Base de dados : MEDLINE
Pesquisa : G03.197 [Categoria DeCS]
Referências encontradas : 4228 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 423 ir para página                         

  1 / 4228 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28463418
[Au] Autor:Liu C; Sekine S; Song B; Ito K
[Ad] Endereço:Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
[Ti] Título:Use of Primary Rat Hepatocytes for Prediction of Drug-Induced Mitochondrial Dysfunction.
[So] Source:Curr Protoc Toxicol;72:14.16.1-14.16.10, 2017 May 02.
[Is] ISSN:1934-9262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction plays a central role in drug-induced liver injury. To evaluate drug-induced mitochondrial impairment, several isolated mitochondria- or cell line-based assays have been reported. Among them, culturing HepG2 cells in galactose provides a remarkable method to assess mitochondrial toxicity by activating mitochondrial aerobic respiration. We applied this assay to primary rat hepatocytes by culturing cells in galactose and hyperoxia to enhance the evaluation of metabolism-related drug-induced mitochondrial toxicity. Conventional culture of primary hepatocytes under high-glucose and hypoxic conditions could force cells to switch energy generation to glycolysis. By contrast, cells cultured in galactose and hyperoxia could maintain energy generation from mitochondrial aerobic respiration, which is consistent with physiological conditions, and consequently improve the susceptibility of cells to mitochondrial toxicants. Measuring the toxicities of test compounds in primary rat hepatocytes cultured in modified conditions provides a useful model to identify mitochondrial dysfunction-mediated drug-induced hepatotoxicity. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Hepatócitos/efeitos dos fármacos
Doenças Mitocondriais/induzido quimicamente
Doenças Mitocondriais/patologia
[Mh] Termos MeSH secundário: Animais
Respiração Celular
Doença Hepática Induzida por Substâncias e Drogas
Meios de Cultura
Metabolismo Energético
Previsões
Galactose/metabolismo
Hepatócitos/enzimologia
Hiperóxia/metabolismo
L-Lactato Desidrogenase/análise
Consumo de Oxigênio
Cultura Primária de Células
Ratos
Ratos Sprague-Dawley
Testes de Toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); EC 1.1.1.27 (L-Lactate Dehydrogenase); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cptx.24


  2 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29478660
[Au] Autor:Li X; Huang Y; Liu HW; Wu C; Bi W; Yuan Y; Liu X
[Ad] Endereço:School of Environmental Science and Engineering, Suzhou University of Science and Technology, Suzhou 215009, China.
[Ti] Título:Simultaneous Fe(III) reduction and ammonia oxidation process in Anammox sludge.
[So] Source:J Environ Sci (China);64:42-50, 2018 Feb.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In recent years, there have been a number of reports on the phenomenon in which ferric iron (Fe(III)) is reduced to ferrous iron [Fe(II)] in anaerobic environments, accompanied by simultaneous oxidation of ammonia to NO , NO , or N However, studies on the relevant reaction characteristics and mechanisms are rare. Recently, in research on the effect of Fe(III) on the activity of Anammox sludge, excess ammonia oxidization has also been found. Hence, in the present study, Fe(III) was used to serve as the electron acceptor instead of NO , and the feasibility and characteristics of Anammox coupled to Fe(III) reduction (termed Feammox) were investigated. After 160days of cultivation, the conversion rate of ammonia in the reactor was above 80%, accompanied by the production of a large amount of NO and a small amount of NO . The total nitrogen removal rate was up to 71.8%. Furthermore, quantities of Fe(II) were detected in the sludge fluorescence in situ hybridization (FISH) and denaturated gradient gel electrophoresis (DGGE) analyses further revealed that in the sludge, some Anammox bacteria were retained, and some microbes were enriched during the acclimatization process. We thus deduced that in Anammox sludge, Fe(III) reduction takes place together with ammonia oxidation to NO and NO along with the Anammox process.
[Mh] Termos MeSH primário: Amônia/química
Ferro/química
Esgotos/microbiologia
[Mh] Termos MeSH secundário: Aclimatação
Amônia/metabolismo
Respiração Celular
Crescimento Quimioautotrófico
Eletroforese em Gel de Gradiente Desnaturante
Meio Ambiente
Compostos Férricos
Hibridização in Situ Fluorescente
Ferro/metabolismo
Nitrogênio
Oxidantes
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ferric Compounds); 0 (Oxidants); 0 (Sewage); 7664-41-7 (Ammonia); E1UOL152H7 (Iron); N762921K75 (Nitrogen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE


  3 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28470519
[Au] Autor:Smolina N; Bruton J; Kostareva A; Sejersen T
[Ad] Endereço:Karolinska Institutet, Stockholm, Sweden. natalia.smolina@ki.se.
[Ti] Título:Assaying Mitochondrial Respiration as an Indicator of Cellular Metabolism and Fitness.
[So] Source:Methods Mol Biol;1601:79-87, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial respiration is the most important generator of cellular energy under most circumstances. It is a process of energy conversion of substrates into ATP. The Seahorse equipment allows measuring oxygen consumption rate (OCR) in living cells and estimates key parameters of mitochondrial respiration in real-time mode. Through use of mitochondrial inhibitors, four key mitochondrial respiration parameters can be measured: basal, ATP production-linked, maximal, and proton leak-linked OCR. This approach requires application of mitochondrial inhibitors-oligomycin to block ATP synthase, FCCP-to make the inner mitochondrial membrane permeable for protons and allow maximum electron flux through the electron transport chain, and rotenone and antimycin A-to inhibit complexes I and III, respectively. This chapter describes the protocol of OCR assessment in the culture of primary myotubes obtained upon satellite cell fusion.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Bioensaio/instrumentação
Mitocôndrias/metabolismo
Fosforilação Oxidativa
Consumo de Oxigênio
[Mh] Termos MeSH secundário: Animais
Antimicina A/farmacologia
Carbonil Cianeto p-Trifluormetoxifenil Hidrazona/farmacologia
Respiração Celular
Sobrevivência Celular
Complexo I de Transporte de Elétrons/antagonistas & inibidores
Complexo III da Cadeia de Transporte de Elétrons/antagonistas & inibidores
Camundongos
Mitocôndrias/efeitos dos fármacos
Fibras Musculares Esqueléticas/efeitos dos fármacos
Fibras Musculares Esqueléticas/metabolismo
Oligomicinas/farmacologia
Cultura Primária de Células
Ionóforos de Próton/farmacologia
Rotenona/farmacologia
Células Satélites de Músculo Esquelético/efeitos dos fármacos
Células Satélites de Músculo Esquelético/metabolismo
Desacopladores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligomycins); 0 (Proton Ionophores); 0 (Uncoupling Agents); 03L9OT429T (Rotenone); 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone); 642-15-9 (Antimycin A); 8L70Q75FXE (Adenosine Triphosphate); EC 1.10.2.2 (Electron Transport Complex III); EC 1.6.5.3 (Electron Transport Complex I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_7


  4 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28456637
[Au] Autor:Vienne JC; Cimetta C; Dubois M; Duburcq T; Favory R; Dessein AF; Fontaine M; Joncquel-Chevalier Curt M; Cuisset JM; Douillard C; Mention-Mulliez K; Dobbelaere D; Vamecq J
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Laboratory of Hormonology, Metabolism-Nutrition & Oncology (HMNO), Center of Biology and Pathology (CBP) Pierre-Marie Degand, CHRU Lille, France.
[Ti] Título:A fast method for high resolution oxymetry study of skeletal muscle mitochondrial respiratory chain complexes.
[So] Source:Anal Biochem;528:57-62, 2017 07 01.
[Is] ISSN:1096-0309
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High resolution oxymetry study (HROS) of skeletal muscle usually requires 90-120 min preparative phase (dissection, permeabilization and washing). This work reports on the suitability of a rapid muscle preparation which by-passes this long preparation. For a few seconds only, muscle biopsy from pigs is submitted to gentle homogenization at 8000 rotations per minute using an ultra-dispersor apparatus. Subsequent HROS is performed using FCCP instead of ADP, compounds crossing and not plasma membrane, respectively. This simplified procedure compares favorably with classical (permeabilized fibers) HROS in terms of respiratory chain complex activities. Mitochondria from cells undergoing ultradispersion were functionally preserved as attested by relative inefficacy of added cytochrome C (not crossing intact mitochondrial outer membrane) to stimulate mitochondrial respiration. Responsiveness of respiration to ADP (in the absence of FCCP) suggested that these intact mitochondria were outside cells disrupted by ultradispersion or within cells permeated by this procedure.
[Mh] Termos MeSH primário: Respiração Celular
Mitocôndrias Musculares/metabolismo
Músculo Esquelético/metabolismo
Consumo de Oxigênio
[Mh] Termos MeSH secundário: Animais
Biópsia
Transporte de Elétrons
Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo
Feminino
Membranas Mitocondriais/metabolismo
Fibras Musculares Esqueléticas/metabolismo
Permeabilidade
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Electron Transport Chain Complex Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  5 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28943350
[Au] Autor:Chen J; Wang PF; Wang C; Liu JJ; Gao H; Wang X
[Ad] Endereço:Key Laboratory of Integrated Regulation and Resource Department on Shallow Lakes, Ministry of Education, Hohai University, 1 Xikang Road, Nanjing 210098, PR China; College of Environment, Hohai University, 1 Xikang Road, Nanjing 210098, PR China; The State Key Laboratory of Lake Science and Environm
[Ti] Título:Spatial distribution and diversity of organohalide-respiring bacteria and their relationships with polybrominated diphenyl ether concentration in Taihu Lake sediments.
[So] Source:Environ Pollut;232:200-211, 2018 Jan.
[Is] ISSN:1873-6424
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It is acknowledged that organohalide-respiring bacteria (OHRB) can degrade polybrominated diphenyl ethers (PBDEs); however, very little is known about the distribution of OHRB or their response to PBDE contamination in natural sediments. We collected sediments from 28 sampling sites in Taihu Lake, China, and investigated the spatial distribution and diversity of OHRB, and the relationships between the PBDE contamination levels and the PBDE removal potential. The abundances of five typical OHRB genera, namely Dehalobacter, Dehalococcoides, Dehalogenimonas, Desulfitobacterium, and Geobacter, ranged from 0.34 × 10 to 19.4 × 10 gene copies g dry sediment, and varied significantly among different areas of Taihu Lake. OHRB were more abundant in sediments from Meiliang and Zhushan Bay, where the PBDE concentrations were higher, and the phylotype diversity of the OHRB belonging to the family Dehalococcoidaceae was lower, than reported for other areas. While the sulfate concentrations explained much of the spatial distribution of OHRB, PBDE concentrations were also a strong influence on the abundance and diversity of OHRB in the sediments. For Dehalococcoides, Dehalogenimonas and Geobacter, the abundance of each genus was positively related to its own potential to remove PBDEs. The dominant OHRB genus, Dehalogenimonas, may contribute most to in situ bioremediation of PBDEs in Taihu Lake.
[Mh] Termos MeSH primário: Biodegradação Ambiental
Monitoramento Ambiental
Éteres Difenil Halogenados/análise
Lagos/microbiologia
Poluentes Químicos da Água/análise
[Mh] Termos MeSH secundário: Bactérias
Respiração Celular
China
Chloroflexi/genética
Desulfitobacterium/genética
Sedimentos Geológicos
Éteres Difenil Halogenados/metabolismo
Lagos/química
Poluentes Químicos da Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Halogenated Diphenyl Ethers); 0 (Water Pollutants, Chemical)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


  6 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29261744
[Au] Autor:Skowronski AA; Ravussin Y; Leibel RL; LeDuc CA
[Ad] Endereço:Institute of Human Nutrition, Columbia University, New York City, New York, United States of America.
[Ti] Título:Energy homeostasis in leptin deficient Lepob/ob mice.
[So] Source:PLoS One;12(12):e0189784, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Maintenance of reduced body weight is associated both with reduced energy expenditure per unit metabolic mass and increased hunger in mice and humans. Lowered circulating leptin concentration, due to decreased fat mass, provides a primary signal for this response. However, leptin deficient (Lepob/ob) mice (and leptin receptor deficient Zucker rats) reduce energy expenditure following weight reduction by a necessarily non-leptin dependent mechanisms. To identify these mechanisms, Lepob/ob mice were fed ad libitum (AL group; n = 21) or restricted to 3 kilocalories of chow per day (CR group, n = 21). After losing 20% of initial weight (in approximately 2 weeks), the CR mice were stabilized at 80% of initial body weight for two weeks by titrated refeeding, and then released from food restriction. CR mice conserved energy (-17% below predicted based on body mass and composition during the day; -52% at night); and, when released to ad libitum feeding, CR mice regained fat and lean mass (to AL levels) within 5 weeks. CR mice did so while their ad libitum caloric intake was equal to that of the AL animals. While calorically restricted, the CR mice had a significantly lower respiratory exchange ratio (RER = 0.89) compared to AL (0.94); after release to ad libitum feeding, RER was significantly higher (1.03) than in the AL group (0.93), consistent with their anabolic state. These results confirm that, in congenitally leptin deficient animals, leptin is not required for compensatory reduction in energy expenditure accompanying weight loss, but suggest that the hyperphagia of the weight-reduced state is leptin-dependent.
[Mh] Termos MeSH primário: Metabolismo Energético
Homeostase
Leptina/deficiência
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Composição Corporal
Temperatura Corporal
Peso Corporal
Restrição Calórica
Respiração Celular
Comportamento Alimentar
Insulina/sangue
Leptina/metabolismo
Masculino
Camundongos
Camundongos Obesos
Projetos Piloto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Leptin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189784


  7 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28452426
[Au] Autor:Chen B; Ma R; Ding D; Wei L; Kang L
[Ad] Endereço:State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
[Ti] Título:Aerobic respiration by haemocyanin in the embryo of the migratory locust.
[So] Source:Insect Mol Biol;26(4):461-468, 2017 08.
[Is] ISSN:1365-2583
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It remains unresolved how insect embryos acquire sufficient oxygen to sustain high rates of respiratory metabolism during embryogenesis in the absence of a fully developed tracheal system. Our previous work showed that the two distinct subunits (Hc1 and Hc2) of haemocyanin (Hc), a copper-containing protein, display embryo-specific high expression that is essential for embryonic development and survival in the migratory locust Locusta migratoria. Here we investigated the role of haemocyanins in oxygen sensing and supply in the embryo of this locust. Putative binding sites for hypoxia-regulated transcription factors were identified in the promoter region of all of the Hc1 and Hc2 genes. Embryonic expression of haemocyanins was highly upregulated by ambient O deprivation, up to 10-fold at 13% O content. The degree of upregulation of haemocyanins increased with increasing levels of hypoxia. Compared with low-altitude locusts, embryonic expression of haemocyanins in high-altitude locusts from Tibetan plateau was constitutively higher and more robust to oxygen deprivation. These findings strongly suggest an active involvement of haemocyanins in oxygen exchange in embryos. We thus propose a mechanistic model for embryo respiration in which haemocyanin plays a key role by complementing the tracheal system for oxygen transport during embryogenesis.
[Mh] Termos MeSH primário: Hemocianinas/metabolismo
Locusta migratoria/embriologia
[Mh] Termos MeSH secundário: Animais
Respiração Celular
Embrião não Mamífero/metabolismo
Regulação da Expressão Gênica
Hipóxia/metabolismo
Locusta migratoria/metabolismo
Oxigênio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9013-72-3 (Hemocyanins); S88TT14065 (Oxygen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/imb.12310


  8 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29176872
[Au] Autor:Scrima R; Menga M; Pacelli C; Agriesti F; Cela O; Piccoli C; Cotoia A; De Gregorio A; Gefter JV; Cinnella G; Capitanio N
[Ad] Endereço:Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.
[Ti] Título:Para-hydroxyphenylpyruvate inhibits the pro-inflammatory stimulation of macrophage preventing LPS-mediated nitro-oxidative unbalance and immunometabolic shift.
[So] Source:PLoS One;12(11):e0188683, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Targeting metabolism is emerging as a promising therapeutic strategy for modulation of the immune response in human diseases. In the presented study we used the lipopolysaccharide (LPS)-mediated activation of RAW 264.7 macrophage-like cell line as a model to investigate changes in the metabolic phenotype and to test the effect of p-hydroxyphenylpyruvate (pHPP) on it. pHPP is an intermediate of the PHE/TYR catabolic pathway, selected as analogue of the ethyl pyruvate (EP), which proved to exhibit antioxidant and anti-inflammatory activities. The results obtained show that LPS-priming of RAW 264.7 cell line to the activated M1 state resulted in up-regulation of the inducible nitric oxide synthase (iNOS) expression and consequently of NO production and in release of the pro-inflammatory cytokine IL-6. All these effects were prevented dose dependently by mM concentrations of pHPP more efficiently than EP. Respirometric and metabolic flux analysis of LPS-treated RAW 264.7 cells unveiled a marked metabolic shift consisting in downregulation of the mitochondrial oxidative phosphorylation and upregulation of aerobic glycolysis respectively. The observed respiratory failure in LPS-treated cells was accompanied with inhibition of the respiratory chain complexes I and IV and enhanced production of reactive oxygen species. Inhibition of the respiratory activity was also observed following incubation of human neonatal fibroblasts (NHDF-neo) with sera from septic patients. pHPP prevented all the observed metabolic alteration caused by LPS on RAW 264.7 or by septic sera on NHDF-neo. Moreover, we provide evidence that pHPP is an efficient reductant of cytochrome c. On the basis of the presented results a working model, linking pathogen-associated molecular patterns (PAMPs)-mediated immune response to mitochondrial oxidative metabolism, is put forward along with suggestions for its therapeutic control.
[Mh] Termos MeSH primário: Inflamação/imunologia
Inflamação/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/imunologia
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Respiração Celular/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Inflamação/patologia
Interleucina-6/metabolismo
Macrófagos/efeitos dos fármacos
Análise do Fluxo Metabólico
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Modelos Biológicos
Nitratos/metabolismo
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo II/metabolismo
Nitritos/metabolismo
Nitrosação
Oxirredução
Peróxidos/metabolismo
Ácidos Fenilpirúvicos/química
Ácidos Fenilpirúvicos/farmacologia
Piruvatos/química
Piruvatos/farmacologia
Células RAW 264.7
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Nitrates); 0 (Nitrites); 0 (Peroxides); 0 (Phenylpyruvic Acids); 0 (Pyruvates); 03O98E01OB (ethyl pyruvate); 156-39-8 (4-hydroxyphenylpyruvic acid); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188683


  9 / 4228 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28991266
[Au] Autor:Marjanovic MP; Hurtado-Bagès S; Lassi M; Valero V; Malinverni R; Delage H; Navarro M; Corujo D; Guberovic I; Douet J; Gama-Perez P; Garcia-Roves PM; Ahel I; Ladurner AG; Yanes O; Bouvet P; Suelves M; Teperino R; Pospisilik JA; Buschbeck M
[Ad] Endereço:Programme of Predictive and Personalized Medicine of Cancer, Germans Trias i Pujol Research Institute (PMPPC-IGTP), Badalona, Spain.
[Ti] Título:MacroH2A1.1 regulates mitochondrial respiration by limiting nuclear NAD consumption.
[So] Source:Nat Struct Mol Biol;24(11):902-910, 2017 Nov.
[Is] ISSN:1545-9985
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Histone variants are structural components of eukaryotic chromatin that can replace replication-coupled histones in the nucleosome. The histone variant macroH2A1.1 contains a macrodomain capable of binding NAD -derived metabolites. Here we report that macroH2A1.1 is rapidly induced during myogenic differentiation through a switch in alternative splicing, and that myotubes that lack macroH2A1.1 have a defect in mitochondrial respiratory capacity. We found that the metabolite-binding macrodomain was essential for sustained optimal mitochondrial function but dispensable for gene regulation. Through direct binding, macroH2A1.1 inhibits basal poly-ADP ribose polymerase 1 (PARP-1) activity and thus reduces nuclear NAD consumption. The resultant accumulation of the NAD precursor NMN allows for maintenance of mitochondrial NAD pools that are critical for respiration. Our data indicate that macroH2A1.1-containing chromatin regulates mitochondrial respiration by limiting nuclear NAD consumption and establishing a buffer of NAD precursors in differentiated cells.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Respiração Celular
Regulação da Expressão Gênica no Desenvolvimento
Histonas/metabolismo
Mitocôndrias/metabolismo
Desenvolvimento Muscular
NAD/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 0 (macroH2A histone); 0U46U6E8UK (NAD)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE
[do] DOI:10.1038/nsmb.3481


  10 / 4228 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28957663
[Au] Autor:Zhao N; Liu CC; Van Ingelgom AJ; Martens YA; Linares C; Knight JA; Painter MM; Sullivan PM; Bu G
[Ad] Endereço:Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
[Ti] Título:Apolipoprotein E4 Impairs Neuronal Insulin Signaling by Trapping Insulin Receptor in the Endosomes.
[So] Source:Neuron;96(1):115-129.e5, 2017 Sep 27.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes and impaired brain insulin signaling are linked to the pathogenesis of Alzheimer's disease (AD). The association between diabetes and AD-associated amyloid pathology is stronger among carriers of the apolipoprotein E (APOE) ε4 gene allele, the strongest genetic risk factor for late-onset AD. Here we report that apoE4 impairs neuronal insulin signaling in human apoE-targeted replacement (TR) mice in an age-dependent manner. High-fat diet (HFD) accelerates these effects in apoE4-TR mice at middle age. In primary neurons, apoE4 interacts with insulin receptor and impairs its trafficking by trapping it in the endosomes, leading to impaired insulin signaling and insulin-stimulated mitochondrial respiration and glycolysis. In aging brains, the increased apoE4 aggregation and compromised endosomal function further exacerbate the inhibitory effects of apoE4 on insulin signaling and related functions. Together, our study provides novel mechanistic insights into the pathogenic mechanisms of apoE4 and insulin resistance in AD.
[Mh] Termos MeSH primário: Apolipoproteína E4/metabolismo
Endossomos/metabolismo
Resistência à Insulina/fisiologia
Insulina/fisiologia
Neurônios/citologia
Neurônios/metabolismo
Receptor de Insulina/metabolismo
[Mh] Termos MeSH secundário: Envelhecimento/metabolismo
Envelhecimento/fisiologia
Animais
Apolipoproteína E3/genética
Apolipoproteína E4/genética
Respiração Celular/fisiologia
Dieta Hiperlipídica
Feminino
Glicólise/fisiologia
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Mitocôndrias/fisiologia
Neurônios/fisiologia
Cultura Primária de Células
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoprotein E3); 0 (Apolipoprotein E4); 0 (Insulin); EC 2.7.10.1 (Receptor, Insulin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE



página 1 de 423 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde