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[PMID]:28453727
[Au] Autor:Lukasz A; Hillgruber C; Oberleithner H; Kusche-Vihrog K; Pavenstädt H; Rovas A; Hesse B; Goerge T; Kümpers P
[Ad] Endereço:Department of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149 Münster, Germany.
[Ti] Título:Endothelial glycocalyx breakdown is mediated by angiopoietin-2.
[So] Source:Cardiovasc Res;113(6):671-680, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: The endothelial glycocalyx (eGC), a carbohydrate-rich layer lining the luminal surface of the endothelium, provides a first vasoprotective barrier against vascular leakage and adhesion in sepsis and vessel inflammation. Angiopoietin-2 (Angpt-2), an antagonist of the endothelium-stabilizing receptor Tie2 secreted by endothelial cells, promotes vascular permeability through cellular contraction and junctional disintegration. We hypothesized that Angpt-2 might also mediate the breakdown of the eGC. Methods and results: Using confocal and atomic force microscopy, we show that exogenous Angpt-2 induces a rapid loss of the eGC in endothelial cells in vitro. Glycocalyx deterioration involves the specific loss of its main constituent heparan sulphate, paralleled by the secretion of the heparan sulphate-specific heparanase from late endosomal/lysosomal stores. Corresponding in vivo experiments revealed that exogenous Angpt-2 leads to heparanase-dependent eGC breakdown, which contributes to plasma leakage and leukocyte recruitment in vivo. Conclusion: Our data indicate that eGC breakdown is mediated by Angpt-2 in a non-redundant manner.
[Mh] Termos MeSH primário: Angiopoietina-2/metabolismo
Glicocálix/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Pele/irrigação sanguínea
[Mh] Termos MeSH secundário: Animais
Permeabilidade Capilar
Linhagem Celular
Glucuronidase/metabolismo
Heparitina Sulfato/metabolismo
Seres Humanos
Camundongos Endogâmicos C57BL
Microscopia de Força Atômica
Microscopia Confocal
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPT2 protein, human); 0 (Angiopoietin-2); 9050-30-0 (Heparitin Sulfate); EC 3.2.1.- (heparanase); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx023


  2 / 13703 MEDLINE  
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[PMID]:27779100
[Au] Autor:Xie B; Cao K; Li J; Chen J; Tang J; Chen X; Xia K; Zhou X; Cheng Y; Zhou J; Xie H
[Ad] Endereço:Deptment of Plastic Surgery, Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China.
[Ti] Título:Hmgb1 inhibits Klotho expression and malignant phenotype in melanoma cells by activating NF-κB.
[So] Source:Oncotarget;7(49):80765-80782, 2016 Dec 06.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular and cellular mechanisms behind the involvement of inflammation in melanoma have not been fully elucidated. In this study, knockdown of Hmgb1 expression increased apoptosis, reduced invasion and p-NF-κB expression, but increased Klotho protein level in melanoma tumor cells. The effect of Hmgb1 knockdown was overcome by LPS. Introduction of exogenous Hmgb1 significantly decreased apoptosis, increased invasion, elevated p-NF-κB, but lowered Klotho protein level in melanoma cells. The effect of exogenous Hmgb1 was agonized by NF-κB inhibitor CAPE. Hmgb1 knockdown activated, but exogenous Hmgb1 inactivated, p-IGF1R/p-PI3K p-85/p-Akt/p-mTOR signaling. Knockdown of Klotho gene expression significantly decreased apoptosis, increased invasion in melanoma cells, and inhibited xenograft A375 tumor growth. A significantly high percentage of cells stained positive for p-NF-κB, but negative for Klotho, in melanoma tissues compared to normal and benign skin tissues. The positive p-NF-κB and negative Klotho protein expression correlated with poor prognosis in melanoma patients. Multivariate analysis revealed an independent association between p-NF-κB / Klotho protein level and overall survival. In conclusion, Hmgb1 can inhibit Klotho gene expression and malignant phenotype in melanoma cells through activation of NF-κB signaling.
[Mh] Termos MeSH primário: Glucuronidase/metabolismo
Proteína HMGB1/metabolismo
Melanoma/metabolismo
NF-kappa B/metabolismo
Neoplasias Cutâneas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Apoptose
Pontos de Checagem do Ciclo Celular
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Distribuição de Qui-Quadrado
Classe Ia de Fosfatidilinositol 3-Quinase/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Glucuronidase/genética
Proteína HMGB1/genética
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Melanoma/genética
Melanoma/patologia
Camundongos Endogâmicos BALB C
Camundongos Nus
Meia-Idade
Análise Multivariada
Invasividade Neoplásica
Fosforilação
Modelos de Riscos Proporcionais
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
Receptores de Somatomedina/metabolismo
Transdução de Sinais
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
Serina-Treonina Quinases TOR/metabolismo
Fatores de Tempo
Transfecção
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HMGB1 Protein); 0 (HMGB1 protein, human); 0 (IGF1R protein, human); 0 (NF-kappa B); 0 (Receptors, Somatomedin); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.137 (Class Ia Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12623


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[PMID]:29297646
[Au] Autor:Milovanova LY; Mukhin NA; Kozlovskaya LV; Milovanov YS; Kiyakbaev GG; Rogova IV; Lebedeva MV; Androsova TV; Milovanova SY; Gil AY; Taranova MV
[Ti] Título:Decreased Serum Levels of Klotho Protein in Chronic Kidney Disease Patients: Clinical Imortance.
[So] Source:Vestn Ross Akad Med Nauk;71(4):288-96, 2016.
[Is] ISSN:0869-6047
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:Objective: To determine the role of serum Klotho (s-Klotho) protein levels changes in patients with different stages of chronic kidney disease (CKD). Methods: The study involved 130 patients with CKD stages 1­5D (mean age ­ 41±6.7 years). Serum levels of parathyroid hormone (PTH), calcium, phosphorus and s-Klotho protein (ELISA method) at baseline and after 1 year of follow-up were examined in all the patients so as the blood pressure (BP), including central (aortic), pulse wave velocity ­ with the help of «Sphygmоcor¼ (Australia), echocardiography, radiography of the abdominal aorta in a lateral projection were also performed. Results: Ehen comparing the s-Klotho levels in patients with different CKD stages, it was found that the level change associated with the reduction of glomerular filtration rate (GFR) ahead of phosphorus and PTH increase in serum, stared at 3A CKD, whereas hyperphosphatemia and PTH increase started at 4­5 CKD stages. According to ROC analysis, decreasing of s-Klotho levels below 387 pg/ml was indicated a calcification risk of abdominal aorta increased with an 80% sensitivity and 75% specificity. In addition, a strong negative relationship of low s-Klotho levels and heart remodeling was found. When comparing the patients with hypertension who were receiving antihypertensive monotherapy, the highest serum levels of Klotho protein were observed in those of them whose target blood pressure level was achieved primarily through Angiotensin II Receptors Blockers (ARB), compared to those who was administered another drug group (p<0.01) or has not reached the target blood pressure level (p=0,008). Conclusion: The change of serum Klotho levels (decrease) in CKD progression is associated with the degree (increase) of cardiovascular calcification and remodeling (the development of left ventricular hypertrophy, and cardiomyopathy) and it can be seen as an early independent marker of the cardiovascular system lesions in CKD. Our preliminary data of the effect of blood pressure correction on s-Klotho levels may indicate the possibility of drug maintaining serum Klotho levels and it requires further research.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/epidemiologia
Glucuronidase/sangue
Insuficiência Renal Crônica
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Coortes
Progressão da Doença
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Masculino
Meia-Idade
Hormônio Paratireóideo/sangue
Gravidade do Paciente
Fósforo/sangue
Insuficiência Renal Crônica/sangue
Insuficiência Renal Crônica/diagnóstico
Insuficiência Renal Crônica/epidemiologia
Insuficiência Renal Crônica/fisiopatologia
Medição de Risco
Fatores de Risco
Federação Russa/epidemiologia
Estatística como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Parathyroid Hormone); 27YLU75U4W (Phosphorus); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE


  4 / 13703 MEDLINE  
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[PMID]:28745686
[Au] Autor:Milovanova SY; Milovanov YS; Taranova MV; Dobrosmyslov IA
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Effects of keto/amino acids and a low-protein diet on the nutritional status of patients with Stages 3B-4 chronic kidney disease].
[Ti] Título:Vliianie keto/aminokislot i ogranicheniia belka na status pitaniia bol'nykh khronicheskoi bolezn'iu pochek IIIB-IV stadii..
[So] Source:Ter Arkh;89(6):30-33, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To evaluate the efficacy of keto/amino acids in maintaining protein balance and preventing mineral metabolic disturbances and the development of uremic hyperparathyroidism in the long-term use of a low-protein diet (LPD) in patients with Stages 3B-4 chronic kidney disease (CKD). SUBJECTS AND METHODS: Ninety patients with CKD caused by chronic latent glomerulonephritis in 65 patients and chronic tubulointerstitial nephritis of various etiologies (gout, drug-induced, and infection) in 25 were examined. The investigators conducted clinical, laboratory, and instrumental examinations, including bioelectrical impedance analysis (body mass index (BMI), the percentages of lean and fat mass), echocardiography and radiography of the abdominal aorta in the lateral projection (the presence of cardiac valvular and aortic calcification), and pulse wave velocity measurements using a Sphygmocor apparatus (vessel stiffness estimation). The stages of CKD were defined according to the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) criteria; glomerular filtration rate was calculated using the CKD EPI equation. According to the diet used, all the patients were divided into 3 groups: 1) 30 patients who took LPD (0.6 g of protein per kg of body weight/day) in combination with the keto/amino acid ketosteril (1 tablet per 5 kg of body weight/day; Diet One); 2) 30 patients who used LPD in combination with the other keto/amino acid ketoaminol at the same dose (Diet Two); 3) 30 patients had LPD without using the keto/amino acids (Diet Three) (a control group). RESULTS: During a follow-up, there were no signs of malnutrition in Groups 1 and 2 patients receiving LPD (0.6 g protein per kg/day) in combination with the keto/amino acids ketosteril and ketaminol, respectively. At the same time, 11 (36.6%) patients in Group 3 (a control group) who did not take the keto/amino acids showed a BMI decrease from 24 (23; 26) kg/m2 to 18.5 (17; 19.2) kg/m2 (p < 0.05), including that of lean body mass from 37.4 (36; 38.8) to 30 (29.1; 34.7)% in the men (p<0.05) and from 29.8 (26.8; 31) to 23.9 (22; 25.7)% in the women (p<0.01). In addition, at the end of the study, there were elevated serum phosphorus levels (p<0.05) and mainly higher parathyroid hormone concentrations in Group 3 patients who received LPD without using the amino/keto acids than in Groups 1 and 2. As compared to Group 3, Groups 1 and 2 displayed no differences in the quantity of cardiac and aortic calcification and in the augmentation index (arterial stiffness). The ketosteril and ketaminol groups versus the control group had also higher s-Klotho levels (p<0.01) that were inversely correlated with glomerular filtration rate (r =-0.467; p<0.01). CONCLUSION: The keto/amino acids ketosteril or ketoaminol are an important component of LPD, which prevents malnutrition and an additional source of calcium that inhibits hyperphosphatemia and slows the development of uremic hyperparathyroidism. Incorporation of keto/amino acids into LPD leads to a less pronounced reduction in s-Klotho protein in relation to the degree of renal failure than does LPD without keto/amino acids.
[Mh] Termos MeSH primário: Aminoácidos Essenciais/farmacologia
Aminoácidos/farmacologia
Dieta com Restrição de Proteínas/métodos
Glucuronidase/sangue
Cetoácidos/farmacologia
Avaliação de Resultados (Cuidados de Saúde)
Insuficiência Renal Crônica
[Mh] Termos MeSH secundário: Adulto
Idoso
Aminoácidos/administração & dosagem
Aminoácidos Essenciais/administração & dosagem
Terapia Combinada
Dieta com Restrição de Proteínas/efeitos adversos
Feminino
Seguimentos
Seres Humanos
Cetoácidos/administração & dosagem
Masculino
Meia-Idade
Insuficiência Renal Crônica/sangue
Insuficiência Renal Crônica/diagnóstico
Insuficiência Renal Crônica/dietoterapia
[Pt] Tipo de publicação:CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Amino Acids, Essential); 0 (Keto Acids); 68934-50-9 (ketosteril); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789630-33


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[PMID]:27772634
[Au] Autor:O'Lone E; Webster AC
[Ad] Endereço:University of Sydney, Sydney, Australia.
[Ti] Título:In Reply to 'Abnormality in FGF-23-α-Klotho Axis: A Possible Mechanism Underlying Hemodialysis-Related Cognitive Dysfunction?'
[So] Source:Am J Kidney Dis;68(5):818, 2016 11.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Disfunção Cognitiva
Fatores de Crescimento de Fibroblastos
[Mh] Termos MeSH secundário: Glucuronidase
Seres Humanos
Diálise Renal
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
62031-54-3 (Fibroblast Growth Factors); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:27772632
[Au] Autor:Shen JQ; Liu JF; Miao LY
[Ad] Endereço:The Third Affiliated Hospital of Soochow University, Changzhou, China.
[Ti] Título:Abnormality in FGF-23-α-Klotho Axis: A Possible Mechanism Underlying Hemodialysis-Related Cognitive Dysfunction?
[So] Source:Am J Kidney Dis;68(5):817-818, 2016 11.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Disfunção Cognitiva
Fatores de Crescimento de Fibroblastos
[Mh] Termos MeSH secundário: Glucuronidase
Seres Humanos
Diálise Renal
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
62031-54-3 (Fibroblast Growth Factors); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29056105
[Au] Autor:Llopart EE; Cian RE; López-Oliva MME; Zuleta Á; Weisstaub A; Drago SR
[Ad] Endereço:1Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ingeniería Química,Instituto de Tecnología de Alimentos,Universidad Nacional del Litoral,Santiago del Estero 2829,Santa Fe,Argentina.
[Ti] Título:Colonic and systemic effects of extruded whole-grain sorghum consumption in growing Wistar rats.
[So] Source:Br J Nutr;118(8):589-597, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Colonic effects of extruded whole-grain sorghum diets were evaluated using a model of growing rats. In all, twenty-four male Wistar rats were fed control (C), extruded white sorghum (EWS) or red sorghum (ERS). Consumption of sorghum diets showed satiety properties, with reduction of caecal pH, and lower activity of ß-glucosidase and ß-glucuronidase enzymes. Decreased copper zinc superoxide dismutase and manganese superoxide dismutase and increased catalase and glutathione peroxidase levels were observed in colonic mucosa. The induction of antioxidant enzymes occurred through the activation of the nuclear factor erythroid 2-related factor 2 protein and its subsequent translocation into the nucleus. ERS was able to decrease the proliferation of proximal mucosa of colon, demonstrating a possible effect against colorectal tumourigenesis. EWS increased proliferation and also apoptosis, ensuring the re-establishment of homoeostasis of the colonic mucosa. No antioxidant systemic effect (serum or hepatic level) was observed. It is likely that despite the extrusion the low bioavailability of the phenolic compounds of sorghum diets caused them to exert mainly acute effects at the colon level. Extruded whole-grain sorghum is a good functional ingredient that might be promising in dietary prevention of intestinal diseases.
[Mh] Termos MeSH primário: Colo/metabolismo
Dieta
Sorghum/química
Grãos Integrais/química
[Mh] Termos MeSH secundário: Animais
Catalase/metabolismo
Modelos Animais de Doenças
Glucuronidase/metabolismo
Glutationa Peroxidase/metabolismo
Concentração de Íons de Hidrogênio
Enteropatias/prevenção & controle
Mucosa Intestinal/metabolismo
Masculino
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Ratos
Ratos Wistar
Saciação
Superóxido Dismutase/metabolismo
beta-Glucosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, rat); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 3.2.1.21 (beta-Glucosidase); EC 3.2.1.31 (Glucuronidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002513


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[PMID]:28993191
[Au] Autor:Prud'homme GJ; Glinka Y; Kurt M; Liu W; Wang Q
[Ad] Endereço:Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada; Department of Laboratory Medicine, St. Michael's Hospital, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Ontario, Canada. Electronic address: prudho
[Ti] Título:The anti-aging protein Klotho is induced by GABA therapy and exerts protective and stimulatory effects on pancreatic beta cells.
[So] Source:Biochem Biophys Res Commun;493(4):1542-1547, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic gamma-aminobutyric acid (GABA) therapy prevents or ameliorates type 1 diabetes (T1D), by suppressing autoimmune responses and stimulating pancreatic beta cells. In beta cells, it increases insulin secretion, prevents apoptosis, and induces regeneration. It is unclear how GABA mediates these effects. We hypothesized that Klotho is involved. It is a multi-functional protein expressed in the kidneys, brain, pancreatic beta cells, other tissues, and is cell-bound or soluble. Klotho knockout mice display accelerated aging, and in humans Klotho circulating levels decline with age, renal disease and diabetes. Here, we report that GABA markedly increased circulating levels of Klotho in streptozotocin (STZ)-induced diabetes. GABA also increased Klotho in the islet of Langerhans of normal mice, as well as the islets and kidneys of STZ-treated mice. In vitro, GABA stimulated production and secretion of Klotho by human islet cells. Knockdown (KD) of Klotho with siRNA in INS-1E insulinoma cells abrogated the protective effects of GABA against STZ toxicity. Following KD, soluble Klotho reversed the effects of Klotho deficiency. In human islet cells soluble Klotho protected against cell death, and stimulated proliferation and insulin secretion. NF-κB activation triggers beta-cell apoptosis, and both GABA and Klotho suppress this pathway. We found Klotho KD augmented NF-κB p65 expression, and abrogated the ability of GABA to block NF-κB activation. This is the first report that GABAergic stimulation increases Klotho expression. Klotho protected and stimulated beta cells and lack of Klotho (KD) was reversed by soluble Klotho. These findings have important implications for the treatment of T1D.
[Mh] Termos MeSH primário: Glucuronidase/biossíntese
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/fisiologia
Ácido gama-Aminobutírico/farmacologia
[Mh] Termos MeSH secundário: Envelhecimento/efeitos dos fármacos
Envelhecimento/metabolismo
Animais
Proliferação Celular/fisiologia
Sobrevivência Celular/fisiologia
Células Cultivadas
Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Experimental/fisiopatologia
Técnicas de Silenciamento de Genes
Glucuronidase/antagonistas & inibidores
Glucuronidase/genética
Seres Humanos
Insulina/secreção
Células Secretoras de Insulina/citologia
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (NF-kappa B); 56-12-2 (gamma-Aminobutyric Acid); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE


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[PMID]:28988528
[Au] Autor:Boksha IS; Prokhorova TA; Savushkina OK; Tereshkina EB
[Ad] Endereço:Mental Health Research Center, Moscow, 115522, Russia. boksha_irina@mail.ru.
[Ti] Título:Klotho Protein: Its Role in Aging and Central Nervous System Pathology.
[So] Source:Biochemistry (Mosc);82(9):990-1005, 2017 Sep.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This review is devoted to Klotho protein and recent evidences for its functions in the brain. Information on transcriptional regulation of the klotho gene and posttranslational modifications of the protein resulting in multiple forms of Klotho is reviewed. Evidence is summarized that Klotho regulates the activity of protein factors, enzymes, and receptors, including data suggesting the importance of its glycosidase activity. Effects of Klotho on components of the glutamatergic neurotransmitter system, signal cascades involving protein kinases and protein phosphorylation, as well as oligodendrocyte differentiation and myelination are discussed. A possible contribution is proposed for Klotho levels in the development of central nervous system pathologies including mental disorders.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Sistema Nervoso Central/patologia
Glucuronidase
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/metabolismo
Seres Humanos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917090024


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[PMID]:28963437
[Au] Autor:Martín-Núñez E; Donate-Correa J; López-Castillo Á; Delgado-Molinos A; Ferri C; Rodríguez-Ramos S; Cerro P; Pérez-Delgado N; Castro V; Hernández-Carballo C; Mora-Fernández C; Navarro-González JF
[Ad] Endereço:Research Unit, University Hospital Nuestra Señora de Candelaria, Carretera del Rosario, 145. 38010 Santa Cruz de Tenerife, Spain.
[Ti] Título:Soluble levels and endogenous vascular gene expression of are related to inflammation in human atherosclerotic disease.
[So] Source:Clin Sci (Lond);131(21):2601-2609, 2017 Nov 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is a chronic inflammatory disorder affecting the artery wall. Klotho, an anti-aging factor expressed in the vessel walls that participates in the maintenance of vascular homeostasis, can be down-regulated by inflammation. In this proof-of-concept work we seek to characterize the arterial expression in the vascular wall, as well as the serum concentration of this protein, in a group of patients with clinical atherosclerotic disease. In addition, we aim to analyze the relationship between Klotho and inflammation. Vascular samples were obtained from 27 patients with atherosclerotic disease under an elective vascular surgery procedure, and from 11 control subjects (cadaveric organ donation programme). qRT-PCR was performed to analyze the gene expression of , and Serum levels of soluble KLOTHO were measured by ELISA. As compared with control subjects, serum concentrations and vascular expression of Klotho were lower in patients with atherosclerotic vascular disease, whereas inflammatory status was significantly higher. There was a negative and significant correlation between inflammatory parameters and Klotho. After controlling for the effect of other variables, partial correlation showed a direct relationship between vascular gene expression and mRNA levels, whereas there was a negative association with serum LDL concentrations and vascular expression. Our study indicates an inverse interrelationship between inflammation and Klotho in atherosclerosis. Further studies are necessary to elucidate whether the inflammatory state causes Klotho deficiency or, on the contrary, reduction of Klotho could be responsible for greater inflammation, and finally, to investigate the potential clinical relevance of this association.
[Mh] Termos MeSH primário: Aterosclerose/genética
Aterosclerose/metabolismo
Expressão Gênica/fisiologia
Glucuronidase/metabolismo
Inflamação/metabolismo
[Mh] Termos MeSH secundário: Feminino
Fatores de Crescimento de Fibroblastos/genética
Fatores de Crescimento de Fibroblastos/metabolismo
Glucuronidase/deficiência
Glucuronidase/genética
Seres Humanos
Inflamação/genética
Interleucina-10/sangue
Masculino
Insuficiência Renal Crônica/sangue
Solubilidade
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, human); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); 62031-54-3 (Fibroblast Growth Factors); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171242



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