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Pesquisa : D03.633.100.759.758.824.751.500 [Categoria DeCS]
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  1 / 5018 MEDLINE  
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[PMID]:28938466
[Au] Autor:Chimerel C; Riccio C; Murison K; Gribble FM; Reimann F
[Ad] Endereço:Metabolic Research Laboratories and Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
[Ti] Título:Optogenetic Analysis of Depolarization-Dependent Glucagonlike Peptide-1 Release.
[So] Source:Endocrinology;158(10):3426-3434, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incretin hormones play an important role in the regulation of food intake and glucose homeostasis. Glucagonlike peptide-1 (GLP-1)-secreting cells have been demonstrated to be electrically excitable and to fire action potentials (APs) with increased frequency in response to nutrient exposure. However, nutrients can also be metabolized or activate G-protein-coupled receptors, thus potentially stimulating GLP-1 secretion independent of their effects on the plasma membrane potential. Here we used channelrhodopsins to manipulate the membrane potential of GLUTag cells, a well-established model of GLP-1-secreting enteroendocrine L cells. Using channelrhodopsins with fast or slow on/off kinetics (CheTA and SSFO, respectively), we found that trains of light pulses could trigger APs and calcium elevation in GLUTag cells stably expressing either CheTA or SSFO. Tetrodotoxin reduced light-triggered AP frequency but did not impair calcium responses, whereas further addition of the calcium-channel blockers nifedipine and ω-conotoxin GVIA abolished both APs and calcium transients. Light pulse trains did not trigger GLP-1 secretion from CheTA-expressing cells under basal conditions but were an effective stimulus when cyclic adenosine monophosphate (cAMP) concentrations were elevated by forskolin plus 3-isobutyl 1-methylxanthine. In SSFO-expressing cells, light-stimulated GLP-1 release was observed at resting and elevated cAMP concentrations and was blocked by nifedipine plus ω-conotoxin GVIA but not tetrodotoxin. We conclude that cAMP elevation or cumulative membrane depolarization triggered by SSFO enhances the efficiency of light-triggered action potential firing, voltage-gated calcium entry, and GLP-1 secretion.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Células Enteroendócrinas/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Animais
Cálcio/metabolismo
Colforsina/farmacologia
Células Enteroendócrinas/metabolismo
Células Enteroendócrinas/secreção
Peptídeo 1 Semelhante ao Glucagon/secreção
Camundongos
Nifedipino/farmacologia
Optogenética
Técnicas de Patch-Clamp
Inibidores de Fosfodiesterase/farmacologia
Rodopsina
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Vasodilatadores/farmacologia
ômega-Conotoxina GVIA/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Phosphodiesterase Inhibitors); 0 (Sodium Channel Blockers); 0 (Vasodilator Agents); 1F7A44V6OU (Colforsin); 4368-28-9 (Tetrodotoxin); 89750-14-1 (Glucagon-Like Peptide 1); 9009-81-8 (Rhodopsin); 92078-76-7 (omega-Conotoxin GVIA); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00434


  2 / 5018 MEDLINE  
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[PMID]:28750324
[Au] Autor:Cheng S; Jiang X; Yang B; Wen L; Zhao F; Zeng WB; Liu XJ; Dong X; Sun JY; Ming YZ; Zhu H; Rayner S; Tang Q; Fortunato E; Luo MH
[Ad] Endereço:State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.
[Ti] Título:Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency.
[So] Source:Virology;510:205-215, 2017 Oct.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T98G cells have been shown to support long-term human cytomegalovirus (HCMV) genome maintenance without infectious virus release. However, it remains unclear whether these viral genomes could be reactivated. To address this question, a recombinant HCMV (rHCMV) containing a GFP gene was used to infect T98G cells, and the infected cells absent of infectious virus production were designated T98G-LrV. Upon dibutyryl cAMP plus IBMX (cAMP/IBMX) treatment, a serial of phenomena were observed, including GFP signal increase, viral genome replication, lytic genes expression and infectious viruses release, indicating the reactivation of HCMV in T98G-LrV cells from a latent status. Mechanistically, HCMV reactivation in the T98G-LrV cells induced by cAMP/IBMX was associated with the PKA-CREB signaling pathway. These results demonstrate that HCMV was latent in T98G-LrV cells and could be reactivated. The T98G-LrV cells represent an effective model for investigating the mechanisms of HCMV reactivation from latency in the context of neural cells.
[Mh] Termos MeSH primário: Citomegalovirus/fisiologia
Ativação Viral
Latência Viral
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/metabolismo
Bucladesina/metabolismo
Linhagem Celular Tumoral
Genes Reporter
Proteínas de Fluorescência Verde/análise
Proteínas de Fluorescência Verde/genética
Seres Humanos
Coloração e Rotulagem/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
147336-22-9 (Green Fluorescent Proteins); 63X7MBT2LQ (Bucladesine); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE


  3 / 5018 MEDLINE  
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[PMID]:28689812
[Au] Autor:Hasan AU; Kittikulsuth W; Yamaguchi F; Musarrat Ansary T; Rahman A; Shibayama Y; Nakano D; Hitomi H; Tokuda M; Nishiyama A
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Kagawa University, 1750-1, Ikenobe, Kita-gun, Miki-cho, Kagawa 761-0793, Japan; Department of Pharmacology, Faculty of Medicine, International University of Health and Welfare, 4-2, Kojunomori, Narita-shi, Chiba 286-8686, Japan. Electronic address: ha
[Ti] Título:IBMX protects human proximal tubular epithelial cells from hypoxic stress through suppressing hypoxia-inducible factor-1α expression.
[So] Source:Exp Cell Res;358(2):343-351, 2017 Sep 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypoxia predisposes renal fibrosis. This study was conducted to identify novel approaches to ameliorate the pathogenic effect of hypoxia. Using human proximal tubular epithelial cells we showed that a pan-phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methylxanthine (IBMX) dose and time dependently downregulated hypoxia-inducible factor 1α (HIF-1α) mRNA expression, which was further augmented by addition of a transcriptional inhibitor, actinomycin D. IBMX also increased the cellular cyclic adenosine monophosphate (cAMP) level. Luciferase assay showed that blocking of protein kinase A (PKA) using H89 reduced, while 8-Br-cAMP agonized the repression of HIF-1α promoter activity in hypoxic condition. Deletion of cAMP response element binding sites from the HIF-1α promoter abrogated the effect of IBMX. Western blot and immunofluorescent study confirmed that the CoCl induced increased HIF-1α protein in whole cell lysate and in nucleus was reduced by the IBMX. Through this process, IBMX attenuated both CoCl and hypoxia induced mRNA expressions of two pro-fibrogenic factors, platelet-derived growth factor B and lysyl oxidase. Moreover, IBMX reduced production of a mesenchymal transformation factor, ß-catenin; as well as protected against hypoxia induced cell-death. Taken together, our study showed novel evidence that the PDE inhibitor IBMX can downregulate the transcription of HIF-1α, and thus may attenuate hypoxia induced renal fibrosis.
[Mh] Termos MeSH primário: 1-Metil-3-Isobutilxantina/farmacologia
Células Epiteliais/efeitos dos fármacos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
[Mh] Termos MeSH secundário: Hipóxia Celular/efeitos dos fármacos
Células Cultivadas
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Células Epiteliais/metabolismo
Seres Humanos
Proteínas Proto-Oncogênicas c-sis/metabolismo
Transdução de Sinais/efeitos dos fármacos
Xantinas/farmacologia
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Proto-Oncogene Proteins c-sis); 0 (Xanthines); 0 (beta Catenin); 28109-92-4 (methylxanthine); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE


  4 / 5018 MEDLINE  
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[PMID]:28536637
[Au] Autor:Pu Y; Veiga-Lopez A
[Ad] Endereço:Department of Animal Science, Michigan State University, 474 S. Shaw Lane Rm 1230 F, East Lansing, MI 48824 USA.
[Ti] Título:PPARγ agonist through the terminal differentiation phase is essential for adipogenic differentiation of fetal ovine preadipocytes.
[So] Source:Cell Mol Biol Lett;22:6, 2017.
[Is] ISSN:1689-1392
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although the 3T3-L1 preadipocyte cell line represents an informative model for adipogenesis research, primary cultured cells are often needed to understand particular human or animal metabolic phenotypes. As demonstrated by cultured preadipocytes from large mammalian species, primary cultured cells require specific adipogenic differentiation conditions different to that of the 3T3-L1 cell line. These conditions are also species-specific and require optimization steps. However, efficient protocols to differentiate primary preadipocytes using alternative species to rodents are scarce. Sheep represent an amenable animal model for fetal biology and developmental origins of health and disease studies. In this work, we present with the first detailed procedure to efficiently differentiate primary fetal and adult ovine preadipocytes. METHODS: Fetal and adult ovine adipose and skin tissue harvest, preadipocyte and fibroblast isolation, proliferation, and standardization and optimization of a new adipogenic differentiation protocol. Use of commercial cell lines (3T3-L1 and NIH-3T3) for validation purposes. Oil red O stain and gene expression were used to validate adipogenic differentiation. ANOVA and Fisher's exact test were used to determine statistical significance. RESULTS: Our optimized adipogenic differentiation method included a prolonged adipogenic cocktail exposure time from 2 to 8 days, higher insulin concentration, and supplementation with the peroxisome proliferator-activated receptor gamma (PPARγ) agonist, rosiglitazone. This protocol was optimized for both, fetal and adult preadipocytes. CONCLUSIONS: Our protocol enables successful adipogenic differentiation of fetal and adult ovine preadipocytes. This work demonstrates that compared to the 3T3-L1 cell line, fetal ovine preadipocytes require a longer exposure to the differentiation cocktail, and the need for IMBX, dexamethasone, and/or the PPARγ agonist rosiglitazone through the terminal differentiation phase. They also require higher insulin concentration during differentiation to enhance lipid accumulation and similar to human primary preadipocytes, PPARγ agonist supplementation is also required for ovine adipogenic differentiation. This work highlights species-specific differences requirements for adipogenic differentiation and the need to develop standardized methods to investigate comparative adipocyte biology.
[Mh] Termos MeSH primário: Adipogenia/efeitos dos fármacos
Técnicas de Cultura de Células/métodos
PPAR gama/agonistas
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Adipócitos/fisiologia
Animais
Dexametasona/farmacologia
Insulina/farmacologia
Camundongos
Células NIH 3T3
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (PPAR gamma); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); 7S5I7G3JQL (Dexamethasone); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1186/s11658-017-0037-1


  5 / 5018 MEDLINE  
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[PMID]:28424169
[Au] Autor:Cuppoletti J; Tewari KP; Chakrabarti J; Malinowska DH
[Ad] Endereço:Department of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio John.Cuppoletti@uc.edu.
[Ti] Título:Identification of the fatty acid activation site on human ClC-2.
[So] Source:Am J Physiol Cell Physiol;312(6):C707-C723, 2017 Jun 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fatty acids (including lubiprostone and cobiprostone) are human ClC-2 (hClC-2) Cl channel activators. Molecular and cellular mechanisms underlying this activation were examined. Role of a four-amino acid PKA activation site, RGET , of hClC-2 was investigated using wild-type (WT) and mutant (AGET, RGEA, and AGAA) hClC-2 expressed in 293EBNA cells as well as involvement of PKA, intracellular cAMP concentration ([cAMP] ), EP , or EP receptor agonist activity. All fatty acids [lubiprostone, cobiprostone, eicosatetraynoic acid (ETYA), oleic acid, and elaidic acid] caused significant rightward shifts in concentration-dependent Cl current activation (increasing EC s) with mutant compared with WT hClC-2 channels, without changing time and voltage dependence, current-voltage rectification, or methadone inhibition of the channel. As with lubiprostone, cobiprostone activation of hClC-2 occurred with PKA inhibitor (myristoylated protein kinase inhibitor) present or when using double PKA activation site (RRAA /RGEA ) mutant. Cobiprostone did not activate human CFTR. Fatty acids did not increase [cAMP] in hClC-2/293EBNA or T84 cells. Using T84 CFTR knockdown cells, cobiprostone increased hClC-2 Cl currents without increasing [cAMP] while PGE and forskolin-IBMX increased both. Fatty acids were not agonists of EP or EP receptors. L-161,982, a supposed EP -selective inhibitor, had no effect on lubiprostone-activated hClC-2 Cl currents but significantly decreased T84 cell barrier function measured by transepithelial resistance and fluorescent dextran transepithelial movement. The present findings show that RGET of hClC-2 (possible binding site) plays an important functional role in fatty acid activation of hClC-2. PKA, [cAMP] , and EP or EP receptors are not involved. These studies provide the molecular basis for fatty acid regulation of hClC-2.
[Mh] Termos MeSH primário: Canais de Cloreto/metabolismo
Lubiprostona/farmacologia
Prostaglandinas/farmacologia
Tiofenos/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Motivos de Aminoácidos
Ácidos Araquidônicos/metabolismo
Sítios de Ligação
Canais de Cloreto/química
Cloretos/metabolismo
Colforsina/farmacologia
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/deficiência
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Células HEK293
Seres Humanos
Transporte de Íons
Cinética
Lubiprostona/química
Metadona/farmacologia
Ácido Oleico/metabolismo
Prostaglandinas/química
Ligação Proteica
Inibidores de Proteínas Quinases/farmacologia
Receptores de Prostaglandina E Subtipo EP2/metabolismo
Receptores de Prostaglandina E Subtipo EP4/metabolismo
Tiofenos/química
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (CFTR protein, human); 0 (Chloride Channels); 0 (Chlorides); 0 (ClC-2 chloride channels); 0 (L-161982); 0 (PTGER2 protein, human); 0 (Prostaglandins); 0 (Protein Kinase Inhibitors); 0 (Receptors, Prostaglandin E, EP2 Subtype); 0 (Receptors, Prostaglandin E, EP4 Subtype); 0 (Thiophenes); 0 (Triazoles); 0 (cobiprostone); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1F7A44V6OU (Colforsin); 2UMI9U37CP (Oleic Acid); 4837010H8C (elaidic acid); 7662KG2R6K (Lubiprostone); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); TBT296U68M (1-Methyl-3-isobutylxanthine); UC6VBE7V1Z (Methadone)
[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:170421
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00267.2016


  6 / 5018 MEDLINE  
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[PMID]:28081948
[Au] Autor:Fukami K; Asano E; Ueda M; Sekiguchi F; Yoshida S; Kawabata A
[Ad] Endereço:Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (Formerly Kinki University), Higashi-Osaka 577-8502, Japan.
[Ti] Título:High glucose induces N-linked glycosylation-mediated functional upregulation and overexpression of Ca 3.2 T-type calcium channels in neuroendocrine-like differentiated human prostate cancer cells.
[So] Source:J Pharmacol Sci;133(1):57-60, 2017 Jan.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Given that Ca 3.2 T-type Ca channels were functionally regulated by asparagine (N)-linked glycosylation, we examined effects of high glucose on the function of Ca 3.2, known to regulate secretory function, in neuroendocrine-like differentiated prostate cancer LNCaP cells. High glucose accelerated the increased channel function and overexpression of Ca 3.2 during neuroendocrine differentiation, the former prevented by enzymatic inhibition of N-glycosylation and cleavage of N-glycans. Hyperglycemia thus appears to induce N-linked glycosylation-mediated functional upregulation and overexpression of Ca 3.2 in neuroendocrine-like differentiated prostate cancer cells.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo T/biossíntese
Diferenciação Celular
Regulação Neoplásica da Expressão Gênica
Glucose/farmacologia
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Bucladesina/farmacologia
Linhagem Celular Tumoral
Glicosilação/efeitos dos fármacos
Seres Humanos
Masculino
Potenciais da Membrana/efeitos dos fármacos
Tunicamicina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CACNA1H protein, human); 0 (Calcium Channels, T-Type); 11089-65-9 (Tunicamycin); 63X7MBT2LQ (Bucladesine); IY9XDZ35W2 (Glucose); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE


  7 / 5018 MEDLINE  
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[PMID]:27973394
[Au] Autor:Neviere R; Delguste F; Durand A; Inamo J; Boulanger E; Preau S
[Ad] Endereço:Département de Physiologie, Faculté de Médecine, Université Lille, 1 Place de Verdun, F-59000 Lille CEDEX 59045, France. rneviere@univ-lille2.fr.
[Ti] Título:Abnormal Mitochondrial cAMP/PKA Signaling Is Involved in Sepsis-Induced Mitochondrial and Myocardial Dysfunction.
[So] Source:Int J Mol Sci;17(12), 2016 Dec 10.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Adrenergic receptors couple to Gs-proteins leading to transmembrane adenylyl cyclase activation and cytosolic cyclic adenosine monophosphate (cAMP) production. Cyclic AMP is also produced in the mitochondrial matrix, where it regulates respiration through protein kinase A (PKA)-dependent phosphorylation of respiratory chain complexes. We hypothesized that a blunted mitochondrial cAMP-PKA pathway would participate in sepsis-induced heart dysfunction. Adult male mice were subjected to intra-abdominal sepsis. Mitochondrial respiration of cardiac fibers and myocardial contractile performance were evaluated in response to 8Br-cAMP, PKA inhibition (H89), soluble adenylyl cyclase inhibition (KH7), and phosphodiesterase inhibition (IBMX; BAY60-7550). Adenosine diphosphate (ADP)-stimulated respiratory rates of cardiac fibers were reduced in septic mice. Compared with controls, stimulatory effects of 8Br-cAMP on respiration rates were enhanced in septic fibers, whereas inhibitory effects of H89 were reduced. Ser-58 phosphorylation of cytochrome c oxidase subunit IV-1 was reduced in septic hearts. In vitro, incubation of septic cardiac fibers with BAY60-7550 increased respiratory control ratio and improved cardiac MVO2 efficiency in isolated septic heart. In vivo, BAY60-7550 pre-treatment of septic mice have limited impact on myocardial function. Mitochondrial cAMP-PKA signaling is impaired in the septic myocardium. PDE2 phosphodiesterase inhibition by BAY60-7550 improves mitochondrial respiration and cardiac MVO2 efficiency in septic mice.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
AMP Cíclico/metabolismo
Mitocôndrias/metabolismo
Miocárdio/metabolismo
Miocárdio/patologia
Sepse/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Animais
Western Blotting
Respiração Celular/efeitos dos fármacos
Nucleotídeo Cíclico Fosfodiesterase do Tipo 2/metabolismo
Transporte de Elétrons/efeitos dos fármacos
Complexo I de Transporte de Elétrons/metabolismo
Imidazóis/farmacologia
Camundongos
Proteínas Mitocondriais/metabolismo
Contração Miocárdica/efeitos dos fármacos
Inibidores de Fosfodiesterase/farmacologia
Fosforilação/efeitos dos fármacos
Fosfosserina/metabolismo
Transdução de Sinais/efeitos dos fármacos
Triazinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3,4-dimethoxybenzyl)-7-(1-(1-hydroxyethyl)-4-phenylbutyl)-5-methylimidazo(5,1-f)(1,2,4)triazin-4 (3H)-one); 0 (Imidazoles); 0 (Mitochondrial Proteins); 0 (Phosphodiesterase Inhibitors); 0 (Triazines); 17885-08-4 (Phosphoserine); E0399OZS9N (Cyclic AMP); EC 1.6.5.3 (Electron Transport Complex I); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 2); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161216
[St] Status:MEDLINE


  8 / 5018 MEDLINE  
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[PMID]:27943300
[Au] Autor:Andersson LE; Nicholas LM; Filipsson K; Sun J; Medina A; Al-Majdoub M; Fex M; Mulder H; Spégel P
[Ad] Endereço:Department of Clinical Sciences, Unit of Molecular Metabolism, Lund University Diabetes Centre, CRC, Malmö, Sweden.
[Ti] Título:Glycogen metabolism in the glucose-sensing and supply-driven ß-cell.
[So] Source:FEBS Lett;590(23):4242-4251, 2016 Dec.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glycogen metabolism in ß-cells may affect downstream metabolic pathways controlling insulin release. We examined glycogen metabolism in human islets and in the rodent-derived INS-1 832/13 ß-cells and found them to express the same isoforms of key enzymes required for glycogen metabolism. Our findings indicate that glycogenesis is insulin-independent but influenced by extracellular glucose concentrations. Levels of glycogen synthase decrease with increasing glucose concentrations, paralleling accumulation of glycogen. We did not find cAMP-elicited glycogenolysis and insulin secretion to be causally related. In conclusion, our results reveal regulated glycogen metabolism in human islets and insulin-secreting cells. Whether glycogen metabolism affects insulin secretion under physiological conditions remains to be determined.
[Mh] Termos MeSH primário: Glucose/farmacologia
Glicogênio/metabolismo
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/metabolismo
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Linhagem Celular
Colforsina/farmacologia
Espaço Extracelular/efeitos dos fármacos
Espaço Extracelular/metabolismo
Glicogênio Sintase/metabolismo
Seres Humanos
Insulina/secreção
Células Secretoras de Insulina/secreção
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Insulin); 1F7A44V6OU (Colforsin); 9005-79-2 (Glycogen); EC 2.4.1.11 (Glycogen Synthase); IY9XDZ35W2 (Glucose); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170510
[Lr] Data última revisão:
170510
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12460


  9 / 5018 MEDLINE  
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[PMID]:27498007
[Au] Autor:Wang YL; Lin SP; Hsieh PC; Hung SC
[Ad] Endereço:Institute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.
[Ti] Título:Concomitant beige adipocyte differentiation upon induction of mesenchymal stem cells into brown adipocytes.
[So] Source:Biochem Biophys Res Commun;478(2):689-95, 2016 09 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The accumulation of fat, which results in obesity, is related to many metabolic disorders. Besides white and brown adipose tissue, beige adipose tissue has recently been recognized as a new type of accumulated fat. Mesenchymal stem cells (MSCs) have been shown to differentiate into brown adipocytes. Through analyzing levels of mRNA and protein markers associated with beige adipocyte, we found concomitant beige adipocyte differentiation upon induction of MSCs into brown adipocytes in a defined medium containing triiodothyronine, insulin, dexamethasone, and indomethacin. Moreover, we found that protein kinase A (PKA) modulators regulated MSC differentiation into brown or beige adipocytes. Activation of PKA by isobutylmethylxanthine or forskolin increased brown adipocyte differentiation and reduced beige adipocyte differentiation, while inactivation of PKA by KT-5720 or SC-3010 or the knockdown of PKA downstream cAMP response element-binding protein (CREB) decreased brown adipocyte differentiation and increased beige adipocyte differentiation. We also showed that increased brown adipocyte differentiation was accompanied by an increase in mitochondrial mass. In conclusion, we propose a model of beige/brown co-differentiation in MSCs and develop a method for controlling this differentiation via PKA modulation.
[Mh] Termos MeSH primário: Adipócitos Bege/efeitos dos fármacos
Adipócitos Marrons/efeitos dos fármacos
Meios de Cultura/farmacologia
Proteínas Quinases Dependentes de AMP Cíclico/genética
Células Mesenquimais Estromais/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Adipócitos Bege/citologia
Adipócitos Bege/metabolismo
Adipócitos Marrons/citologia
Adipócitos Marrons/metabolismo
Carbazóis/farmacologia
Diferenciação Celular/efeitos dos fármacos
Colforsina/farmacologia
Meios de Cultura/química
AMP Cíclico/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/antagonistas & inibidores
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Dexametasona/farmacologia
Regulação da Expressão Gênica
Seres Humanos
Indometacina/farmacologia
Insulina/farmacologia
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Cultura Primária de Células
Pirróis/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Tri-Iodotironina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CREB1 protein, human); 0 (Carbazoles); 0 (Culture Media); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Insulin); 0 (Pyrroles); 0 (RNA, Small Interfering); 06LU7C9H1V (Triiodothyronine); 1F7A44V6OU (Colforsin); 58HV29I28S (KT 5720); 7S5I7G3JQL (Dexamethasone); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); TBT296U68M (1-Methyl-3-isobutylxanthine); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160808
[St] Status:MEDLINE


  10 / 5018 MEDLINE  
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[PMID]:27401133
[Au] Autor:Wei D; Hurd C; Galleguillos D; Singh J; Fenrich KK; Webber CA; Sipione S; Fouad K
[Ad] Endereço:Neuroscience and Mental Health Institute, University of Alberta, Edmonton T6G 2E1, Canada.
[Ti] Título:Inhibiting cortical protein kinase A in spinal cord injured rats enhances efficacy of rehabilitative training.
[So] Source:Exp Neurol;283(Pt A):365-74, 2016 Sep.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated levels of the second messenger molecule cyclic adenosine monophosphate (cAMP) are often associated with neuron sprouting and neurite extension (i.e., neuroplasticity). Phosphokinase A (PKA) is a prominent downstream target of cAMP that has been associated with neurite outgrowth. We hypothesized that rehabilitative motor training following spinal cord injuries promotes neuroplasticity via PKA activation. However, in two independent experiments, inhibition of cortical PKA using Rp-cAMPS throughout rehabilitative training robustly increased functional recovery and collateral sprouting of injured corticospinal tract axons, an indicator of neuroplasticity. Consistent with these in vivo findings, using cultured STHdh neurons, we found that Rp-cAMPS had no effect on the phosphorylation of CREB (cAMP response element-binding protein), a prominent downstream target of PKA, even with the concomitant application of the adenylate cyclase agonist forskolin to increase cAMP levels. Conversely, when cAMP levels were increased using the phosphodiesterase inhibitor IBMX, Rp-cAMPS potently inhibited CREB phosphorylation. Taken together, our results suggest that an alternate cAMP dependent pathway was involved in increasing CREB phosphorylation and neuroplasticity. This idea was supported by an in vitro neurite outgrowth assay, where inhibiting PKA did enhance neurite outgrowth. However, when PKA inhibition was combined with inhibition of EPAC2 (exchange protein directly activated by cAMP), another downstream target of cAMP in neurons, neurite outgrowth was significantly reduced. In conclusion, blocking PKA in cortical neurons of spinal cord injured rats increases neurite outgrowth of the lesioned corticospinal tract fibres and the efficacy of rehabilitative training, likely via EPAC.
[Mh] Termos MeSH primário: Córtex Cerebral/enzimologia
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/reabilitação
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Análise de Variância
Animais
Proteína de Ligação a CREB/metabolismo
Linhagem Celular Transformada/metabolismo
Linhagem Celular Transformada/patologia
Células Cultivadas
Córtex Cerebral/metabolismo
AMP Cíclico/análogos & derivados
AMP Cíclico/metabolismo
Modelos Animais de Doenças
Feminino
Gânglios Espinais/citologia
Microglia/metabolismo
Microglia/patologia
Neuritos/efeitos dos fármacos
Neuritos/fisiologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Inibidores de Fosfodiesterase/farmacologia
Tratos Piramidais/metabolismo
Ratos
Ratos Endogâmicos Lew
Recuperação de Função Fisiológica/fisiologia
Tionucleotídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphodiesterase Inhibitors); 0 (Thionucleotides); 23645-17-2 (adenosine-3',5'-cyclic phosphorothioate); E0399OZS9N (Cyclic AMP); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, rat); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE



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