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Pesquisa : D12.644.276.374.750.186 [Categoria DeCS]
Referências encontradas : 613 [refinar]
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  1 / 613 MEDLINE  
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[PMID]:29254303
[Au] Autor:Abbasi MH; Fatima S; Khawar MB; Naz N; Mujeeb KA; Akhtar T; Sheikh N
[Ad] Endereço:Department of Zoology, Government College of Science, Lahore, Pakistan.
[Ti] Título:Dose-dependent acute phase response of aqueous leaf decoction of Nerium oleander in Wistar rats.
[So] Source:J Biol Regul Homeost Agents;31(4):985-989, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Many studies have been carried out in order to determine the toxicity of medicinal plants. The objective of this study was to compare and analyze the hepatic response against two doses of Nerium oleander, (N. oleander) “kaner” leaf decoction. Aqueous leaf decoction was injected intramuscularly into both hind limbs of male rats (200∓10g), assigned into three categories (n=4): control group with no treatment; group I, injected with 5 ml/ kg; and group II injected with 10 ml/ kg of leaf decoction, respectively. Animals were sacrificed 6 h after administration and hepato-histological changes were then observed. The decoction induced an acute phase reaction reflected by a more significant recruitment of inflammatory cells in group II than in group I and controls, as observed by histological studies. These results indicated that both doses can induce an acute-phase condition. Hence, traditional practice of medicinal plants without preliminary dose assessment must not be administered.
[Mh] Termos MeSH primário: Reação de Fase Aguda/induzido quimicamente
Fígado/efeitos dos fármacos
Nerium/química
Extratos Vegetais/efeitos adversos
Folhas de Planta/química
[Mh] Termos MeSH secundário: Reação de Fase Aguda/imunologia
Reação de Fase Aguda/patologia
Animais
Biomarcadores/metabolismo
Relação Dose-Resposta Imunológica
Ectodisplasinas/imunologia
Ectodisplasinas/metabolismo
Imuno-Histoquímica
Injeções Intramusculares
Fígado/imunologia
Fígado/patologia
Masculino
Plantas Medicinais
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Ectodysplasins); 0 (Plant Extracts)
[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:171220
[St] Status:MEDLINE


  2 / 613 MEDLINE  
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[PMID]:28877528
[Au] Autor:Savasta S; Carlone G; Castagnoli R; Chiappe F; Bassanese F; Piras R; Salpietro V; Brazzelli V; Verrotti A; Marseglia GL
[Ad] Endereço:Department of Pediatrics, Fondazione Policlinico San Matteo IRCCS, University of Pavia, Pavia, Italy.
[Ti] Título:X-Linked Hypohidrotic Ectodermal Dysplasia: New Features and a Novel EDA Gene Mutation.
[So] Source:Cytogenet Genome Res;152(3):111-116, 2017.
[Is] ISSN:1424-859X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:We described a 5-year-old male with hypodontia, hypohidrosis, and facial dysmorphisms characterized by a depressed nasal bridge, maxillary hypoplasia, and protuberant lips. Chromosomal analysis revealed a normal 46,XY male karyotype. Due to the presence of clinical features of hypohidrotic ectodermal dysplasia (HED), the EDA gene, located at Xq12q13.1, of the patient and his family was sequenced. Analysis of the proband's sequence revealed a missense mutation (T to A transversion) in hemizygosity state at nucleotide position 158 in exon 1 of the EDA gene, which changes codon 53 from leucine to histidine, while heterozygosity at this position was detected in the slightly affected mother; moreover, this mutation was not found in the publically available Human Gene Mutation Database. To date, our findings indicate that a novel mutation in EDA is associated with X-linked HED, adding it to the repertoire of EDA mutations.
[Mh] Termos MeSH primário: Displasia Ectodérmica Anidrótica Tipo 1/genética
Ectodisplasinas/genética
Mutação de Sentido Incorreto
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Anodontia/genética
Anodontia/patologia
Pré-Escolar
Códon
Análise Mutacional de DNA
Displasia Ectodérmica Anidrótica Tipo 1/patologia
Feminino
Genes Ligados ao Cromossomo X
Hemizigoto
Heterozigoto
Histidina/genética
Seres Humanos
Hipo-Hidrose/genética
Hipo-Hidrose/patologia
Leucina/genética
Lábio/anormalidades
Masculino
Maxila/anormalidades
Osso Nasal/anormalidades
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); 0 (EDA protein, human); 0 (Ectodysplasins); 4QD397987E (Histidine); GMW67QNF9C (Leucine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1159/000478922


  3 / 613 MEDLINE  
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[PMID]:28813629
[Au] Autor:Fons Romero JM; Star H; Lav R; Watkins S; Harrison M; Hovorakova M; Headon D; Tucker AS
[Ad] Endereço:1 Department of Craniofacial Development and Stem Cell Biology, King's College London, London, UK.
[Ti] Título:The Impact of the Eda Pathway on Tooth Root Development.
[So] Source:J Dent Res;96(11):1290-1297, 2017 Oct.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Eda pathway ( Eda, Edar, Edaradd) plays an important role in tooth development, determining tooth number, crown shape, and enamel formation. Here we show that the Eda pathway also plays a key role in root development. Edar (the receptor) is expressed in Hertwig's epithelial root sheath (HERS) during root development, with mutant mice showing a high incidence of taurodontism: large pulp chambers lacking or showing delayed bifurcation or trifurcation of the roots. The mouse upper second molars in the Eda pathway mutants show the highest incidence of taurodontism, this enhanced susceptibility being matched in human patients with mutations in EDA-A1. These taurodont teeth form due to defects in the direction of extension of the HERS from the crown, associated with a more extensive area of proliferation of the neighboring root mesenchyme. In those teeth where the angle at which the HERS extends from the crown is very wide and therefore more vertical, the mutant HERSs fail to reach toward the center of the tooth in the normal furcation region, and taurodont teeth are created. The phenotype is variable, however, with milder changes in angle and proliferation leading to normal or delayed furcation. This is the first analysis of the role of Eda in the root, showing a direct role for this pathway during postnatal mouse development, and it suggests that changes in proliferation and angle of HERS may underlie taurodontism in a range of syndromes.
[Mh] Termos MeSH primário: Cavidade Pulpar/anormalidades
Ectodisplasinas/genética
Dente Molar/anormalidades
Dente Molar/embriologia
Anormalidades Dentárias/genética
Raiz Dentária/anormalidades
Raiz Dentária/embriologia
[Mh] Termos MeSH secundário: Adolescente
Animais
Criança
Seres Humanos
Masculino
Camundongos
Odontogênese/genética
Fenótipo
Transdução de Sinais
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDA protein, human); 0 (Ectodysplasins); 0 (Eda protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517725692


  4 / 613 MEDLINE  
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[PMID]:28655773
[Au] Autor:Li S; Zhou J; Bu J; Ning K; Zhang L; Li J; Guo Y; He X; He H; Cai X; Chen Y; Reinach PS; Liu Z; Li W
[Ad] Endereço:From the Eye Institute of Xiamen University, Xiamen, Fujian 361102.
[Ti] Título:Ectodysplasin A protein promotes corneal epithelial cell proliferation.
[So] Source:J Biol Chem;292(32):13391-13401, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gene encodes ectodysplasin A (Eda), which if mutated causes X-linked hypohidrotic ectodermal dysplasia (XLHED) disease in humans. Ocular surface changes occur in XLHED patients whereas its underlying mechanism remains elusive. In this study, we found Eda was highly expressed in meibomian glands, and it was detected in human tears but not serum. Corneal epithelial integrity was defective and the thickness was reduced in the early postnatal stage of mutant mice. Corneal epithelial cell proliferation decreased and the epithelial wound healing was delayed in mice, whereas it was restored by exogenous Eda. Eda exposure promoted mouse corneal epithelial wound healing during organ culture, whereas scratch wound assay showed that it did not affect human corneal epithelial cell line migration. Epidermal growth factor receptor (EGFR), phosphorylated EGFR (p-EGFR), and phosphorylated ERK1/2 (p-ERK) were down-regulated in mice corneal epithelium. Eda treatment up-regulated the expression of Ki67, EGFR, EGFR, and ERK in human corneal epithelial cells in a dose-dependent manner. In conclusion, Eda protein can be secreted from meibomian glands and promotes corneal epithelial cell proliferation through regulation of the EGFR signaling pathway. Eda release into the tears plays an essential role in the maintenance of corneal epithelial homeostasis.
[Mh] Termos MeSH primário: Displasia Ectodérmica Anidrótica Tipo 1/metabolismo
Ectodisplasinas/metabolismo
Epitélio Anterior/metabolismo
Doenças Palpebrais/metabolismo
Glândulas Tarsais/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Displasia Ectodérmica Anidrótica Tipo 1/tratamento farmacológico
Displasia Ectodérmica Anidrótica Tipo 1/patologia
Displasia Ectodérmica Anidrótica Tipo 1/fisiopatologia
Ectodisplasinas/genética
Ectodisplasinas/farmacologia
Ectodisplasinas/uso terapêutico
Epitélio Anterior/efeitos dos fármacos
Epitélio Anterior/lesões
Epitélio Anterior/patologia
Doenças Palpebrais/patologia
Doenças Palpebrais/fisiopatologia
Feminino
Seres Humanos
Masculino
Glândulas Tarsais/patologia
Glândulas Tarsais/fisiopatologia
Camundongos Mutantes
Técnicas de Cultura de Órgãos
Fosforilação
Processamento de Proteína Pós-Traducional
Receptor do Fator de Crescimento Epidérmico/metabolismo
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/farmacologia
Proteínas Recombinantes/uso terapêutico
Transdução de Sinais
Lágrimas/metabolismo
Cicatrização/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDA protein, human); 0 (Ectodysplasins); 0 (Eda protein, mouse); 0 (Recombinant Proteins); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.803809


  5 / 613 MEDLINE  
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[PMID]:28106506
[Au] Autor:Podzus J; Kowalczyk-Quintas C; Schuepbach-Mallepell S; Willen L; Staehlin G; Vigolo M; Tardivel A; Headon D; Kirby N; Mikkola ML; Schneider H; Schneider P
[Ad] Endereço:1 Department of Pediatrics, University Hospital Erlangen, Germany.
[Ti] Título:Ectodysplasin A in Biological Fluids and Diagnosis of Ectodermal Dysplasia.
[So] Source:J Dent Res;96(2):217-224, 2017 Feb.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor necrosis factor (TNF) family ligand ectodysplasin A (EDA) is produced as 2 full-length splice variants, EDA1 and EDA2, that bind to EDA receptor (EDAR) and X-linked EDA receptor (XEDAR/EDA2R), respectively. Inactivating mutations in Eda or Edar cause hypohidrotic ectodermal dysplasia (HED), a condition characterized by malformations of the teeth, hair and glands, with milder deficiencies affecting only the teeth. EDA acts early during the development of ectodermal appendages-as early as the embryonic placode stage-and plays a role in adult appendage function. In this study, the authors measured EDA in serum, saliva and dried blood spots. The authors detected 3- to 4-fold higher levels of circulating EDA in cord blood than in adult sera. A receptor binding-competent form of EDA1 was the main form of EDA but a minor fraction of EDA2 was also found in fetal bovine serum. Sera of EDA-deficient patients contained either background EDA levels or low levels of EDA that could not bind to recombinant EDAR. The serum of a patient with a V262F missense mutation in Eda, which caused a milder form of X-linked HED (XLHED), contained low levels of EDA capable of binding to EDAR. In 2 mildly affected carriers, intermediate levels of EDA were detected, whereas a severely affected carrier had no active EDA in the serum. Small amounts of EDA were also detectable in normal adult saliva. Finally, EDA could be measured in spots of wild-type adult or cord blood dried onto filter paper at levels significantly higher than that measured in EDA-deficient blood. Measurement of EDA levels combined with receptor-binding assays might be of relevance to aid in the diagnosis of total or partial EDA deficiencies.
[Mh] Termos MeSH primário: Displasia Ectodérmica/diagnóstico
Ectodisplasinas/análise
[Mh] Termos MeSH secundário: Adulto
Animais
Biomarcadores/análise
Biomarcadores/sangue
Western Blotting
Bovinos/sangue
Teste em Amostras de Sangue Seco
Displasia Ectodérmica/genética
Ectodisplasinas/sangue
Feminino
Seres Humanos
Imunoprecipitação
Masculino
Camundongos
Camundongos Transgênicos
Meia-Idade
Mutação de Sentido Incorreto/genética
Saliva/química
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Ectodysplasins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170525
[Lr] Data última revisão:
170525
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.1177/0022034516673562


  6 / 613 MEDLINE  
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[PMID]:26659383
[Au] Autor:Sisto M; Lorusso L; Lisi S
[Ad] Endereço:Department of Basic Medical Sciences, Neurosciences and Sense Organs, Section of Human Anatomy and Histology, Laboratory of Cell Biology, University of Bari Medical School, Piazza Giulio Cesare 1, 70124, Bari, Italy. margherita.sisto@uniba.it.
[Ti] Título:X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren's syndrome.
[So] Source:Clin Exp Med;17(1):111-119, 2017 Feb.
[Is] ISSN:1591-9528
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Despite recent advancements in the knowledge of the etiology and pathogenic mechanisms, treatment of the autoimmune disease Sjögren's syndrome (SS) remains mostly empiric and symptom-based, indicating the need for novel therapeutic approaches. Ectodysplasin-A2 (EDA-A2) is a recently isolated member of the tumor necrosis factor superfamily that binds to X-linked ectodermal dysplasia receptor (XEDAR). In this report, we have analyzed the expression and the biological activity of EDA-A2 in human salivary gland epithelial cells (SGEC) from primary Sjögren's syndrome (pSS) patients. We report that EDA-A2 and its receptor XEDAR are overexpressed in pSS SGEC in comparison with healthy individuals and that the EDA-A2/XEDAR system in these cells is involved in the induction of apoptosis via caspases activation. Collectively, our results suggest that EDA-A2/XEDAR system may be a promising agent for the gene therapy of pSS.
[Mh] Termos MeSH primário: Caspase 3/genética
Ectodisplasinas/genética
Células Epiteliais/metabolismo
Glândulas Salivares/metabolismo
Síndrome de Sjogren/genética
Receptor Xedar/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Estudos de Casos e Controles
Caspase 3/metabolismo
Ectodisplasinas/metabolismo
Células Epiteliais/patologia
Regulação da Expressão Gênica
Seres Humanos
Cultura Primária de Células
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Glândulas Salivares/patologia
Transdução de Sinais
Síndrome de Sjogren/metabolismo
Síndrome de Sjogren/patologia
Receptor Xedar/antagonistas & inibidores
Receptor Xedar/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDA protein, human); 0 (EDA2R protein, human); 0 (Ectodysplasins); 0 (RNA, Small Interfering); 0 (Xedar Receptor); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.1007/s10238-015-0404-z


  7 / 613 MEDLINE  
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[PMID]:27685774
[Au] Autor:Ono H; Imai H; Miyawaki S; Nakatomi H; Saito N
[Ad] Endereço:Department of Neurosurgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
[Ti] Título:Rat white matter injury model induced by endothelin-1 injection: technical modification and pathological evaluation.
[So] Source:Acta Neurobiol Exp (Wars);76(3):212-24, 2016.
[Is] ISSN:1689-0035
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:White matter injury is an important cause of functional disability of the brain. We comprehensively analyzed a modified endothelin-1 (ET­1) injection-induced white matter injury model in the rat which is very valuable for investigating the underlying mechanisms of subcortical ischemic stroke. ET-1 was stereotactically injected into the internal capsule of the rat. To avoid complications with leakage of ET-1 into the lateral ventricle, the safest trajectory angle to the target was established. Rats with white matter injury were extensively evaluated for structural changes and functional sequelae, using motor function tests, magnetic resonance (MR) imaging, histopathology evolution, volume estimation of the lesion, and neuroanatomical identification of affected neurons using the retrograde tracer hydroxystilbamidine. Optimization of the trajectory of the ET-1 injection needle provided excellent survival rate. MR imaging visualized the white matter injury 2 days after surgery. Motor function deficit appeared temporarily after the operation. Histological studies confirmed damage of axons and myelin sheaths followed by inflammatory reaction and gliosis similar to lacunar infarction, with lesion volume of less than 1% of the whole brain. Hydroxystilbamidine injected into the lesion revealed wide spatial distribution of the affected neuronal population. Compared with prior ET-1 injection models, this method induced standardized amount of white matter damage and temporary motor function deficit in a reproducible and safe manner. The present model is valuable for studying the pathophysiology of not only ischemia, but a broader set of white matter damage conditions in the lissencephalic brain.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Endotelina-1/toxicidade
Leucoencefalopatias/induzido quimicamente
Leucoencefalopatias/patologia
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/metabolismo
Animais
Ectodisplasinas/metabolismo
Lateralidade Funcional/efeitos dos fármacos
Proteína Glial Fibrilar Ácida/metabolismo
Cápsula Interna/efeitos dos fármacos
Leucoencefalopatias/diagnóstico por imagem
Leucoencefalopatias/fisiopatologia
Locomoção/efeitos dos fármacos
Locomoção/fisiologia
Imagem por Ressonância Magnética
Exame Neurológico
Desempenho Psicomotor/efeitos dos fármacos
Desempenho Psicomotor/fisiologia
Ratos
Ratos Sprague-Dawley
Estilbamidinas/farmacocinética
Natação/psicologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt); 0 (Amyloid beta-Protein Precursor); 0 (Ectodysplasins); 0 (Endothelin-1); 0 (Glial Fibrillary Acidic Protein); 0 (Stilbamidines)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170209
[Lr] Data última revisão:
170209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160930
[St] Status:MEDLINE


  8 / 613 MEDLINE  
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[PMID]:27629711
[Au] Autor:Luo B; Han F; Xu K; Wang J; Liu Z; Shen Z; Li J; Liu Y; Jiang M; Zhang ZY; Zhang Z
[Ad] Endereço:Institute of Immunology of PLA, Third Military Medical University, Chongqing 400038, China.
[Ti] Título:Resolvin D1 Programs Inflammation Resolution by Increasing TGF-ß Expression Induced by Dying Cell Clearance in Experimental Autoimmune Neuritis.
[So] Source:J Neurosci;36(37):9590-603, 2016 Sep 14.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Experimental autoimmune neuritis (EAN) is the animal model of human acute inflammatory demyelinating polyradiculoneuropathies (AIDP), an auto-immune inflammatory demyelination disease of the peripheral nervous system (PNS) and the world's leading cause of acute autoimmune neuromuscular paralysis. EAN and AIDP are characterized by self-limitation with spontaneous recovery; however, endogenous pathways that regulate inflammation resolution in EAN and AIDP remain elusive. A pathway of endogenous mediators, especially resolvins and clearance of apoptotic cells, may be involved. Here, we determined that resolvin D1 (RvD1), its synthetic enzyme, and its receptor were greatly increased in PNS during the recovery stage of EAN. Both endogenous and exogenous RvD1 increased regulatory T (Treg) cell and anti-inflammatory macrophage counts in PNS, enhanced inflammation resolution, and promoted disease recovery in EAN rats. Moreover, RvD1 upregulated the transforming growth factor-ß (TGF-ß) level and pharmacologic inhibition of TGF-ß signaling suppressed RvD1-induced Treg cell counts, but not anti-inflammatory macrophage counts, and RvD1-improved inflammation resolution and disease recovery in EAN rats. Mechanistically, the RvD1-enhanced macrophage phagocytosis of apoptotic T cells leading to reduced apoptotic T-cell accumulation in PNS induced TGF-ß production and caused Treg cells to promote inflammation resolution and disease recovery in EAN. Therefore, these data highlight the crucial role of RvD1 as an important pro-resolving molecule in EAN and suggest its potential as a therapeutic target in human neuropathies. SIGNIFICANCE STATEMENT: Experimental autoimmune neuritis (EAN) is the animal model of human acute inflammatory demyelinating polyradiculoneuropathies, an auto-immune inflammatory demyelination disease of the peripheral nervous system (PNS) and the world's leading cause of acute autoimmune neuromuscular paralysis. Here, we demonstrated that resolvin D1 (RvD1) promoted macrophage phagocytosis of apoptotic T cells in PNS, thereby upregulating transforming growth factor-ß by macrophages, increased local Treg cell counts, and finally promoted inflammation resolution and disease recovery in EAN. These data highlight the crucial role of RvD1 as an important pro-resolving molecule in EAN and suggest that it has potential as a therapeutic target in human neuritis.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Ácidos Docosa-Hexaenoicos/uso terapêutico
Regulação da Expressão Gênica/efeitos dos fármacos
Neurite Autoimune Experimental/tratamento farmacológico
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Cultivadas
Modelos Animais de Doenças
Ácidos Docosa-Hexaenoicos/metabolismo
Ectodisplasinas/metabolismo
Inibidores Enzimáticos/uso terapêutico
Fatores de Transcrição Forkhead/metabolismo
Macrófagos/efeitos dos fármacos
Masculino
Neurite Autoimune Experimental/metabolismo
Neurite Autoimune Experimental/patologia
Fagocitose/efeitos dos fármacos
Pteridinas/uso terapêutico
Ratos
Ratos Endogâmicos Lew
Receptores de Lipoxinas/antagonistas & inibidores
Receptores de Lipoxinas/metabolismo
Nervo Isquiático/patologia
Nervo Isquiático/ultraestrutura
Linfócitos T Reguladores/metabolismo
Linfócitos T Reguladores/patologia
Linfócitos T Reguladores/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Ectodysplasins); 0 (Enzyme Inhibitors); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, rat); 0 (Pteridines); 0 (Receptors, Lipoxin); 0 (SD-208); 0 (Transforming Growth Factor beta); 0 (lipoxin A(4) receptor, rat); 0 (resolvin D1); 25167-62-8 (Docosahexaenoic Acids)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0020-16.2016


  9 / 613 MEDLINE  
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[PMID]:27621364
[Au] Autor:Ahtiainen L; Uski I; Thesleff I; Mikkola ML
[Ad] Endereço:Developmental Biology Program, Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland laura.ahtiainen@helsinki.fi marja.mikkola@helsinki.fi.
[Ti] Título:Early epithelial signaling center governs tooth budding morphogenesis.
[So] Source:J Cell Biol;214(6):753-67, 2016 Sep 12.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During organogenesis, cell fate specification and patterning are regulated by signaling centers, specialized clusters of morphogen-expressing cells. In many organs, initiation of development is marked by bud formation, but the cellular mechanisms involved are ill defined. Here, we use the mouse incisor tooth as a model to study budding morphogenesis. We show that a group of nonproliferative epithelial cells emerges in the early tooth primordium and identify these cells as a signaling center. Confocal live imaging of tissue explants revealed that although these cells reorganize dynamically, they do not reenter the cell cycle or contribute to the growing tooth bud. Instead, budding is driven by proliferation of the neighboring cells. We demonstrate that the activity of the ectodysplasin/Edar/nuclear factor κB pathway is restricted to the signaling center, and its inactivation leads to fewer quiescent cells and a smaller bud. These data functionally link the signaling center size to organ size and imply that the early signaling center is a prerequisite for budding morphogenesis.
[Mh] Termos MeSH primário: Movimento Celular
Proliferação Celular
Células Epiteliais/fisiologia
Incisivo/embriologia
[Mh] Termos MeSH secundário: Animais
Ectodisplasinas/genética
Ectodisplasinas/metabolismo
Receptor Edar/genética
Receptor Edar/metabolismo
Células Epiteliais/metabolismo
Fase G1
Regulação da Expressão Gênica no Desenvolvimento
Genótipo
Idade Gestacional
Incisivo/metabolismo
Camundongos Transgênicos
Microscopia Confocal
Morfogênese
NF-kappa B/genética
NF-kappa B/metabolismo
Tamanho do Órgão
Fenótipo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Ectodysplasins); 0 (Edar Receptor); 0 (Edar protein, mouse); 0 (NF-kappa B)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201512074


  10 / 613 MEDLINE  
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[PMID]:27612287
[Au] Autor:Bauer PM; Zalis MC; Abdshill H; Deierborg T; Johansson F; Englund-Johansson U
[Ad] Endereço:Dept. of Biology, Sec. Functional Zoology, Lund University, Lund, Sweden.
[Ti] Título:Inflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.
[So] Source:PLoS One;11(9):e0161723, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Disease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments. Therefore, we have used the explanted retina as a model to explore the immune response and expression of the immune modulator galectin-3 (Gal-3), induced by the cultivation per se and after additional immune stimulation with lipopolysaccharide (LPS), and how this correlates with retinal neurotoxicity. METHODS: Post-natal mouse retinas were cultured in a defined medium. One group was stimulated with LPS (100 ng/ml, 24 h). Retinal architecture, apoptotic cell death, and micro- and macroglial activity were studied at the time of cultivation (0 days in vitro (DIV)) and at 3, 4 and 7 DIV using morphological staining, biochemical- and immunohistochemical techniques. RESULTS: Our results show that sustained activation of macro- and microglia, characterized by no detectable cytokine release and limited expression of Gal-3, is not further inducing apoptosis additional to the axotomy-induced apoptosis in innermost nuclear layer. An elevated immune response was detected after LPS stimulation, as demonstrated primarily by release of immune mediators (i.e. interleukin 2 (IL-2), IL-6, KC/GRO (also known as CLCX1) and tumour necrosis factor-α (TNF-α)), increased numbers of microglia displaying morphologies of late activation stages as well as Gal-3 expression. This was accompanied with increased apoptosis in the two additional nuclear layers, and damage to retinal gross architecture. CONCLUSION: We demonstrate that an immune response characterized by sustained and increased release of cytokines, along with an increase in Gal-3 expression, is accompanied by significant increased neurotoxicity in the explanted retina. Further investigations using the current setting may lead to increased understanding on the mechanisms involved in neuronal loss in retinal neurodegenerations.
[Mh] Termos MeSH primário: Galectina 3/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Retina/citologia
Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas de Ligação ao Cálcio/metabolismo
Ectodisplasinas/metabolismo
Galectina 3/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Técnicas In Vitro
Inflamação/induzido quimicamente
Interleucina-2/metabolismo
Interleucina-6/metabolismo
Antígeno Ki-67/metabolismo
Lipopolissacarídeos/toxicidade
Camundongos
Proteínas dos Microfilamentos/metabolismo
Microglia/citologia
Microglia/efeitos dos fármacos
Microglia/metabolismo
Retina/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Ectodysplasins); 0 (Eda protein, mouse); 0 (Galectin 3); 0 (Glial Fibrillary Acidic Protein); 0 (Interleukin-2); 0 (Interleukin-6); 0 (Ki-67 Antigen); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 0 (Tumor Necrosis Factor-alpha); 0 (glial fibrillary astrocytic protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161723



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