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Pesquisa : A10.272.491 [Categoria DeCS]
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[PMID]:28457941
[Au] Autor:Menazza S; Sun J; Appachi S; Chambliss KL; Kim SH; Aponte A; Khan S; Katzenellenbogen JA; Katzenellenbogen BS; Shaul PW; Murphy E
[Ad] Endereço:Systems Biology Center, National Heart Lung and Blood Institute, NIH, Bethesda, MD, United States.
[Ti] Título:Non-nuclear estrogen receptor alpha activation in endothelium reduces cardiac ischemia-reperfusion injury in mice.
[So] Source:J Mol Cell Cardiol;107:41-51, 2017 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERß, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with estradiol significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocked the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERß, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERß. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Isquemia/genética
Traumatismo por Reperfusão/genética
[Mh] Termos MeSH secundário: Animais
Endotélio/metabolismo
Endotélio/patologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Isquemia/metabolismo
Isquemia/patologia
Camundongos
Ovariectomia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Receptores Estrogênicos/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens); 0 (GPR30 protein, mouse); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  2 / 18535 MEDLINE  
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[PMID]:29249275
[Au] Autor:Litvinov RI
[Ad] Endereço:Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA; Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russian Federation. Electronic address: litvinov@pennmedicine.upenn.edu.
[Ti] Título:Fibrin opens the "gate" for leukocytes in the endothelium.
[So] Source:Thromb Res;162:101-103, 2018 02.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Fibrina
Leucócitos
[Mh] Termos MeSH secundário: Endotélio
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
9001-31-4 (Fibrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


  3 / 18535 MEDLINE  
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[PMID]:29388836
[Au] Autor:Kwapiszewska G; Crnkovic S; Stenmark KR
[Ad] Endereço:1 Ludwig Boltzmann Institute for Lung Vascular Research Graz, Austria and.
[Ti] Título:A Twist on Pulmonary Vascular Remodeling: Endothelial to Mesenchymal Transition?
[So] Source:Am J Respir Cell Mol Biol;58(2):140-141, 2018 02.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Actinas/metabolismo
Endotélio/citologia
Hipertensão Pulmonar/patologia
Proteínas Nucleares/metabolismo
Proteína 1 Relacionada a Twist/metabolismo
Remodelação Vascular/fisiologia
[Mh] Termos MeSH secundário: Transição Epitelial-Mesenquimal/fisiologia
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Nuclear Proteins); 0 (TWIST1 protein, human); 0 (Twist-Related Protein 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0314ED


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[PMID]:29172521
[Au] Autor:Wang Z; Cui Y; Liu P; Zhao Y; Wang L; Liu Y; Xie J
[Ad] Endereço:Laboratory of Quality & Safety Risk Assessment for Aquatic Products on Storage and Preservation (Shanghai), Ministry of Agriculture , Shanghai 201306, China.
[Ti] Título:Small Peptides Isolated from Enzymatic Hydrolyzate of Fermented Soybean Meal Promote Endothelium-Independent Vasorelaxation and ACE Inhibition.
[So] Source:J Agric Food Chem;65(50):10844-10850, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fermentation of soybean is a process in which soy proteins are broken down into small peptides to exert various physiological functions beyond their nutritional value and to improve food source bioactive components responsible for health benefits. Enzymatic hydrolysis could speed up the degradation of proteins during fermentation of soybean, thus resulting in higher peptide production. In the present study, fermented soy meal (fermented with Bacillus subtilis from Douchi) was hydrolyzed by thermolysin, and the water extraction was then separated into four fractions using ultrafiltration membranes. Their vasorelaxation activities were screened, and the most potent fraction was further isolated and purified to obtain four peptides. Briefly, three peptides exerted a dose-dependent vasorelaxation (0.01-4.10 µM) in the phenylephrine preconstricted thoracic aorta ring of Sprague-Dawley rat (relaxation actions were all endothelium-independent), while one peptide induced vasoconstriction. Furthermore, an independent causal relationship between vasorelaxation and angiotensin converting enzyme (ACE) inhibition activities was found.
[Mh] Termos MeSH primário: Inibidores da Enzima Conversora de Angiotensina/administração & dosagem
Bacillus subtilis/metabolismo
Endotélio/efeitos dos fármacos
Hipertensão/tratamento farmacológico
Peptídeos/administração & dosagem
Feijão de Soja/química
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/química
Inibidores da Enzima Conversora de Angiotensina/metabolismo
Animais
Endotélio/fisiopatologia
Fermentação
Seres Humanos
Hidrólise
Hipertensão/fisiopatologia
Masculino
Peptídeos/química
Peptídeos/metabolismo
Ratos
Ratos Sprague-Dawley
Proteínas de Soja/química
Proteínas de Soja/metabolismo
Feijão de Soja/metabolismo
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Peptides); 0 (Soybean Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b05026


  5 / 18535 MEDLINE  
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[PMID]:27770854
[Au] Autor:Das ND; Yin GN; Choi MJ; Song KM; Park JM; Limanjaya A; Ghatak K; Minh NN; Ock J; Park SH; Kim HM; Ryu JK; Suh JK
[Ad] Endereço:National Research Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, Incheon, Republic of Korea; Epigenetics Drug Discovery Unit, Division of Structural and Synthetic Biology, RIKEN Center for Life Science Technologies, Suehiro-cho, Yokohama, Japan.
[Ti] Título:Effectiveness of Intracavernous Delivery of Recombinant Human Hepatocyte Growth Factor on Erectile Function in the Streptozotocin-Induced Diabetic Mouse.
[So] Source:J Sex Med;13(11):1618-1628, 2016 11.
[Is] ISSN:1743-6109
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Diabetic erectile dysfunction is a disease mostly of vascular origin and men with diabetic erectile dysfunction respond poorly to oral phosphodiesterase-5 inhibitors. Hepatocyte growth factor (HGF) is a pleiotropic factor that plays an essential role in the regulation of cell proliferation, survival, and angiogenesis. AIM: To determine the effectiveness of recombinant human (rh)-HGF in restoring erectile function in diabetic mice. METHODS: Four groups of mice were used: control non-diabetic mice and streptozotocin-induced diabetic mice receiving two successive intracavernous injections of phosphate buffered saline (days -3 and 0), a single intracavernous injection of rh-HGF (day 0), or two successive intracavernous injections of rh-HGF (days -3 and 0). We also examined the effect of rh-HGF in primary cultured mouse cavernous endothelial cells and in major pelvic ganglion culture in vitro, which was incubated under a normal-glucose (5 mmol/L) or a high-glucose (30 mmol/L) condition. MAIN OUTCOME MEASURES: Two weeks after treatment, we measured erectile function by electrical stimulation of the cavernous nerve and the penis was harvested for histologic studies. RESULTS: Repeated intracavernous injections of rh-HGF protein induced significant restoration of erectile function in diabetic mice (89-100% of control values), whereas a single intracavernous injection of rh-HGF protein elicited modest improvement. Rh-HGF significantly induced phosphorylation of its receptor c-Met, increased the content of endothelial cells and smooth muscle cells, and decreased the generation of reactive oxygen species (superoxide anion and peroxynitrite) and extravasation of oxidized low-density lipoprotein in diabetic mice. Under the high-glucose condition, rh-HGF protein also promoted tube formation in mouse cavernous endothelial cells and enhanced neurite sprouting in major pelvic ganglion culture in vitro. CONCLUSION: The dual angiogenic and neurotrophic effects of HGF could open a new avenue through which diabetic erectile dysfunction can be treated.
[Mh] Termos MeSH primário: Disfunção Erétil/tratamento farmacológico
Fator de Crescimento de Hepatócito/farmacologia
Ereção Peniana/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/fisiologia
Diabetes Mellitus Experimental/fisiopatologia
Células Endoteliais/citologia
Células Endoteliais/fisiologia
Endotélio/metabolismo
Disfunção Erétil/fisiopatologia
Seres Humanos
Injeções Intralesionais
Lipoproteínas LDL/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Óxido Nítrico Sintase Tipo III/metabolismo
Pênis/irrigação sanguínea
Inibidores da Fosfodiesterase 5/farmacologia
Fosforilação/fisiologia
Ratos Sprague-Dawley
Proteínas Recombinantes/farmacologia
Regeneração/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipoproteins, LDL); 0 (Phosphodiesterase 5 Inhibitors); 0 (Recombinant Proteins); 0 (oxidized low density lipoprotein); 67256-21-7 (Hepatocyte Growth Factor); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171207
[Lr] Data última revisão:
171207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  6 / 18535 MEDLINE  
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[PMID]:28922850
[Au] Autor:Korkmaz E; Kleinloog R; Verweij BH; Allijn IE; Hekking LHP; Regli L; Rinkel GJE; Ruigrok YM; Andries Post J
[Ad] Endereço:Department of Biology, Biomolecular Imaging and Cell Biology, Faculty of Science, Utrecht University, Utrecht, The Netherlands; Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands; Department of Neurosurgery, University Ho
[Ti] Título:Comparative Ultrastructural and Stereological Analyses of Unruptured and Ruptured Saccular Intracranial Aneurysms.
[So] Source:J Neuropathol Exp Neurol;76(10):908-916, 2017 Oct 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Insight into processes leading to rupture of intracranial aneurysms (IAs) may identify biomarkers for rupture or lead to management strategies reducing the risk of rupture. We characterized and quantified (ultra)structural differences between unruptured and ruptured aneurysmal walls. Six unruptured and 6 ruptured IA fundi were resected after microsurgical clipping and analyzed by correlative light microscopy for quantitative analysis (proportion of the vessel wall area) and transmission electron microscopy for qualitative ultrastructural analysis. Quantitative analysis revealed extensive internal elastic lamina (IEL) thickening in ruptured IA (36.3% ± 15%), while thin and fragmented IEL were common in unruptured IA (5.6% ± 7.1%). Macrophages were increased in ruptured IA (28.3 ± 24%) versus unruptured IA (2.7% ± 5.5%), as were leukocytes (12.85% ± 10% vs 0%). Vasa vasorum in ruptured but not in unruptured IA contained vast numbers of inflammatory cells and extravasation of these cells into the vessel wall. In conclusion, detection of thickened IEL, leaky vasa vasorum, and heavy inflammation as seen in ruptured IA in comparison to unruptured IA may identify aneurysms at risk of rupture, and management strategies preventing development of vasa vasorum or inflammation may reduce the risk of aneurysmal rupture.
[Mh] Termos MeSH primário: Aneurisma Roto/patologia
Vasos Sanguíneos/patologia
Vasos Sanguíneos/ultraestrutura
Aneurisma Intracraniano/patologia
Técnicas Estereotáxicas
[Mh] Termos MeSH secundário: Adulto
Idoso
Endotélio/patologia
Endotélio/ultraestrutura
Feminino
Seres Humanos
Masculino
Microscopia Eletrônica de Transmissão
Meia-Idade
Músculo Liso/patologia
Músculo Liso/ultraestrutura
Plasmócitos/patologia
Plasmócitos/ultraestrutura
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx075


  7 / 18535 MEDLINE  
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[PMID]:28919237
[Au] Autor:Vercellino M; Trebini C; Capello E; Mancardi GL; Giordana MT; Cavalla P
[Ad] Endereço:Città della Salute e della Scienza di Torino University Hospital, Department of Neuroscience, Via Cherasco 15, 10126 Torino, Italy. Electronic address: mvercellino@cittadellasalute.to.it.
[Ti] Título:Inflammatory responses in Multiple Sclerosis normal-appearing white matter and in non-immune mediated neurological conditions with wallerian axonal degeneration: A comparative study.
[So] Source:J Neuroimmunol;312:49-58, 2017 Nov 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Inflammatory-like changes in the white matter (WM) are commonly observed in conditions of axonal degeneration by different etiologies. This study is a systematic comparison of the principal features of the inflammatory-like changes in the WM in different pathological conditions characterized by axonal damage/degeneration, focusing in particular on Multiple Sclerosis (MS) normal-appearing white matter (NAWM) compared to non immune-mediated disorders. The study was performed on sections of NAWM from 15 MS cases, 11 cases of non immune-mediated disorders with wallerian axonal degeneration (stroke, trauma, amyotrophic lateral sclerosis), 3 cases of viral encephalitis, 6 control cases. Common features of the inflammatory-like changes observed in all of the conditions of WM pathology were diffuse endothelial expression of VCAM-1, microglial activation with expression of M2 markers, increased expression of sphingosine receptors. Inflammation in MS NAWM was characterized, compared to non immune-mediated conditions, by higher VCAM-1 expression, higher density of perivascular lymphocytes, focal perivascular inflammation with microglial expression of M1 markers, ongoing acute axonal damage correlating with VCAM-1 expression but not with microglia activation. Inflammatory changes in MS NAWM share all the main features observed in the WM in non immune-mediated conditions with wallerian axonal degeneration (with differences to a large extent more quantitative than qualitative), but with superimposition of disease-specific perivascular inflammation and ongoing acute axonal damage.
[Mh] Termos MeSH primário: Inflamação/etiologia
Esclerose Múltipla/complicações
Degeneração Walleriana/complicações
Substância Branca/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD/metabolismo
Barreira Hematoencefálica/fisiopatologia
Encefalite Viral/metabolismo
Encefalite Viral/patologia
Endotélio/metabolismo
Endotélio/patologia
Feminino
Seres Humanos
Linfócitos/metabolismo
Linfócitos/patologia
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Esclerose Múltipla/patologia
Óxido Nítrico Sintase Tipo II/metabolismo
Molécula 1 de Adesão de Célula Vascular/metabolismo
Degeneração Walleriana/patologia
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Vascular Cell Adhesion Molecule-1); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28806774
[Au] Autor:Sahni A; Patel J; Narra HP; Schroeder CLC; Walker DH; Sahni SK
[Ad] Endereço:Department of Pathology, University of Texas Medical Branch, Galveston, Texas, United States of America.
[Ti] Título:Fibroblast growth factor receptor-1 mediates internalization of pathogenic spotted fever rickettsiae into host endothelium.
[So] Source:PLoS One;12(8):e0183181, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rickettsial infections continue to cause serious morbidity and mortality in severe human cases around the world. Host cell adhesion and invasion is an essential requisite for intracellular growth, replication, and subsequent dissemination of pathogenic rickettsiae. Heparan sulfate proteoglycans [HSPGs] facilitate the interactions between fibroblast growth factor(s) and their tyrosine kinase receptors resulting in receptor dimerization/activation and have been implicated in bacterial adhesion to target host cells. In the present study, we have investigated the contributions of fibroblast growth factor receptors [FGFRs] in rickettsial entry into the host cells. Inhibition of HSPGs by heparinase and FGFRs by AZD4547 (a selective small-molecule inhibitor) results in significant reduction in rickettsial internalization into cultured human microvascular endothelial cells (ECs), which represent the primary targets of pathogenic rickettsiae during human infections. Administration of AZD4547 during R. conorii infection in a murine model of endothelial-target spotted fever rickettsiosis also diminishes pulmonary rickettsial burden in comparison to mock-treated controls. Silencing of FGFR1 expression using a small interfering RNA also leads to similar inhibition of R. rickettsii invasion into ECs. Consistent with these findings, R. rickettsii infection of ECs also results in phosphorylation of tyrosine 653/654, suggesting activation of FGFR1. Using isobaric tag for relative and absolute quantitation [iTRAQ]-based proteomics approach, we further demonstrate association of ß-peptide of rickettsial outer membrane protein OmpA with FGFR1. Mechanistically, FGFR1 binds to caveolin-1 and mediates bacterial entry via caveolin-1 dependent endocytosis. Together, these results identify host cell FGFR1 and rickettsial OmpA as another novel receptor-ligand pair contributing to the internalization of pathogenic rickettsiae into host endothelial cells and the potential application of FGFR-inhibitor drugs as adjunct therapeutics against spotted fever rickettsioses.
[Mh] Termos MeSH primário: Febre Botonosa/metabolismo
Febre Botonosa/microbiologia
Endocitose
Endotélio/microbiologia
Interações Hospedeiro-Patógeno
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/metabolismo
Rickettsia/fisiologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Proteínas da Membrana Bacteriana Externa/química
Proteínas da Membrana Bacteriana Externa/metabolismo
Caveolina 1/metabolismo
Caveolina 2/metabolismo
Modelos Animais de Doenças
Endotélio/patologia
Técnicas de Silenciamento de Genes
Proteoglicanas de Heparan Sulfato/metabolismo
Seres Humanos
Peptídeos/química
Peptídeos/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Outer Membrane Proteins); 0 (Caveolin 1); 0 (Caveolin 2); 0 (Heparan Sulfate Proteoglycans); 0 (Peptides); 149024-69-1 (OMPA outer membrane proteins); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183181


  9 / 18535 MEDLINE  
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[PMID]:28715462
[Au] Autor:Itoh Y; Voskuhl RR
[Ad] Endereço:Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, United States of America.
[Ti] Título:Cell specificity dictates similarities in gene expression in multiple sclerosis, Parkinson's disease, and Alzheimer's disease.
[So] Source:PLoS One;12(7):e0181349, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Drug repurposing is an efficient approach in new treatment development since it leverages previous work from one disease to another. While multiple sclerosis (MS), Parkinson's disease (PD), and Alzheimer's disease (AD) are all neurodegenerative diseases of the central nervous system (CNS) and differ in many clinical and pathological aspects, it is possible that they may share some mechanistic features. We hypothesized that focusing on gene expression in a CNS cell type specific manner might uncover similarities between diseases that could be missed using whole tissue gene expression analyses. We found similarities and differences in gene expression in these three distinct diseases, depending upon cell type. Microglia genes were increased in all three diseases, and gene expression levels were correlated strongly among these three neurodegenerative diseases. In astrocytes and endothelia, upregulation and correlations were observed only between MS and PD, but not AD. Neuronal genes were down-regulated in all three diseases, but correlations of changes of individual genes between diseases were not strong. Oligodendrocyte showed gene expression changes that were not shared among the three diseases. Together these data suggest that treatments targeting microglia are most amenable to drug repurposing in MS, PD, and AD, while treatments targeting other CNS cells must be tailored to each disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Misturas Complexas/metabolismo
Expressão Gênica/fisiologia
Esclerose Múltipla/metabolismo
Doença de Parkinson/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Astrócitos/metabolismo
Endotélio/metabolismo
Feminino
Seres Humanos
Masculino
Análise em Microsséries
Microglia/metabolismo
Meia-Idade
Neurônios/metabolismo
Oligodendroglia/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complex Mixtures); 0 (Frondanol-A5P)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181349


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[PMID]:28696548
[Au] Autor:Ly H; Verma N; Wu F; Liu M; Saatman KE; Nelson PT; Slevin JT; Goldstein LB; Biessels GJ; Despa F
[Ad] Endereço:Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY.
[Ti] Título:Brain microvascular injury and white matter disease provoked by diabetes-associated hyperamylinemia.
[So] Source:Ann Neurol;82(2):208-222, 2017 Aug.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The brain blood vessels of patients with type 2 diabetes and dementia have deposition of amylin, an amyloidogenic hormone cosecreted with insulin. It is not known whether vascular amylin deposition is a consequence or a trigger of vascular injury. We tested the hypothesis that the vascular amylin deposits cause endothelial dysfunction and microvascular injury and are modulated by amylin transport in the brain via plasma apolipoproteins. METHODS: Rats overexpressing amyloidogenic (human) amylin in the pancreas (HIP rats) and amylin knockout (AKO) rats intravenously infused with aggregated amylin were used for in vivo phenotyping. We also carried out biochemical analyses of human brain tissues and studied the effects of the aggregated amylin on endothelial cells ex vivo. RESULTS: Amylin deposition in brain blood vessels is associated with vessel wall disruption and abnormal surrounding neuropil in patients with type 2 diabetes and dementia, in HIP rats, and in AKO rats infused with aggregated amylin. HIP rats have brain microhemorrhages, white matter injury, and neurologic deficits. Vascular amylin deposition provokes loss of endothelial cell coverage and tight junctions. Intravenous infusion in AKO rats of human amylin, or combined human amylin and apolipoprotein E4, showed that amylin binds to plasma apolipoproteins. The intravenous infusion of apolipoprotein E4 exacerbated the brain accumulation of aggregated amylin and vascular pathology in HIP rats. INTERPRETATION: These data identify vascular amylin deposition as a trigger of brain endothelial dysfunction that is modulated by plasma apolipoproteins and represents a potential therapeutic target in diabetes-associated dementia and stroke. Ann Neurol 2017;82:208-222.
[Mh] Termos MeSH primário: Encéfalo/patologia
Diabetes Mellitus Tipo 2/patologia
Polipeptídeo Amiloide das Ilhotas Pancreáticas/efeitos adversos
Leucoencefalopatias/induzido quimicamente
Leucoencefalopatias/patologia
Microvasos/metabolismo
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Animais
Apolipoproteína E4/administração & dosagem
Apolipoproteína E4/efeitos adversos
Encéfalo/irrigação sanguínea
Encéfalo/efeitos dos fármacos
Células Cultivadas
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/complicações
Sinergismo Farmacológico
Endotélio/metabolismo
Técnicas de Inativação de Genes
Seres Humanos
Hemorragias Intracranianas/induzido quimicamente
Polipeptídeo Amiloide das Ilhotas Pancreáticas/sangue
Polipeptídeo Amiloide das Ilhotas Pancreáticas/metabolismo
Leucoencefalopatias/sangue
Leucoencefalopatias/complicações
Imagem por Ressonância Magnética
Aprendizagem em Labirinto/efeitos dos fármacos
Destreza Motora/efeitos dos fármacos
Neuroimagem
Pâncreas/metabolismo
Ratos
Ratos Mutantes
Junções Íntimas/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoprotein E4); 0 (Islet Amyloid Polypeptide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24992



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