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[PMID]:29340527
[Au] Autor:Ribeiro LP; Freitas-Lima LC; Naumann GB; Meyrelles SS; Lunz W; Pires SF; Andrade HM; Carnielli JBT; Figueiredo SG
[Ad] Endereço:Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.
[Ti] Título:Cardiac protein expression patterns are associated with distinct inborn exercise capacity in non-selectively bred rats.
[So] Source:Braz J Med Biol Res;51(3):e7033, 2018 Jan 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:In the present study, we successfully demonstrated for the first time the existence of cardiac proteomic differences between non-selectively bred rats with distinct intrinsic exercise capacities. A proteomic approach based on two-dimensional gel electrophoresis coupled to mass spectrometry was used to study the left ventricle (LV) tissue proteome of rats with distinct intrinsic exercise capacity. Low running performance (LRP) and high running performance (HRP) rats were categorized by a treadmill exercise test, according to distance run to exhaustion. The running capacity of HRPs was 3.5-fold greater than LRPs. Protein profiling revealed 29 differences between HRP and LRP rats (15 proteins were identified). We detected alterations in components involved in metabolism, antioxidant and stress response, microfibrillar and cytoskeletal proteins. Contractile proteins were upregulated in the LVs of HRP rats (α-myosin heavy chain-6, myosin light chain-1 and creatine kinase), whereas the LVs of LRP rats exhibited upregulation in proteins associated with stress response (aldehyde dehydrogenase 2, α-crystallin B chain and HSPß-2). In addition, the cytoskeletal proteins desmin and α-actin were upregulated in LRPs. Taken together, our results suggest that the increased contractile protein levels in HRP rats partly accounted for their improved exercise capacity, and that proteins considered risk factors to the development of cardiovascular disease were expressed in higher amounts in LRP animals.
[Mh] Termos MeSH primário: Testes de Função Cardíaca/métodos
Miocárdio/metabolismo
Condicionamento Físico Animal/fisiologia
Proteínas/metabolismo
Corrida/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas Contráteis/metabolismo
Proteínas do Citoesqueleto/metabolismo
Desmina/metabolismo
Eletroforese em Gel Bidimensional
Ventrículos do Coração/metabolismo
Proteínas de Choque Térmico/metabolismo
Masculino
Espectrometria de Massas
Tamanho do Órgão
Proteínas/isolamento & purificação
Proteômica
Ratos
Ratos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contractile Proteins); 0 (Cytoskeletal Proteins); 0 (Desmin); 0 (Heat-Shock Proteins); 0 (Proteins)
[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:180118
[St] Status:MEDLINE


  2 / 211873 MEDLINE  
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[PMID]:28465283
[Au] Autor:Pinto SK; Lamon S; Stephenson EJ; Kalanon M; Mikovic J; Koch LG; Britton SL; Hawley JA; Camera DM
[Ad] Endereço:Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, Victoria, Australia.
[Ti] Título:Expression of microRNAs and target proteins in skeletal muscle of rats selectively bred for high and low running capacity.
[So] Source:Am J Physiol Endocrinol Metab;313(3):E335-E343, 2017 09 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Impairments in mitochondrial function and substrate metabolism are implicated in the etiology of obesity and Type 2 diabetes. MicroRNAs (miRNAs) can degrade mRNA or repress protein translation and have been implicated in the development of such disorders. We used a contrasting rat model system of selectively bred high- (HCR) or low- (LCR) intrinsic running capacity with established differences in metabolic health to investigate the molecular mechanisms through which miRNAs regulate target proteins mediating mitochondrial function and substrate oxidation processes. Quantification of select miRNAs using the rat miFinder miRNA PCR array revealed differential expression of 15 skeletal muscles (musculus tibialis anterior) miRNAs between HCR and LCR rats (14 with higher expression in LCR; < 0.05). Ingenuity Pathway Analysis predicted these altered miRNAs to collectively target multiple proteins implicated in mitochondrial dysfunction and energy substrate metabolism. Total protein abundance of citrate synthase (CS; miR-19 target) and voltage-dependent anion channel 1 (miR-7a target) were higher in HCR compared with LCR cohorts (~57 and ~26%, respectively; < 0.05). A negative correlation was observed for miR-19a-3p and CS ( = 0.32, = 0.015) protein expression. To determine whether miR-19a-3p can regulate CS in vitro, we performed luciferase reporter and transfection assays in C2C12 myotubes. MiR-19a-3p binding to the CS untranslated region did not change luciferase reporter activity; however, miR-19a-3p transfection decreased CS protein expression (∼70%; < 0.05). The differential miRNA expression targeting proteins implicated in mitochondrial dysfunction and energy substrate metabolism may contribute to the molecular basis, mediating the divergent metabolic health profiles of LCR and HCR rats.
[Mh] Termos MeSH primário: Tolerância ao Exercício/genética
MicroRNAs/metabolismo
Mitocôndrias Musculares/metabolismo
Músculo Esquelético/metabolismo
Corrida
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Citrato (si)-Sintase/metabolismo
Metabolismo Energético/genética
Técnicas In Vitro
Camundongos
Fibras Musculares Esqueléticas/metabolismo
RNA Mensageiro/metabolismo
Ratos
Ratos Endogâmicos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Canal de Ânion 1 Dependente de Voltagem/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN103 microRNA, rat); 0 (MIRN181 microRNA, rat); 0 (MIRN19 microRNA, rat); 0 (MIRN194 microRNA, rat); 0 (MIRN223 microRNA, rat); 0 (MIRN24 microRNA, rat); 0 (MIRN26 microRNA, rat); 0 (MIRN30 microRNA, rat); 0 (MicroRNAs); 0 (RNA, Messenger); EC 1.6.- (Voltage-Dependent Anion Channel 1); EC 2.3.3.1 (Citrate (si)-Synthase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00043.2017


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[PMID]:29227592
[Au] Autor:Chekhun VF; Lozovska YV; Burlaka AP; Ganusevich LI; Shvets YV; Lukyanova NY; Todor IM; Tregubova NA; Naleskina LA
[Ti] Título:Remodulating effect of doxorubicin on the state of iron-containing proteins, and redox characteristics of tumor with allowance for its sensitivity to cytostatic agents.
[So] Source:Ukr Biochem J;88(1):99-108, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The study was aimed at determining the changes of metal-containing proteins in blood serum and tumor tissue of animals with parental and doxorubicin-resistant strains of Walker-256 carcinosarcoma before and after the cytostatic administration. It has been shown that upon doxorubicin action the levels of total iron and transferrin in the tissues from the both groups of animals decreased while that of ferritine simultaneously increased with more pronounced pattern in the group of animals with resistant tumor strain. It has been shown that upon the action of doxorubicin in tumor tissue of animals with different sensitivity to the cytostatic there could be observed oppositely directed changes in the redox state of these cells that in turn determined the content of " free iron" complexes, RO S generation and concentration of active forms of matrix metaloproteinase- 2 and matrix metaloproteinase-9, namely, the increase of these indexes in animals with parental strain and their decrease in animals with the resistant one. So, our study has demonstrated the remodulating effect of doxorubicin on the state of metal-containing proteins and redox characteristics of tumor dependent on its sensitivity to cytostatic, at the levels of the tumor and an organism. These data may serve as a criterion for the development of programs for the correction of malfunction of iron metabolism aimed at elevating tumor sensitivity to cytostatic agents.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/farmacologia
Carcinoma 256 de Walker/tratamento farmacológico
Doxorrubicina/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Ferro/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma 256 de Walker/genética
Carcinoma 256 de Walker/metabolismo
Carcinoma 256 de Walker/patologia
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Ferritinas/genética
Ferritinas/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Transplante de Neoplasias
Ratos
Ratos Endogâmicos
Espécies Reativas de Oxigênio/metabolismo
Transferrina/genética
Transferrina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Reactive Oxygen Species); 0 (Transferrin); 80168379AG (Doxorubicin); 9007-73-2 (Ferritins); E1UOL152H7 (Iron); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, rat); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, rat)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.099


  4 / 211873 MEDLINE  
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[PMID]:27770464
[Au] Autor:Raschke M; Igl BW; Kenny J; Collins J; Dertinger SD; Labash C; Bhalli JA; Tebbe CC; McNeil KM; Sutter A
[Ad] Endereço:Bayer Pharma AG, Muellerstrasse 178, Berlin, 13353, Germany.
[Ti] Título:In Vivo Pig-a gene mutation assay: Guidance for 3Rs-friendly implementation.
[So] Source:Environ Mol Mutagen;57(9):678-686, 2016 12.
[Is] ISSN:1098-2280
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The rodent Pig-a assay is an in vivo method for the detection of gene mutation, where lack of glycosylphosphatidylinositol-anchored proteins on the surface of circulating red blood cells (RBCs) serves as a reporter for Pig-a gene mutation. In the case of rats, the frequency of mutant phenotype RBCs is measured via fluorescent anti-CD59 antibodies and flow cytometry. The Pig-a assay meets the growing expectations for novel approaches in animal experimentation not only focusing on the scientific value of the assay but also on animal welfare aspects (3Rs principles), for example, amenable to integration into pivotal rodent 28-day general toxicology studies. However, as recommended in the Organisation for Economic Co-operation and Development Test Guidelines for genotoxicity testing, laboratories are expected to demonstrate their proficiency. While this has historically involved the extensive use of animals, here we describe an alternative approach based on a series of blood dilutions covering a range of mutant frequencies. The experiments described herein utilized either non-fluorescent anti-CD59 antibodies to provide elevated numbers of mutant-like cells, or a low volume blood sample from a single N-ethyl-N-nitrosourea treated animal. Results from these so-called reconstruction experiments from four independent laboratories showed good overall precision (correlation coefficients: 0.9979-0.9999) and accuracy (estimated slope: 0.71-1.09) of mutant cell scoring, which was further confirmed by Bland-Altman analysis. These data strongly support the use of reconstruction experiments for training purposes and demonstrating laboratory proficiency with very few animals, an ideal situation given the typically conflicting goals of demonstrating laboratory proficiency and reducing the use of animals. Environ. Mol. Mutagen. 57:678-686, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Alternativas ao Uso de Animais
Etilnitrosoureia/toxicidade
Proteínas de Membrana/genética
Testes de Mutagenicidade/métodos
Mutagênicos/toxicidade
Mutação
[Mh] Termos MeSH secundário: Bem-Estar do Animal
Animais
Antígenos CD59/análise
Eritrócitos/efeitos dos fármacos
Eritrócitos/metabolismo
Citometria de Fluxo
Guias como Assunto
Laboratórios/normas
Masculino
Ratos Endogâmicos
Reticulócitos/efeitos dos fármacos
Reticulócitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD59 Antigens); 0 (Membrane Proteins); 0 (Mutagens); 0 (phosphatidylinositol glycan-class A protein); P8M1T4190R (Ethylnitrosourea)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/em.22060


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[PMID]:28371602
[Au] Autor:Repkova MN; Levina AS; Seryapina AA; Shikina NV; Bessudnova EV; Zarytova VF; Markel AL
[Ad] Endereço:Novosibirsk State University, Novosibirsk, 630090, Russia. markel@bionet.nsc.ru.
[Ti] Título:Toward Gene Therapy of Hypertension: Experimental Study on Hypertensive ISIAH Rats.
[So] Source:Biochemistry (Mosc);82(4):454-457, 2017 Apr.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TiO -based nanocomposites were prepared to deliver oligonucleotides into cells. The nanocomposites were designed by the immobilization of polylysine-containing oligonucleotides on TiO -nanoparticles (TiO ·PL-DNA). We showed for the first time the possibility of using the proposed nanocomposites for treatment of hypertensive disease by introducing them into hypertensive ISIAH rats developed as a model of stress-sensitive arterial hypertension. The mRNA of the gene encoding angiotensin I-converting enzyme (ACE1) involved in the synthesis of angiotensin II was chosen as a target. Administration (intraperitoneal injection and inhalation) of the nanocomposite showed a significant (by 20-30 mm Hg) decrease in systolic blood pressure when the nanocomposite contained the ACE1 gene-targeted oligonucleotide. When using the oligonucleotide with a random sequence, no effect was observed. Further development and improvement of the inhalation nanocomposite drug delivery to systemic hypertensive disease treatment promises new possibilities for clinical practice.
[Mh] Termos MeSH primário: Terapia Genética
Hipertensão/terapia
Oligonucleotídeos/administração & dosagem
Peptidil Dipeptidase A/genética
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Endogâmicos
Titânio/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligonucleotides); 15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium); EC 3.4.15.1 (Peptidyl-Dipeptidase A)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1134/S000629791704006X


  6 / 211873 MEDLINE  
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[PMID]:28315676
[Au] Autor:Yau ACY; Tuncel J; Holmdahl R
[Ad] Endereço:Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:The Major Histocompatibility Complex Class III Haplotype Ltab-Ncr3 Regulates Adjuvant-Induced but Not Antigen-Induced Autoimmunity.
[So] Source:Am J Pathol;187(5):987-998, 2017 May.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis is a complex disease associated with >100 risk loci, with the strongest association from the major histocompatibility complex (MHC) region. Here, we analyzed a new genetic association in the MHC class-III region (MHC-III) using adjuvant- and antigen-induced arthritis models. In addition, we used models for multiple sclerosis for comparison and dissected the MHC-III-mediated mechanisms of importance for antibody and T-cell responses to antigens. With the use of a panel of MHC-III recombinant inbred strains, we found that the 33-kb Ltab-Ncr3 haplotype in MHC-III was linked to the induction of arthritis with incomplete Freund's adjuvant, with similar effects in arthritis induced by several oil adjuvants (hexadecane, heptadecane, squalene, arlacel). Adoptive T-cell transfer experiment showed that this arthritis-protective effect operated during the priming of T cells by controlling their arthritogenicity. Interestingly, Ltab-Ncr3 did not regulate autoimmune diseases induced with tissue-specific antigens emulsified in adjuvant oils, such as collagen-induced arthritis or experimental autoimmune encephalomyelitis. No effect on antibody or T-cell response to tissue antigens in the Ltab-Ncr3 could be demonstrated. The finding that Ltab-Ncr3 is specific in regulating adjuvant-induced arthritis but not antigen-induced autoimmunity, and with unique effects on priming of autoreactive and arthritogenic T cells, provides new insight for understanding the regulation of autoimmune diseases.
[Mh] Termos MeSH primário: Autoimunidade/fisiologia
Complexo Principal de Histocompatibilidade/imunologia
Proteínas do Tecido Nervoso/fisiologia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/toxicidade
Animais
Área Sob a Curva
Artrite/induzido quimicamente
Artrite/imunologia
Colágeno/fisiologia
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/imunologia
Feminino
Adjuvante de Freund/toxicidade
Lipídeos/toxicidade
Masculino
Ratos Endogâmicos
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Lipids); 0 (Nerve Tissue Proteins); 0 (Vangl2 protein, rat); 0 (incomplete Freund's adjuvant); 9007-34-5 (Collagen); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE


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[PMID]:28298521
[Au] Autor:Kottom TJ; Hebrink DM; Jenson PE; Nandakumar V; Wüthrich M; Wang H; Klein B; Yamasaki S; Lepenies B; Limper AH
[Ad] Endereço:Thoracic Diseases Research Unit, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905.
[Ti] Título:The Interaction of with the C-Type Lectin Receptor Mincle Exerts a Significant Role in Host Defense against Infection.
[So] Source:J Immunol;198(9):3515-3525, 2017 May 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:pneumonia (PCP) remains a major cause of morbidity and mortality within immunocompromised patients. In this study, we examined the potential role of macrophage-inducible C-type lectin (Mincle) for host defense against Binding assays implementing soluble Mincle carbohydrate recognition domain fusion proteins demonstrated binding to intact as well as to organism homogenates, and they purified major surface glycoprotein/glycoprotein A derived from the organism. Additional experiments showed that rats with PCP expressed increased Mincle mRNA levels. Mouse macrophages overexpressing Mincle displayed increased binding to life forms and enhanced protein tyrosine phosphorylation. The binding of to Mincle resulted in activation of FcRγ-mediated cell signaling. RNA silencing of Mincle in mouse macrophages resulted in decreased activation of Syk kinase after challenge, critical in downstream inflammatory signaling. Mincle-deficient CD4-depleted (Mincle ) mice showed a significant defect in organism clearance from the lungs with higher organism burdens and altered lung cytokine responses during pneumonia. Interestingly, Mincle mice did not demonstrate worsened survival during PCP compared with wild-type mice, despite the markedly increased organism burdens. This may be related to increased expression of anti-inflammatory factors such as IL-1Ra during infection in the Mincle mice. Of note, the -infected Mincle mice demonstrated increased expression of known C-type lectin receptors Dectin-1, Dectin-2, and MCL compared with infected wild-type mice. Taken together, these data support a significant role for Mincle in modulating host defense during infection.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno
Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Proteínas de Membrana/metabolismo
Pneumocystis carinii/imunologia
Pneumonia por Pneumocystis/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Lectinas Tipo C/genética
Macrófagos/microbiologia
Masculino
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células RAW 264.7
RNA Interferente Pequeno/genética
Ratos
Ratos Endogâmicos
Transdução de Sinais/genética
Quinase Syk/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Clecsf8 protein, mouse); 0 (Lectins, C-Type); 0 (Membrane Proteins); 0 (RNA, Small Interfering); EC 2.7.10.2 (Syk Kinase); EC 2.7.10.2 (Syk protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170510
[Lr] Data última revisão:
170510
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600744


  8 / 211873 MEDLINE  
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[PMID]:28163042
[Au] Autor:Qin T; Liang T; Zhu D; Kang Y; Xie L; Dolai S; Sugita S; Takahashi N; Ostenson CG; Banks K; Gaisano HY
[Ad] Endereço:Department of Medicine, University of Toronto, Toronto, ON M5S 1A8, Canada.
[Ti] Título:Munc18b Increases Insulin Granule Fusion, Restoring Deficient Insulin Secretion in Type-2 Diabetes Human and Goto-Kakizaki Rat Islets with Improvement in Glucose Homeostasis.
[So] Source:EBioMedicine;16:262-274, 2017 Feb.
[Is] ISSN:2352-3964
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Reduced pancreatic islet levels of Munc18a/SNARE complex proteins have been postulated to contribute to the deficient glucose-stimulated insulin secretion (GSIS) in type-2 diabetes (T2D). Whereas much previous work has purported Munc18a/SNARE complex (Syntaxin-1A/VAMP-2/SNAP25) to be primarily involved in predocked secretory granule (SG) fusion, less is known about newcomer SGs that undergo minimal docking time at the plasma membrane before fusion. Newcomer SG fusion has been postulated to involve a distinct SM/SNARE complex (Munc18b/Syntaxin-3/VAMP8/SNAP25), whose levels we find also reduced in islets of T2D humans and T2D Goto-Kakizaki (GK) rats. Munc18b overexpression by adenovirus infection (Ad-Munc18b), by increasing assembly of Munc18b/SNARE complexes, mediated increased fusion of not only newcomer SGs but also predocked SGs in T2D human and GK rat islets, resulting in rescue of the deficient biphasic GSIS. Infusion of Ad-Munc18b into GK rat pancreas led to sustained improvement in glucose homeostasis. However, Munc18b overexpression in normal islets increased only newcomer SG fusion. Therefore, Munc18b could potentially be deployed in human T2D to rescue the deficient GSIS.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Glucose/metabolismo
Homeostase
Insulina/secreção
Ilhotas Pancreáticas/metabolismo
Proteínas Munc18/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
Western Blotting
Diabetes Mellitus Tipo 2/genética
Feminino
Seres Humanos
Masculino
Microscopia Confocal
Meia-Idade
Complexos Multiproteicos/metabolismo
Proteínas Munc18/genética
Proteínas Qa-SNARE/metabolismo
Proteínas R-SNARE/metabolismo
Ratos Endogâmicos
Proteína 25 Associada a Sinaptossoma/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Multiprotein Complexes); 0 (Munc18 Proteins); 0 (Qa-SNARE Proteins); 0 (R-SNARE Proteins); 0 (Synaptosomal-Associated Protein 25); 0 (VAMP8 protein, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE


  9 / 211873 MEDLINE  
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[PMID]:28130419
[Au] Autor:Matsuoka H; Shima A; Uda A; Ezaki H; Michihara A
[Ad] Endereço:Laboratory of Genome Function and Pathophysiology, Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama University, Fukuyama, Hiroshima 729-0292, Japan.
[Ti] Título:The retinoic acid receptor-related orphan receptor α positively regulates tight junction protein claudin domain-containing 1 mRNA expression in human brain endothelial cells.
[So] Source:J Biochem;161(5):441-450, 2017 May 01.
[Is] ISSN:1756-2651
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Members of the claudin family play important roles in the formation of tight junctions (TJs) in several tissues. Claudin domain containing 1 (CLDND1) is homologous to this family and localizes to TJs and the cytoplasm when exogenously expressed in cultured epithelial cell lines. Furthermore, serum antibody levels of CLDND1-derived peptides are elevated in patients with cerebral infection, cardiovascular disease or diabetes mellitus as compared to healthy controls. However, CLDND1 transcriptional regulation remains poorly analyzed and most regional transcription factor binding sites remain to be defined. Notably, the CLDND1 promoter contains a putative response element for retinoic acid receptor-related orphan receptor α (RORα), which is involved in the above-mentioned disorders. In this study, we found that Cldnd1 and Rora mRNA levels are correlated in rat tissues and that RORα overexpression in human brain endothelial cells enhanced CLDND1 transcript expression. In addition, siRNA-mediated knockdown of RORα significantly decreased CLDND1 transcription. An electrophoresis mobility shift assay indicated that RORα binds to the identified response element in a sequence-specific manner. Furthermore, luciferase reporter assays confirmed that RORα interacts with the CLDND1 promoter to enhance transcription. Taken together, our findings strongly suggest that CLDND1 is a direct RORα target.
[Mh] Termos MeSH primário: Encéfalo/citologia
Claudinas/genética
Células Endoteliais/metabolismo
Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo
RNA Mensageiro/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Células Endoteliais/efeitos dos fármacos
Perfilação da Expressão Gênica
Seres Humanos
Masculino
RNA Mensageiro/biossíntese
RNA Interferente Pequeno/farmacologia
Ratos
Ratos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CLDND1 protein, human); 0 (Claudins); 0 (Nuclear Receptor Subfamily 1, Group F, Member 1); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (RORA protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE
[do] DOI:10.1093/jb/mvw092


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[PMID]:28103056
[Au] Autor:Maruyama K; Kagota S; McGuire JJ; Wakuda H; Yoshikawa N; Nakamura K; Shinozuka K
[Ad] Endereço:a Department of Pharmacology, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, 11-68 Koshien Kyuban-cho, Nishinomiya 663-8179, Japan.
[Ti] Título:Age-related changes to vascular protease-activated receptor 2 in metabolic syndrome: a relationship between oxidative stress, receptor expression, and endothelium-dependent vasodilation.
[So] Source:Can J Physiol Pharmacol;95(4):356-364, 2017 Apr.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Protease-activated receptor 2 (PAR2) is expressed in vascular endothelium. Nitric oxide (NO) - cyclic GMP-mediated vasodilation in response to 2-furoyl-LIGRLO-amide (2fLIGRLO), a PAR2-activating peptide, is impaired in aortas from aged SHRSP.Z-Lepr /IzmDmcr (SHRSP.ZF) rats with metabolic syndrome. Here we investigated mechanisms linking PAR2's vascular effects to phenotypic characteristics of male SHRSP.ZF rats at 10, 20, and 30 weeks of age. We found vasodilation responses to either 2fLIGRLO or enzyme-mediated PAR2 activation by trypsin were sustained until 20 weeks and lessened at 30 weeks. PAR2 protein and mRNA levels were lower in aortas at 30 weeks than at 10 and 20 weeks. PAR2-mediated responses positively correlated with PAR2 protein and mRNA levels. Decreased cGMP accumulation in the presence of 2fLIGRLO paralleled the decreased relaxations elicited by nitroprusside and the cGMP analog 8-pCPT-cGMP, and the less soluble guanylyl cyclase protein at 30 weeks. 2fLIGRLO-induced relaxation was negatively correlated with serum thiobarbituric acid reactive substances, an index of oxidative stress, which increased with age. Forward stepwise data regression supported a model of age-related decreases in PAR2 function resulting from decreased PAR2 mRNA and increased oxidative stress. We conclude that decreased responsiveness of aortic smooth muscle to NO and downregulation of receptor expression impair PAR2 functions at later stages of metabolic syndrome in SHRSP.ZF rats.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Endotélio Vascular/metabolismo
Síndrome Metabólica/metabolismo
Estresse Oxidativo/fisiologia
Receptor PAR-2/metabolismo
Vasodilatação/fisiologia
[Mh] Termos MeSH secundário: Animais
Aorta/metabolismo
GMP Cíclico/análogos & derivados
GMP Cíclico/metabolismo
GMP Cíclico/farmacologia
Modelos Animais de Doenças
Regulação para Baixo
Expressão Gênica/fisiologia
Masculino
Óxido Nítrico/metabolismo
Nitroprussiato/farmacologia
Oligopeptídeos/farmacologia
RNA Mensageiro/metabolismo
Ratos
Ratos Endogâmicos
Receptor PAR-2/agonistas
Substâncias Reativas com Ácido Tiobarbitúrico/análise
Tionucleotídeos/farmacologia
Tripsina/farmacologia
Vasodilatadores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-furoyl-LIGRLO-amide); 0 (Oligopeptides); 0 (RNA, Messenger); 0 (Receptor, PAR-2); 0 (Thiobarbituric Acid Reactive Substances); 0 (Thionucleotides); 0 (Vasodilator Agents); 169D1260KM (Nitroprusside); 31C4KY9ESH (Nitric Oxide); 54364-02-2 (8-((4-chlorophenyl)thio)cyclic-3',5'-GMP); EC 3.4.21.4 (Trypsin); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0298



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