário: Animais
Transtorno do Espectro Autista/complicações
Encéfalo/patologia
Bumetanida/uso terapêutico
Criança
Pré-Escolar
Cloretos/metabolismo
Endocanabinoides/metabolismo
Seres Humanos
Modelos Teóricos
Bainha de Mielina/química
Neurônios/metabolismo
Oligodendroglia/metabolismo
Ocitocina/metabolismo
Transtornos Psicóticos/complicações
Síndrome de Rett/tratamento farmacológico
Esquizofrenia/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Endocannabinoids); 0 (IGF1 protein, human); 0 (SLC12A2 protein, human); 0 (Solute Carrier Family 12, Member 2); 0Y2S3XUQ5H (Bumetanide); 50-56-6 (Oxytocin); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE


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[PMID]:28087701
[Au] Autor:Jiang C; Kawabe H; Rotin D
[Ad] Endereço:From The Hospital for Sick Children and University of Toronto, Toronto, Ontario M5G 0A4, Canada and.
[Ti] Título:The Ubiquitin Ligase Nedd4L Regulates the Na/K/2Cl Co-transporter NKCC1/SLC12A2 in the Colon.
[So] Source:J Biol Chem;292(8):3137-3145, 2017 Feb 24.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ubiquitin ligase Nedd4-like (Nedd4L, or Nedd4-2) binds to and regulates stability of the epithelial Na channel (ENaC) in salt-absorbing epithelia in the kidney, lung, and other tissues. Its role in the distal colon, which also absorbs salt and fluid and expresses ENaC, is unknown. Using a conditional knock-out approach to knock out in mice intestinal epithelium ( ; ) we show here that depletion leads to a higher steady-state short circuit current (Isc) in mouse distal colon tissue relative to controls. This higher Isc was partially reduced by the addition of apical amiloride and strongly reduced by basolateral bumetanide as well as by depletion of basolateral Cl , suggesting that Na /K /2Cl (NKCC1/SLC12A2) co-transporter and ENaC are targets of Nedd4L in the colon. In accordance, NKCC1 (and γENaC) protein abundance in the colon of the Nedd4L knock-out animals was increased, indicating that Nedd4L normally suppresses these proteins. However, we did not observe co-immunoprecipitation between Nedd4L and NKCC1, suggesting that Nedd4L indirectly suppresses NKCC1 expression. Low salt diet resulted in a strong increase in ß and γ (but not α) ENaC mRNA and protein expression and ENaC activity. Although salt restriction also increased NKCC1 protein and mRNA abundance, it did not lead to its elevated activity (Isc). These results identify NKCC1 as a novel target for Nedd4L-mediated down-regulation , which modulates ion and fluid transport in the distal colon together with ENaC.
[Mh] Termos MeSH primário: Colo/metabolismo
Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Canais Epiteliais de Sódio/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Cloretos/metabolismo
Complexos Endossomais de Distribuição Requeridos para Transporte/genética
Canais Epiteliais de Sódio/genética
Células HEK293
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ubiquitina-Proteína Ligases Nedd4
Potássio/metabolismo
Sais/metabolismo
Transdução de Sinais
Sódio/metabolismo
Membro 2 da Família 12 de Carreador de Soluto/genética
Ubiquitina-Proteína Ligases/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Endosomal Sorting Complexes Required for Transport); 0 (Epithelial Sodium Channels); 0 (Salts); 0 (Slc12a2 protein, mouse); 0 (Solute Carrier Family 12, Member 2); 9NEZ333N27 (Sodium); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, human); EC 2.3.2.26 (Nedd4L protein, human); EC 2.3.2.26 (Nedd4l protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); RWP5GA015D (Potassium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770065


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[PMID]:28074534
[Au] Autor:Kourdougli N; Pellegrino C; Renko JM; Khirug S; Chazal G; Kukko-Lukjanov TK; Lauri SE; Gaiarsa JL; Zhou L; Peret A; Castrén E; Tuominen RK; Crépel V; Rivera C
[Ad] Endereço:Inserm Unit 901, Inmed, Marseille, France.
[Ti] Título:Depolarizing γ-aminobutyric acid contributes to glutamatergic network rewiring in epilepsy.
[So] Source:Ann Neurol;81(2):251-265, 2017 Feb.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Rewiring of excitatory glutamatergic neuronal circuits is a major abnormality in epilepsy. Besides the rewiring of excitatory circuits, an abnormal depolarizing γ-aminobutyric acidergic (GABAergic) drive has been hypothesized to participate in the epileptogenic processes. However, a remaining clinically relevant question is whether early post-status epilepticus (SE) evoked chloride dysregulation is important for the remodeling of aberrant glutamatergic neuronal circuits. METHODS: Osmotic minipumps were used to infuse intracerebrally a specific inhibitor of depolarizing GABAergic transmission as well as a functionally blocking antibody toward the pan-neurotrophin receptor p75 (p75 ). The compounds were infused between 2 and 5 days after pilocarpine-induced SE. Immunohistochemistry for NKCC1, KCC2, and ectopic recurrent mossy fiber (rMF) sprouting as well as telemetric electroencephalographic and electrophysiological recordings were performed at day 5 and 2 months post-SE. RESULTS: Blockade of NKCC1 after SE with the specific inhibitor bumetanide restored NKCC1 and KCC2 expression, normalized chloride homeostasis, and significantly reduced the glutamatergic rMF sprouting within the dentate gyrus. This mechanism partially involves p75 signaling, as bumetanide application reduced SE-induced p75 expression and functional blockade of p75 decreased rMF sprouting. The early transient (3 days) post-SE infusion of bumetanide reduced rMF sprouting and recurrent seizures in the chronic epileptic phase. INTERPRETATION: Our findings show that early post-SE abnormal depolarizing GABA and p75 signaling fosters a long-lasting rearrangement of glutamatergic network that contributes to the epileptogenic process. This finding defines promising and novel targets to constrain reactive glutamatergic network rewiring in adult epilepsy. Ann Neurol 2017;81:251-265.
[Mh] Termos MeSH primário: Bumetanida/farmacologia
Fibras Musgosas Hipocampais/efeitos dos fármacos
Receptores de Fator de Crescimento Neural/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Membro 2 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Estado Epiléptico/metabolismo
Simportadores/efeitos dos fármacos
Ácido gama-Aminobutírico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Bumetanida/administração & dosagem
Masculino
Ratos
Ratos Wistar
Inibidores de Simportadores de Cloreto de Sódio e Potássio/administração & dosagem
Estado Epiléptico/tratamento farmacológico
Estado Epiléptico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Nerve Growth Factor); 0 (Slc12a2 protein, rat); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 2); 0 (Symporters); 0 (TNFRSF16 protein, rat); 0 (potassium-chloride symporters); 0Y2S3XUQ5H (Bumetanide); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24870



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