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[PMID]:28467721
[Au] Autor:Sareila O; Hagert C; Kelkka T; Linja M; Xu B; Kihlberg J; Holmdahl R
[Ad] Endereço:1 Medicity Research Laboratory, University of Turku , Turku, Finland .
[Ti] Título:Reactive Oxygen Species Regulate Both Priming and Established Arthritis, but with Different Mechanisms.
[So] Source:Antioxid Redox Signal;27(18):1473-1490, 2017 Dec 20.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Neutrophil cytosolic factor 1 (NCF1) is a key regulatory component of the phagocytic NOX2 complex, which produces reactive oxygen species (ROS). Polymorphism of the Ncf1 gene is associated with increased arthritis severity. In this study, we generated targeted Ncf1 knock-in mice with inducible Ncf1 expression and determined the critical time window during which the NOX2-derived ROS protect the mice from arthritis. RESULTS: Targeted Ncf1 knock-in mice lacked NOX2-derived ROS, and in vivo allelic conversion of Ncf1 by the CreER recombinase led to full protein expression and ROS production within 10 days. Mice in which Ncf1 had been activated before immunization with type II collagen (CII) developed only mild clinical symptoms of collagen-induced arthritis (CIA), whereas the ROS-deficient littermates had severe arthritis. The functional Ncf1 restricted the expansion of IL-17A-producing T cells specific for the immunodominant CII peptide. When the Ncf1 gene was activated after the priming phase, Ncf1-dependent protection from autoimmune arthritis was still observed, together with a reduced number of splenic monocytes but it was not associated with alterations in peptide-specific T cell response. The Ncf1-deficient mice expressed pronounced interferon signature, which could be normalized by conditional expression of Ncf1 and was also present in the Ncf1-mutated mouse during arthritis. Innovation and Conclusion: Ncf1 deficiency has been known to predispose to autoimmunity in both humans and rodents. Our in vivo results point to a regulatory role of NOX2-derived ROS not only during priming but also during the effector phase of CIA, most likely via different mechanisms. Antioxid. Redox Signal. 27, 1473-1490.
[Mh] Termos MeSH primário: Artrite Experimental/metabolismo
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/induzido quimicamente
Artrite Experimental/genética
Colágeno Tipo II/efeitos adversos
Modelos Animais de Doenças
Técnicas de Introdução de Genes
Seres Humanos
Interleucina-17/metabolismo
Camundongos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Interleukin-17); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (neutrophil cytosolic factor 1)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2016.6981


  2 / 8253 MEDLINE  
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[PMID]:29343683
[Au] Autor:Meng X; Grötsch B; Luo Y; Knaup KX; Wiesener MS; Chen XX; Jantsch J; Fillatreau S; Schett G; Bozec A
[Ad] Endereço:Department of Internal Medicine 3, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Hypoxia-inducible factor-1α is a critical transcription factor for IL-10-producing B cells in autoimmune disease.
[So] Source:Nat Commun;9(1):251, 2018 01 17.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypoxia-inducible factors (HIFs) are key elements for controlling immune cell metabolism and functions. While HIFs are known to be involved in T cells and macrophages activation, their functions in B lymphocytes are poorly defined. Here, we show that hypoxia-inducible factor-1α (HIF-1α) contributes to IL-10 production by B cells. HIF-1α regulates IL-10 expression, and HIF-1α-dependent glycolysis facilitates CD1d CD5 B cells expansion. Mice with B cell-specific deletion of Hif1a have reduced number of IL-10-producing B cells, which result in exacerbated collagen-induced arthritis and experimental autoimmune encephalomyelitis. Wild-type CD1d CD5 B cells, but not Hif1a-deficient CD1d CD5 B cells, protect recipient mice from autoimmune disease, while the protective function of Hif1a-deficient CD1d CD5 B cells is restored when their defective IL-10 expression is genetically corrected. Taken together, this study demonstrates the key function of the hypoxia-associated transcription factor HIF-1α in driving IL-10 expression in CD1d CD5 B cells, and in controlling their protective activity in autoimmune disease.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Linfócitos B/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Interleucina-10/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/imunologia
Artrite Experimental/metabolismo
Doenças Autoimunes/metabolismo
Encefalomielite/imunologia
Encefalomielite/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02683-x


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[PMID]:29315314
[Au] Autor:Vidal B; Cascão R; Finnilä MAJ; Lopes IP; Saarakkala S; Zioupos P; Canhão H; Fonseca JE
[Ad] Endereço:Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
[Ti] Título:Early arthritis induces disturbances at bone nanostructural level reflected in decreased tissue hardness in an animal model of arthritis.
[So] Source:PLoS One;13(1):e0190920, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Arthritis induces joint erosions and skeletal bone fragility. OBJECTIVES: The main goal of this work was to analyze the early arthritis induced events at bone architecture and mechanical properties at tissue level. METHODS: Eighty-eight Wistar rats were randomly housed in experimental groups, as follows: adjuvant induced arthritis (AIA) (N = 47) and a control healthy group (N = 41). Rats were monitored during 22 days for the inflammatory score, ankle perimeter and body weight and sacrificed at different time points (11 and 22 days post disease induction). Bone samples were collected for histology, micro computed tomography (micro-CT), 3-point bending and nanoindentation. Blood samples were also collected for bone turnover markers and systemic cytokine quantification. RESULTS: At bone tissue level, measured by nanoindentation, there was a reduction of hardness in the arthritic group, associated with an increase of the ratio of bone concentric to parallel lamellae and of the area of the osteocyte lacuna. In addition, increased bone turnover and changes in the microstructure and mechanical properties were observed in arthritic animals, since the early phase of arthritis, when compared with healthy controls. CONCLUSION: We have shown in an AIA rat model that arthritis induces very early changes at bone turnover, structural degradation and mechanical weakness. Bone tissue level is also affected since the early phase of arthritis, characterized by decreased tissue hardness associated with changes in bone lamella organization and osteocyte lacuna surface. These observations highlight the pertinence of immediate control of inflammation in the initial stages of arthritis.
[Mh] Termos MeSH primário: Artrite Experimental/patologia
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/diagnóstico por imagem
Remodelação Óssea
Progressão da Doença
Feminino
Dureza
Ratos
Ratos Wistar
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180110
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190920


  4 / 8253 MEDLINE  
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[PMID]:28461107
[Au] Autor:Gertel S; Mahagna H; Karmon G; Watad A; Amital H
[Ad] Endereço:Zabludowicz Center For Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer 5262100, Israel; Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 6997801, Israel. Electronic address: smadar.gertel@sheba.health.gov.il.
[Ti] Título:Tofacitinib attenuates arthritis manifestations and reduces the pathogenic CD4 T cells in adjuvant arthritis rats.
[So] Source:Clin Immunol;184:77-81, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis (RA) is an autoimmune disease characterized by pronounced inflammation and leukocyte infiltration in affected joints. Tofacitinib is new agent, a selective inhibitor of Janus kinase (JAK) signaling pathways mediated by JAK1 and JAK3 and inhibits the key transcription factors STAT1 and STAT3. We investigated the action mechanisms of tofacitinib in rats with adjuvant-induced-arthritis (AIA). AIA-rats were treated orally with tofacitinib or with methotrexate. Arthritis severity and serum C-reactive protein (CRP) levels were evaluated, splenic cells were examined by flow cytometry and cytokines were analyzed by real-time PCR. Tofacitinib markedly reduced the clinical status of treated rats in comparison to control group. Reduced joints inflammation and down-regulated serum CRP levels reflected the clinical manifestations of the treated rats. Tofacitinib down-regulated significantly the frequency of CD4 IFN-γ T cells and reduced IL-1ß mRNA expression levels in the spleen of the treated rats. These results show that tofacitinib attenuated arthritis severity, modified splenic populations and cytokine imbalance.
[Mh] Termos MeSH primário: Artrite Experimental/imunologia
Artrite Reumatoide/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Articulações do Pé/efeitos dos fármacos
Piperidinas/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Animais
Antirreumáticos/farmacologia
Artrite Experimental/fisiopatologia
Artrite Reumatoide/fisiopatologia
Proteína C-Reativa/efeitos dos fármacos
Proteína C-Reativa/imunologia
Linfócitos T CD4-Positivos/imunologia

Articulações do Pé/patologia
Membro Anterior
Membro Posterior
Interferon gama/imunologia
Interleucina-1beta/efeitos dos fármacos
Interleucina-1beta/genética
Metotrexato/farmacologia
RNA Mensageiro/efeitos dos fármacos
RNA Mensageiro/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Baço/citologia
Baço/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Piperidines); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); 0 (RNA, Messenger); 82115-62-6 (Interferon-gamma); 87LA6FU830 (tofacitinib); 9007-41-4 (C-Reactive Protein); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  5 / 8253 MEDLINE  
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[PMID]:27771442
[Au] Autor:Liu X; Wang J; Chu Y; Zhou X
[Ad] Endereço:School of Pharmaceutical Engineering and Life Science, Changzhou University, 213164, Jiangsu, China.
[Ti] Título:Serum based fluorescent assay for evaluating dipeptidyl peptidase I activity in collagen induced arthritis rat model.
[So] Source:Mol Cell Probes;32:5-12, 2017 04.
[Is] ISSN:1096-1194
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dipeptidyl peptidase I (DPPI) is a lysosomal cysteine protease and derived from immune granule cells. It has been suggested playing an important role in the development of rheumatoid arthritis. In this study, a coumarin based fluorescent probe (GF-AFC) was designed and synthesized to evaluate DPPI activity in serum or tissue homogenates of collagen-induced arthritis (CIA) rats, an inflammatory arthropathy model. It was revealed that the fluorescent intensity was significantly increased in a very short time after specific substrate GF-AFC reacted with the DPPI. The fluorophore (AFC) was released to shine after the cleavage reaction which was examined by F NMR spectroscopy. It has been shown that DPPI hydrolyzed the GF-AFC in a robust, linear, and time dependent manner at a significant high rate. A serum-based DPPI activity assay was validated by spiking and gradient dilution methods, there were no interferences or auto-fluorescence observed. The Coefficient of Variance calculated for serum-based DPPI activity assays indicates the good reproducibility. The good correlation has been seen between serum DPPI levels and the severity of arthritis during RA development in CIA rats. Our study has demonstrated a new serum based diagnostic assay for detecting DPPI activity using coumarin conjugated fluorescent (GF-AFC) as a substrate. The successful implementation of the case would provide beneficial experience in rheumatoid arthritis research.
[Mh] Termos MeSH primário: Artrite Experimental/sangue
Artrite Experimental/enzimologia
Bioensaio/métodos
Catepsina C/sangue
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/diagnóstico
Modelos Animais de Doenças
Fluorescência
Corantes Fluorescentes/síntese química
Corantes Fluorescentes/química
Corantes Fluorescentes/metabolismo
Cinética
Espectroscopia de Ressonância Magnética
Masculino
Ratos Wistar
Reprodutibilidade dos Testes
Espectrofotometria Ultravioleta
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorescent Dyes); EC 3.4.14.1 (Cathepsin C)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29228993
[Au] Autor:Yuan F; Wang J; Zhang K; Li Z; Guan Z
[Ad] Endereço:Arthritis Clinic & Research Center, Peking University People's Hospital, 11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
[Ti] Título:Programmed cell death 5 transgenic mice attenuates adjuvant induced arthritis by 2 modifying the T lymphocytes balance.
[So] Source:Biol Res;50(1):40, 2017 Dec 11.
[Is] ISSN:0717-6287
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Programmed cell death 5 (PDCD5) is an apoptosis-related gene cloned from TF-1 cells whose primary biological functions are to promote apoptosis and immune regulation. The effects and mechanisms exerted by key mediators of arthritic inflammation remain unclear in PDCD5 transgenic (PDCD5 tg) mice. RESULTS: In the current study, PDCD5 tg mice inhibited the progression of adjuvant-induced arthritis, specifically decreasing clinical signs and histological damage, compared with arthritis control mice. Additionally, the ratio of CD4 IFN-γ cells (Th1) and CD4 IL-17A cells (Th17), as well as the mRNA expression of the pro-inflammatory mediators IFN-γ, IL-6, IL-17A and TNF-α, were decreased in PDCD5 tg mice, while CD4 CD25 Foxp3 regulatory T (Treg) cells and the anti-inflammatory mediators IL-4 and IL-10 were increased. Furthermore, PDCD5 tg mice demonstrated reduced serum levels of IFN-γ, IL-6, IL-17A and TNF-α and increased levels of IL-4. CONCLUSIONS: Based on our data, PDCD5 exerts anti-inflammatory effects by modifying the T lymphocytes balance, inhibiting the production of pro-inflammatory mediators and promoting the secretion of anti-inflammatory cytokines, validating PDCD5 protein as a possible treatment for RA.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/fisiologia
Artrite Experimental/metabolismo
Proteínas de Neoplasias/fisiologia
Linfócitos T Reguladores/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/genética
Artrite Experimental/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas de Neoplasias/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Neoplasm Proteins); 0 (Pdcd5 protein, mouse)
[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:171213
[St] Status:MEDLINE
[do] DOI:10.1186/s40659-017-0145-4


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[PMID]:28467992
[Au] Autor:Sun CL; Wei J; Bi LQ
[Ad] Endereço:Department of Rheumatology and Immunology, The First College of Clinical Medical Science, China Three Gorges University, Yichang, and Department of Rheumatology and Immunology, China-Japan Union Hospital of Jilin University, Changchun, China.
[Ti] Título:Rutin Attenuates Oxidative Stress and Proinflammatory Cytokine Level in Adjuvant Induced Rheumatoid Arthritis via Inhibition of NF-κB.
[So] Source:Pharmacology;100(1-2):40-49, 2017.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The present study was intended to elucidate the effect of rutin, a flavonoid, on arthritis in complete Freund's adjuvant-induced arthritic rats. The present study showed that more pronounced effect has been observed in the case of 15 mg/kg dose of rutin, with significant reduction in paw diameter together with positive modulation of hematological parameters as compared to 2 other tested doses. A significant upsurge in the level of superoxide dismutase, glutathione peroxidase and glutathione were observed together with decrease in the level of malondialdehyde after treatment with rutin in a dose-dependent manner. Furthermore, the effect of rutin on the tumor necrosis factor-α and interleukin-1ß in arthritic rats showed does-dependent lowering of these cytokines with maximum benefit at 15 mg/kg dose and the level of both NF-κB p65 and NF-κBp65 (Ser536) has been significantly reduced in the presence of rutin. Histopathological examination showed that the inflammatory cells infiltration, synovial hyperplasia, pannus formation and cartilage and bone erosion had considerably improved on administration of rutin. In conclusion, our paper strongly demonstrated the protective effect of rutin against the rheumatoid arthritis involved via suppression of NF-κB p65 protein expression.
[Mh] Termos MeSH primário: Artrite Experimental/tratamento farmacológico
Artrite Reumatoide/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Rutina/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Anti-Inflamatórios/farmacologia
Artrite Experimental/patologia
Artrite Reumatoide/patologia
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Adjuvante de Freund
Interleucina-1beta/metabolismo
Malondialdeído/metabolismo
Ratos
Ratos Wistar
Rutina/administração & dosagem
Fator de Transcrição RelA/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Interleukin-1beta); 0 (Transcription Factor RelA); 0 (Tumor Necrosis Factor-alpha); 4Y8F71G49Q (Malondialdehyde); 5G06TVY3R7 (Rutin); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1159/000451027


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[PMID]:29190705
[Au] Autor:Jung H; Jung SM; Rim YA; Park N; Nam Y; Lee J; Park SH; Ju JH
[Ad] Endereço:Catholic iPSC Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
[Ti] Título:Arthritic role of Porphyromonas gingivalis in collagen-induced arthritis mice.
[So] Source:PLoS One;12(11):e0188698, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiological studies show an association between rheumatoid arthritis (RA) and periodontal disease. Porphyromonas gingivalis (P.gingivalis) is a well-known pathogen in periodontitis. This study investigated the pathogenic effects of P.gingivalis on autoimmune arthritis in vivo. Collagen-induced arthritis (CIA) mice were intraperitoneally injected with W83 and 2561 strains of P.gingivalis. Infection with P.gingivalis exacerbated arthritis score in CIA mice. Synovial inflammation and bone destruction in CIA mice infected with P.gingivalis were more severe than in uninfected CIA mice. Both W83 and 2561 strains were more pro-arthritic after arthritis symptom was fully activated. Interestingly, only W83 strain was arthritogenic before autoimmune reaction initiated. Citrullination was detected in synovial tissue of CIA mice and CIA mice inoculated with P.gingivalis, but not in normal control mice. The citrullinated area was greater in P.gingivalis-infected CIA mice than in non-infected CIA mice. This study showed that P.gingivalis exacerbated disease in a mouse model of autoimmune arthritis and increased the expression of citrullinated antigens in the synovium. The arthritogenic effects of P.gingivalis were at least in part, dependent upon the bacterial strain with or without fimbriae expression, route and time of infection. P.gingivalis-mediated citrullination may explain the possible link between periodontal disease and RA.
[Mh] Termos MeSH primário: Artrite Experimental/microbiologia
Colágeno/administração & dosagem
Porphyromonas gingivalis/patogenicidade
[Mh] Termos MeSH secundário: Animais
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9007-34-5 (Collagen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188698


  9 / 8253 MEDLINE  
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[PMID]:28747638
[Au] Autor:Hong SS; Marotte H; Courbon G; Firestein GS; Boulanger P; Miossec P
[Ad] Endereço:University of Lyon, Lyon, 69007, France. saw-see.hong@univ-lyon1.fr.
[Ti] Título:PUMA gene delivery to synoviocytes reduces inflammation and degeneration of arthritic joints.
[So] Source:Nat Commun;8(1):146, 2017 07 27.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In rheumatoid arthritis (RA), the proliferation of fibroblast-like synoviocytes (FLS) is the cause of chronic inflammation in joints and of joint damage. Delivery of the pro-apoptotic gene PUMA to FLS via human adenovirus type 5 (HAdV5) vectors has been tested as a therapeutic approach, but efficiency is hampered by low transduction, as FLS do not express HAdV5 receptors on the cell surface. Here we show that efficient transduction of PUMA in FLS can be achieved by conjugating HAdV5 to a baculovirus, which binds to the cell surface via the envelope glycoprotein Gp64. Intra-articular injection in an adjuvant-induced rat model of RA induces apoptosis of FLS, leading to significant decrease in joint inflammation, joint damage, and bone loss with improvement in joint function and mobility. Our results demonstrate the therapeutic potential of PUMA gene therapy as a local treatment in various forms of arthritis in which abnormal FLS proliferation is implicated.Proliferation of synoviocytes contributes to joint damage in rheumatoid arthritis. Here the authors show that targeting of these cells by a vector, consisting of a baculovirus conjugated to an adenovirus carrying the pro-apoptotic gene PUMA, has therapeutic efficacy in a rat arthritis model.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Artrite Reumatoide/genética
Proteínas Proto-Oncogênicas/genética
Sinoviócitos/metabolismo
Sinovite/genética
[Mh] Termos MeSH secundário: Adenovírus Humanos/genética
Animais
Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Artrite Experimental/genética
Artrite Experimental/metabolismo
Artrite Experimental/terapia
Artrite Reumatoide/terapia
Baculoviridae/genética
Proliferação Celular/genética
Células Cultivadas
Feminino
Técnicas de Transferência de Genes
Terapia Genética/métodos
Vetores Genéticos/genética
Células HEK293
Seres Humanos
Proteínas Proto-Oncogênicas/metabolismo
Ratos Endogâmicos Lew
Sinovite/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (BBC3 protein, human); 0 (Proto-Oncogene Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00142-1


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[PMID]:28957555
[Au] Autor:Tao Y; Wang Z; Wang L; Shi J; Guo X; Zhou W; Wu X; Liu Y; Zhang W; Yang H; Shi Q; Xu Y; Geng D
[Ad] Endereço:Department of Orthopedics, First Affiliated Hospital of Soochow University, Suzhou.
[Ti] Título:Downregulation of miR-106b attenuates inflammatory responses and joint damage in collagen-induced arthritis.
[So] Source:Rheumatology (Oxford);56(10):1804-1813, 2017 Oct 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objective: miRNAs are small, signal-strand, non-coding RNAs that function in post-transcriptional regulation. We analysed the in vivo effect of miR-106b (miR-106b-5p) on inflammatory bone loss in CIA mice. Methods: CIA mice are developed by injecting DAB/1 mice with bovine type II collagen containing Freund's adjuvant and then the in vivo effect of miR-106b is examined. On day 22, mice were given lentiviral negative control, lentiviral-mediated miR-106b mimics or lentiviral-mediated miR-106b inhibitor via orbital injection on a weekly basis. Morphological changes in the ankle joints were assessed via micro-CT and histopathology and cytokine expression levels were examined via immunohistochemical staining, ELISA or flow cytometric analysis. miR-106b and osteoclastic-related gene expression was evaluated via quantitative real-time PCR. Results: CIA mice were found to have increased miR-106b expression and CIA-associated bone loss and inflammatory infiltration. miR-106b inhibitor treatment markedly decreased arthritis incidence and attenuated bone destruction and histological severity compared with the control group. Moreover, miR-106b inhibitor treatment suppressed RANK ligand (RANKL) expression, increased osteoprotegerin (OPG) expression and reduced the RANKL:OPG ratio in CIA mice. miR-106b inhibition also significantly decreased inflammatory mediator production in joint sections and reduced serum pro-inflammatory cytokine levels when compared with the control group. Additionally, miR-106b inhibition decreased tartrate-resistant acid phosphatase-positive cell numbers and suppressed murine bone marrow macrophage differentiation. Conclusion: These findings indicate that miR-106b inhibition can ameliorate CIA-associated inflammation and bone destruction and thus may serve as a potential therapeutic for human RA treatment.
[Mh] Termos MeSH primário: Artrite Experimental/genética
Osso e Ossos/patologia
Regulação para Baixo
Articulações/patologia
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/induzido quimicamente
Artrite Experimental/tratamento farmacológico
Osso e Ossos/metabolismo
Colágeno Tipo II
Citocinas/sangue
Regulação da Expressão Gênica/efeitos dos fármacos
Mediadores da Inflamação/fisiologia
Articulações/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos DBA
MicroRNAs/antagonistas & inibidores
Osteoclastos/metabolismo
Osteoprotegerina/metabolismo
Ligante RANK/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Cytokines); 0 (Inflammation Mediators); 0 (MicroRNAs); 0 (Mirn106 microRNA, mouse); 0 (Osteoprotegerin); 0 (RANK Ligand); 0 (Tnfrsf11b protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kex233



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