Base de dados : MEDLINE
Pesquisa : D27.505.519.914.500.204 [Categoria DeCS]
Referências encontradas : 106 [refinar]
Mostrando: 1 .. 10   no formato [Longo]

página 1 de 11 ir para página                         

  1 / 106 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:29217191
Autor:Yoshida K; Nakai A; Kaneshiro K; Hashimoto N; Suzuki K; Uchida K; Hashimoto T; Kawasaki Y; Tateishi K; Nakagawa N; Shibanuma N; Sakai Y; Hashiramoto A
Endereço:Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe 654-0142, Japan.
Título:TNF-α induces expression of the circadian clock gene Bmal1 via dual calcium-dependent pathways in rheumatoid synovial cells.
Fonte:Biochem Biophys Res Commun; 495(2):1675-1680, 2018 01 08.
ISSN:1090-2104
País de publicação:United States
Idioma:eng
Resumo:Tumor necrosis factor (TNF)-α is responsible for expressions of several clock genes and affects joint symptoms of rheumatoid arthritis (RA) with diurnal fluctuation. We tried to determine the mechanism involved in over-expression of Bmal1, induced by TNF-α, in primary cultured rheumatoid synovial cells. Cells were incubated with intra-cellular Ca chelator BAPTA-AM, calcineurin inhibitor FK506 and p300/CBP (CREB binding protein) inhibitor C646, respectively, or transfected with p300 and CBP small interfering RNA (siRNA) before stimulation with TNF-α. Oscillation phase and amplitude of Bmal1, transcriptional activator Rorα, transcriptional repressor Rev-erbα, and histone acetyltransferases (p300 and Cbp) were evaluated by quantitative real-time PCR. As results, TNF-α did not influence the oscillation phase of Rev-erbα, while enhanced those of Rorα, resulting in over-expression of Bmal1. When Ca influx was inhibited by BAPTA-AM, TNF-α-mediated up-regulation of Rorα was cancelled, however, that of Bmal1 was still apparent. When we further explored another pathway between TNF-α and Bmal1, TNF-α suppressed the expression of Rev-erbα in the absence of Ca influx, as well as those of p300 and Cbp genes. Finally, actions of TNF-α, in increasing Bmal1/Rorα and decreasing Rev-erbα, were cancelled by C646 treatment or silencing of both p300 and Cbp. In conclusion, we determined a novel role of TNF-α in inducing Bmal1 via dual calcium dependent pathways; Rorα was up-regulated in the presence of Ca influx and Rev-erbα was down-regulated in the absence of that. Results proposed that inhibition of p300/CBP could be new therapeutic targets for RA.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (ARNTL Transcription Factors); 0 (ARNTL protein, human); 0 (Benzoates); 0 (C646 compound); 0 (Calcium Chelating Agents); 0 (NR1D1 protein, human); 0 (Nuclear Receptor Subfamily 1, Group D, Member 1); 0 (Nuclear Receptor Subfamily 1, Group F, Member 1); 0 (Pyrazoles); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (RORA protein, human); 0 (Tumor Necrosis Factor-alpha); 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester); 526U7A2651 (Egtazic Acid); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human)


  2 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28470526
Autor:Friedrich O; Head SI
Endereço:Friedrich-Alexander University (FAU) Erlangen-Nürnberg, Institute of Medical Biotechnology, Paul-Gordan-Street 3, Erlangen, 91052, Germany. oliver.friedrich@fau.de.
Título:Quantitative Ratiometric Ca Imaging to Assess Cell Viability.
Fonte:Methods Mol Biol; 1601:171-193, 2017.
ISSN:1940-6029
País de publicação:United States
Idioma:eng
Resumo:Viability of cells is strongly related to their Ca homeostasis. Ca signal fluctuations can be on a slow time scale, e.g., in non-excitable cells, but also in the range of tens of milliseconds for excitable cells, such as nerve and muscle. Muscle fibers respond to electrical stimulation with Ca transients that exceed their resting basal level about 100 times. Fluorescent Ca dyes have become an indispensable means to monitor Ca fluctuations in living cells online. Fluorescence intensity of such "environmental dyes" relies on a buffer-ligand interaction which is not only governed by laws of mass action but also by binding and unbinding kinetics that have to be considered for proper Ca kinetics and amplitude validation. The concept of Ca dyes including the different approaches using ratiometric and non-ratiometric dyes, the way to correctly choose dyes according to their low-/high-affinity properties and kinetics as well as staining techniques, and in situ calibration are reviewed and explained. We provide detailed protocols to apply ratiometric Fura-2 imaging of resting Ca and Ca fluctuations during field-stimulation in single isolated skeletal muscle cells and how to translate fluorescence intensities into absolute Ca concentrations using appropriate calibration techniques.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Fluorescent Dyes); SY7Q814VUP (Calcium); TSN3DL106G (Fura-2)


  3 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28887310
Autor:Yanda MK; Liu Q; Cebotaru V; Guggino WB; Cebotaru L
Endereço:From the Division of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 and.
Título:Histone deacetylase 6 inhibition reduces cysts by decreasing cAMP and Ca in knock-out mouse models of polycystic kidney disease.
Fonte:J Biol Chem; 292(43):17897-17908, 2017 Oct 27.
ISSN:1083-351X
País de publicação:United States
Idioma:eng
Resumo:Autosomal dominant polycystic kidney disease (ADPKD) is associated with progressive enlargement of multiple renal cysts, often leading to renal failure that cannot be prevented by a current treatment. Two proteins encoded by two genes are associated with ADPKD: PC1 ( ), primarily a signaling molecule, and PC2 ( ), a Ca channel. Dysregulation of cAMP signaling is central to ADPKD, but the molecular mechanism is unresolved. Here, we studied the role of histone deacetylase 6 (HDAC6) in regulating cyst growth to test the possibility that inhibiting HDAC6 might help manage ADPKD. Chemical inhibition of HDAC6 reduced cyst growth in PC1-knock-out mice. In proximal tubule-derived, PC1-knock-out cells, adenylyl cyclase 6 and 3 (AC6 and -3) are both expressed. AC6 protein expression was higher in cells lacking PC1, compared with control cells containing PC1. Intracellular Ca was higher in PC1-knock-out cells than in control cells. HDAC inhibition caused a drop in intracellular Ca and increased ATP-simulated Ca release. HDAC6 inhibition reduced the release of Ca from the endoplasmic reticulum induced by thapsigargin, an inhibitor of endoplasmic reticulum Ca -ATPase. HDAC6 inhibition and treatment of cells with the intracellular Ca chelator 1,2-bis(2-aminophenoxy)ethane- , , ', '-tetraacetic acid tetrakis(acetoxymethyl ester) reduced cAMP levels in PC1-knock-out cells. Finally, the calmodulin inhibitors W-7 and W-13 reduced cAMP levels, and W-7 reduced cyst growth, suggesting that AC3 is involved in cyst growth regulated by HDAC6. We conclude that HDAC6 inhibition reduces cell growth primarily by reducing intracellular cAMP and Ca levels. Our results provide potential therapeutic targets that may be useful as treatments for ADPKD.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Histone Deacetylase Inhibitors); 0 (TRPP Cation Channels); 0 (polycystic kidney disease 2 protein); 67526-95-8 (Thapsigargin); E0399OZS9N (Cyclic AMP); EC 2.7.10.- (protein kinase D); EC 2.7.11.13 (Protein Kinase C); EC 3.5.1.98 (Hdac6 protein, mouse); EC 3.5.1.98 (Histone Deacetylase 6); EC 3.5.1.98 (Histone Deacetylases); SY7Q814VUP (Calcium)


  4 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28764041
Autor:McIntyre I; O'Sullivan M; O'Riordan D
Endereço:UCD Institute of Food & Health, University College Dublin, Belfield, Dublin 4, Ireland.
Título:Monitoring the progression of calcium and protein solubilisation as affected by calcium chelators during small-scale manufacture of casein-based food matrices.
Fonte:Food Chem; 237:597-604, 2017 Dec 15.
ISSN:0308-8146
País de publicação:England
Idioma:eng
Resumo:Calcium and protein solubilisation during small-scale manufacture of semi-solid casein-based food matrices was investigated and found to be very different in the presence or absence of calcium chelating salts. Calcium concentrations in the dispersed phase increased and calcium-ion activity (A ) decreased during manufacture of the matrices containing calcium chelating salts; with ∼23% of total calcium solubilised by the end of manufacture. In the absence of calcium chelating salts, these concentrations were significantly lower at equivalent processing times and remained unchanged as did A , throughout manufacture. The protein content of the dispersed phase was low (≤3% of total protein), but was significantly higher for matrices containing calcium chelating salts. This study elucidates the critical role of calcium chelating salts in modulating casein hydration and dispersion and gives an indication of the levels of soluble calcium and protein required to allow matrix formation during manufacture of casein-based food structures e.g. processed and analogue cheese.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Caseins); SY7Q814VUP (Calcium)


  5 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28739328
Autor:Marques S; Santos S; Fremin K; Fogo AB
Endereço:Department of Nephrology, Centro Hospitalar São João, Porto, Portugal; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN. Electronic address: sofiahomemdemelo@gmail.com.
Título:A Case of Oxalate Nephropathy: When a Single Cause Is Not Crystal Clear.
Fonte:Am J Kidney Dis; 70(5):722-724, 2017 Nov.
ISSN:1523-6838
País de publicação:United States
Idioma:eng
Resumo:Hyperoxaluria can result in oxalate nephropathy with intratubular calcium oxalate crystallization and acute tubular injury. Primary inherited enzymatic deficiency or secondary causes such as excessive dietary intake, enteric increased absorption, or high doses of vitamin C, which is metabolized to oxalate, may underlie hyperoxaluria and oxalate nephropathy. We report a case of acute kidney injury due to oxalate nephropathy in a patient using chelating therapy with oral ethylenediamine tetra acetic acid (EDTA), intravenous supplementation with vitamin C, and chronic diarrhea and discuss the potential kidney damage these factors can cause in particular settings. To our knowledge, this is the first report suggesting an association between oral EDTA and oxalate nephropathy.
Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Vitamins); 2612HC57YE (Calcium Oxalate); 9G34HU7RV0 (Edetic Acid); PQ6CK8PD0R (Ascorbic Acid)


  6 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28689036
Autor:Arenas IA; Navas-Acien A; Ergui I; Lamas GA
Endereço:The Columbia University Division of Cardiology at Mount Sinai Medical Center, Miami Beach, FL, USA.
Título:Enhanced vasculotoxic metal excretion in post-myocardial infarction patients following a single edetate disodium-based infusion.
Fonte:Environ Res; 158:443-449, 2017 10.
ISSN:1096-0953
País de publicação:Netherlands
Idioma:eng
Resumo:Toxic metals have been associated with cardiovascular mortality and morbidity. We have hypothesized that enhanced excretion of vasculotoxic metals might explain the positive results of the Trial to Assess Chelation Therapy (TACT). The purpose of this study was to determine whether a single infusion of the edetate disodium- based infusion used in TACT led to enhanced excretion of toxic metals known to be associated with cardiovascular events. METHODS: Twenty six patients (post-MI, age > 50 years, serum creatinine ≤ 2.0mg/dL) were enrolled in this open-label study. Urinary levels of 20 toxic metals normalized to urinary creatinine concentrations were measured at baseline in overnight urine collections, for 6h following a placebo infusion of 500mL normal saline and 1.2% dextrose, and for 6h following a 3g edetate disodium-based infusion. Self-reported metal exposure, smoking status, food frequency, occupational history, drinking water source, housing and hobbies were collected at baseline by a metal exposure questionnaire. RESULTS: The mean age was 65 years (range 51-81 years). All patients were male. 50% had diabetes mellitus and 58% were former smokers. Mean (SD) serum creatinine was 0.95 (0.31) mg/dL. Toxic metals were detected in the baseline urine of >80% of patients. After placebo infusion there were no significant changes in total urinary metal levels. After edetate infusion, total urinary metal level increased by 71% compared to baseline (1500 vs. 2580µg/g creatinine; P<0.0001). The effect of edetate was particularly large for lead (3835% increase) and cadmium (633% increase). CONCLUSIONS: Edetate disodium-based infusions markedly enhanced the urinary excretion of lead and cadmium, toxic metals with established epidemiologic evidence and mechanisms linking them to coronary and vascular events.
Tipo de publicação: JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Calcium Chelating Agents); 0 (Environmental Pollutants); 0 (Metals); 9G34HU7RV0 (Edetic Acid)


  7 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28422989
Autor:Cavaliere FM; Prezzo A; Bilotta C; Iacobini M; Quinti I
Endereço:Department of Molecular Medicine, Sapienza University of Rome, Roma, Italy.
Título:The lack of BTK does not impair monocytes and polymorphonuclear cells functions in X-linked agammaglobulinemia under treatment with intravenous immunoglobulin replacement.
Fonte:PLoS One; 12(4):e0175961, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:The lack of BTK in X-linked agammaglobulinemia (XLA) patients does not affect monocytes and polymorphonuclear cells (PMN) phenotype and functions. In this study, we show that XLA patients had an increased frequency of the intermediate monocytes subset and that BTK-deficient monocytes and PMN had a normal expression of receptors involved in the activation and cellular responses. We demonstrate that BTK is not required for migration, phagocytosis and the production of reactive oxygen species (ROS) following engagement of FC gamma receptors (FcγR). XLA monocytes and PMN showed an efficient calcium (Ca2+)-independent activation of oxidative burst, suggesting that oxidative burst is less dependent by Ca2+ mobilization. The phagocytosis was functional and it remained unaltered also after Ca2+ chelation, confirming the independence of phagocytosis on Ca2+ mobilization. Intravenous immunoglobulin (IVIg) infusion exerted an anti-inflammatory effect by reducing the frequency of pro-inflammatory monocytes. In monocytes, the IVIg reduce the oxidative burst and phagocytosis even if these functions remained efficient.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Immunoglobulins, Intravenous); 0 (Reactive Oxygen Species); 0 (Receptors, IgG); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); SY7Q814VUP (Calcium)


  8 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28332248
Autor:Ou Y; Liu Z; Li S; Zhu X; Lin Y; Han J; Duan Z; Jia L; Gui B
Endereço:Department of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Título:Citrate attenuates vascular calcification in chronic renal failure rats.
Fonte:APMIS; 125(5):452-458, 2017 May.
ISSN:1600-0463
País de publicação:Denmark
Idioma:eng
Resumo:Vascular calcification (VC) is a major contributor of cardiovascular dysfunction in chronic renal failure (CRF). Citrate binds calcium and inhibits the growth of calcium crystals. This present study intends to evaluate the effect of citrate on VC in adenine-induced CRF rats. The rats were randomly divided into five groups: the control group, the citrate control group, model group, model rats with low-dose treatment of citrate (216 mg/kg) and model rats with high-dose treatment of citrate (746 mg/kg). The rats were euthanized at 5 weeks with their blood and aorta in detection. The results showed that serum level of blood urea nitrogen, serum creatinine, phosphorus, calcium, and related renal failure function marker were elevated in the model group. Furthermore, the aortic calcium accumulation and alkaline phosphatase activity were significantly increased in the model group compared with control groups. Additionally, hematoxylin-eosin staining results demonstrated that the vascular calcification in aorta is significantly increased in the model group. Finally, the expression of VC-related proteins including bone morphogenetic protein and osteocalcin were increased in the model group, whereas alpha-smooth muscle actin was decreased in the model group compared with the control group. However, treatment with citrate caused a reversal effect of all the above events in a dose-dependent manner. In conclusion, citrate may attenuate vascular calcification in adenine-induced CRF rats.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 2968PHW8QP (Citric Acid)


  9 / 106 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28319173
Autor:Nguyen HH; Varadi M; Tompa P; Pauwels K
Endereço:VIB Center for Structural Biology (CSB), Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium.
Título:Affinity purification of human m-calpain through an intrinsically disordered inhibitor, calpastatin.
Fonte:PLoS One; 12(3):e0174125, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Calpains are calcium-activated proteases that have biomedical and biotechnological potential. Their activity is tightly regulated by their endogenous inhibitor, calpastatin that binds to the enzyme only in the presence of calcium. Conventional approaches to purify calpain comprise multiple chromatographic steps, and are labor-intensive, leading to low yields. Here we report a new purification procedure for the human m-calpain based on its reversible calcium-mediated interaction with the intrinsically disordered calpastatin. We exploit the specific binding properties of human calpastatin domain 1 (hCSD1) to physically capture human m-calpain from a complex biological mixture. The dissociation of the complex is mediated by chelating calcium, upon which heterodimeric calpain elutes while hCSD1 remains immobilized onto the stationary phase. This novel affinity-based purification was compared to the conventional multistep purification strategy and we find that it is robust, it yields a homogeneous preparation, it can be scaled up easily and it rests on a non-disruptive step that maintains close to physiological conditions that allow further biophysical and functional studies.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Calcium Chelating Agents); 0 (Calcium-Binding Proteins); 0 (Recombinant Proteins); 79079-11-1 (calpastatin); EC 3.4.22.- (Calpain); EC 3.4.22.53 (CAPN2 protein, human)


  10 / 106 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
PMID:28216372
Autor:Chen S; Dong Z; Yang P; Wang X; Jin G; Yu H; Chen L; Li L; Tang L; Bai S; Yan H; Shen F; Cong W; Wen W; Wang H
Endereço:National Center for Liver Cancer, Second Military Medical University, 225 Changhai Road, Shanghai 200438, China; International Cooperation Laboratory on Signal Transduction of Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China.
Título:Hepatitis B virus X protein stimulates high mobility group box 1 secretion and enhances hepatocellular carcinoma metastasis.
Fonte:Cancer Lett; 394:22-32, 2017 May 28.
ISSN:1872-7980
País de publicação:Ireland
Idioma:eng
Resumo:Hepatitis B virus X protein (HBx) plays an important role in the progression of hepatocellular carcinoma. Here we reported that overexpression of HBx in hepatocellular carcinoma (HCC) cells could induce the secretion of high-mobility group box 1 (HMGB1) to promote invasion and metastasis of HCC in an autocrine/paracrine manner. HBx triggered an increase of cytoplasmic calcium and activated CAMKK/CAMKIV pathway, leading to subsequent translocation and release of HMGB1. HMGB1 neutralizing antibody, as well as calcium chelator or inhibitors of CAMKK/CAMKIV, could remarkably reduce invasion and metastasis of HCC cells in vitro and in a murine HCC metastasis model in vivo. Furthermore, the level of HMGB1 in patient serum and tumor tissues was positively correlated with HBV DNA load. We demonstrate an inverse relationship between HMGB1 in tumor cytoplasm and overall prognosis of HCC patients. CONCLUSION: HBx promotes the progression of HCC through translocation and secretion of HMGB1 from tumor cells via calcium dependent cascades. These data indicates that HMGB1 could serve as a novel prognostic biomarker and potential therapeutic target for HBV-related HCC.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies); 0 (Antineoplastic Agents); 0 (Calcium Chelating Agents); 0 (DNA, Viral); 0 (HMGB1 Protein); 0 (HMGB1 protein, human); 0 (Protein Kinase Inhibitors); 0 (Trans-Activators); 0 (hepatitis B virus X protein); EC 2.7.11.17 (CAMK4 protein, human); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Kinase); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 4)



página 1 de 11 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