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[PMID]:29465573
[Au] Autor:Li X; Zhang Z; Latif M; Chen W; Cui J; Peng Z
[Ad] Endereço:Department of Radiology, the Third Hospital of Hebei Medical University.
[Ti] Título:Synovium as a widespread pathway to the adjacent joint in undifferentiated high-grade pleomorphic sarcoma of the tibia: A case report.
[So] Source:Medicine (Baltimore);97(8):e9870, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Undifferentiated high-grade pleomorphic sarcoma (UPS), originated from bone, is a rare tumor, accounting for 2% to 5% of all primary maligment bone neoplasms. Skip lesion can be found in undifferentiated high-grade pleomorphic sarcoma of bone (UPS-B). However, the direct invasion across the articular synovium to bone has not been reported previously. PATIENT CONCERNS: We report an unusual case of a 65-year-old man complained of a year history of pain, swelling, and limitation of activity in the left knee joint. At the proximal tibia, there was extensive invasion of articular synovium, which provides a direct anatomic pathway for the tumor invasion to the adjacent bone, including patella and femoral condyle. DIAGNOSES: Magnetic resonance imaging was important in defining the marrow involvement and joint invasion, including the thickening articular synovium. Subsequent pathological examination confirmed the diagnosis of UPS. INTERVENTIONS: The patient underwent an extensive resection of the knee joint, except for the patellar. OUTCOMES: After operation, routine chemotherapy was performed. Unfortunately, half a year later, soft tissue swelling of whole thigh was found. Then this patient came our hospital again. Positron emission tomography imaging showed there was recurrence of UPS with lung metastasis. A week later, this patient died. LESSONS: In contrast to frequent infiltration pathway, the articular synovium as a media for this tumor spread is rare. This study adds a better understanding of this direct invasion way to the medical literature.
[Mh] Termos MeSH primário: Neoplasias Ósseas/patologia
Histiocitoma Fibroso Maligno/patologia
Membrana Sinovial/patologia
Tíbia/patologia
[Mh] Termos MeSH secundário: Idoso
Neoplasias Ósseas/diagnóstico por imagem
Neoplasias Ósseas/cirurgia
Evolução Fatal
Neoplasias Femorais/diagnóstico por imagem
Neoplasias Femorais/patologia
Neoplasias Femorais/cirurgia
Histiocitoma Fibroso Maligno/diagnóstico por imagem
Histiocitoma Fibroso Maligno/cirurgia
Seres Humanos
Articulação do Joelho/diagnóstico por imagem
Articulação do Joelho/patologia
Articulação do Joelho/cirurgia
Neoplasias Pulmonares/secundário
Imagem por Ressonância Magnética
Masculino
Invasividade Neoplásica
Patela/diagnóstico por imagem
Patela/patologia
Patela/cirurgia
Membrana Sinovial/diagnóstico por imagem
Coxa da Perna/diagnóstico por imagem
Coxa da Perna/patologia
Tíbia/diagnóstico por imagem
Tíbia/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009870


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[PMID]:29367523
[Au] Autor:Umeda N; Matsumoto I; Sumida T
[Ad] Endereço:Department of Rheumatology, Tsuchiura Kyodo General Hospital.
[Ti] Título:[The pathogenic role of ACPA in rheumatoid arthritis].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(6):391-395, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.
[Mh] Termos MeSH primário: Anticorpos Anti-Proteína Citrulinada/efeitos adversos
Anticorpos Anti-Proteína Citrulinada/imunologia
Artrite Reumatoide/imunologia
[Mh] Termos MeSH secundário: Antígenos CD
Antígenos de Diferenciação Mielomonocítica
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Reabsorção Óssea/imunologia
Osso e Ossos/patologia
Cartilagem/patologia
Citrulina/imunologia
Citrulina/metabolismo
Antígenos HLA-DR
Seres Humanos
Mediadores da Inflamação/metabolismo
Osteogênese/imunologia
Doenças Periodontais
Desiminases de Arginina em Proteínas/metabolismo
Fumar
Membrana Sinovial/citologia
Membrana Sinovial/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Citrullinated Protein Antibodies); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (HLA-DR Antigens); 0 (Inflammation Mediators); 0 (Tumor Necrosis Factor-alpha); 29VT07BGDA (Citrulline); EC 3.5.3.15 (Protein-Arginine Deiminases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.391


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[PMID]:29217191
[Au] Autor:Yoshida K; Nakai A; Kaneshiro K; Hashimoto N; Suzuki K; Uchida K; Hashimoto T; Kawasaki Y; Tateishi K; Nakagawa N; Shibanuma N; Sakai Y; Hashiramoto A
[Ad] Endereço:Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe 654-0142, Japan.
[Ti] Título:TNF-α induces expression of the circadian clock gene Bmal1 via dual calcium-dependent pathways in rheumatoid synovial cells.
[So] Source:Biochem Biophys Res Commun;495(2):1675-1680, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor (TNF)-α is responsible for expressions of several clock genes and affects joint symptoms of rheumatoid arthritis (RA) with diurnal fluctuation. We tried to determine the mechanism involved in over-expression of Bmal1, induced by TNF-α, in primary cultured rheumatoid synovial cells. Cells were incubated with intra-cellular Ca chelator BAPTA-AM, calcineurin inhibitor FK506 and p300/CBP (CREB binding protein) inhibitor C646, respectively, or transfected with p300 and CBP small interfering RNA (siRNA) before stimulation with TNF-α. Oscillation phase and amplitude of Bmal1, transcriptional activator Rorα, transcriptional repressor Rev-erbα, and histone acetyltransferases (p300 and Cbp) were evaluated by quantitative real-time PCR. As results, TNF-α did not influence the oscillation phase of Rev-erbα, while enhanced those of Rorα, resulting in over-expression of Bmal1. When Ca influx was inhibited by BAPTA-AM, TNF-α-mediated up-regulation of Rorα was cancelled, however, that of Bmal1 was still apparent. When we further explored another pathway between TNF-α and Bmal1, TNF-α suppressed the expression of Rev-erbα in the absence of Ca influx, as well as those of p300 and Cbp genes. Finally, actions of TNF-α, in increasing Bmal1/Rorα and decreasing Rev-erbα, were cancelled by C646 treatment or silencing of both p300 and Cbp. In conclusion, we determined a novel role of TNF-α in inducing Bmal1 via dual calcium dependent pathways; Rorα was up-regulated in the presence of Ca influx and Rev-erbα was down-regulated in the absence of that. Results proposed that inhibition of p300/CBP could be new therapeutic targets for RA.
[Mh] Termos MeSH primário: Fatores de Transcrição ARNTL/genética
Artrite Reumatoide/genética
Artrite Reumatoide/metabolismo
Sinalização do Cálcio
Relógios Circadianos/genética
Membrana Sinovial/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Artrite Reumatoide/patologia
Benzoatos/farmacologia
Proteína de Ligação a CREB/antagonistas & inibidores
Proteína de Ligação a CREB/genética
Quelantes de Cálcio/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Células Cultivadas
Proteína p300 Associada a E1A/antagonistas & inibidores
Proteína p300 Associada a E1A/genética
Ácido Egtázico/análogos & derivados
Ácido Egtázico/farmacologia
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Membro 1 do Grupo D da Subfamília 1 de Receptores Nucleares/genética
Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Pirazóis/farmacologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
Membrana Sinovial/efeitos dos fármacos
Membrana Sinovial/patologia
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (ARNTL protein, human); 0 (Benzoates); 0 (C646 compound); 0 (Calcium Chelating Agents); 0 (NR1D1 protein, human); 0 (Nuclear Receptor Subfamily 1, Group D, Member 1); 0 (Nuclear Receptor Subfamily 1, Group F, Member 1); 0 (Pyrazoles); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (RORA protein, human); 0 (Tumor Necrosis Factor-alpha); 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester); 526U7A2651 (Egtazic Acid); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:29221756
[Au] Autor:Lesniak A; Aarnio M; Diwakarla S; Norberg T; Nyberg F; Gordh T
[Ad] Endereço:Uppsala University, Department of Pharmaceutical Biosciences, SE 751 24 Uppsala, Sweden; Medical University of Warsaw, Department of Pharmacodynamics, Centre for Preclinical Research and Technology, 02-097 Warsaw, Poland. Electronic address: anna.lesniak@wum.edu.pl.
[Ti] Título:Characterization of the binding site for d-deprenyl in human inflamed synovial membrane.
[So] Source:Life Sci;194:26-33, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: d-Deprenyl when used as a positron emission tomography tracer visualizes peripheral inflammation. The major aim of the current study was to identify and investigate the properties of the binding target for d-deprenyl in synovial membrane explants from arthritic patients. MAIN METHODS: Thirty patients diagnosed with arthritis or osteoarthritis were enrolled into the study. Homologous and competitive radioligand binding assays utilizing [ H]d-deprenyl were performed to investigate the biochemical characteristics of the binding site and assess differences in the binding profile in synovial membranes exhibiting varying levels of inflammation. KEY FINDINGS: The [ H]d-deprenyl binding assay confirmed the existence of a single, saturable population of membrane-bound protein binding sites in synovial membrane homogenates. The macroscopically determined level of inflammation correlated with an increase in [ H]d-deprenyl binding affinity, without significant alterations in binding site density. Selective monoamine oxidase B inhibitor, selegiline competed for the same site as [ H]d-deprenyl, but failed to differentiate the samples with regard to their inflammation grade. A monoamine oxidase A inhibitor, pirlindole mesylate showed only weak displacement of [ H]d-deprenyl binding. No significant alterations in monoamine oxidase B expression was detected, thus it was not confirmed whether it could serve as a marker for ongoing inflammation. SIGNIFICANCE: Our study was the first to show the biochemical characteristics of the [ H]d-deprenyl binding site in inflamed human synovium. We confirmed that d-deprenyl could differentiate between patients with varying severity of synovitis in the knee joint by binding to a protein target distinct from monoamine oxidase B.
[Mh] Termos MeSH primário: Artrite/diagnóstico
Inibidores da Monoaminoxidase/metabolismo
Monoaminoxidase/análise
Selegilina/metabolismo
Membrana Sinovial/patologia
Sinovite/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Artrite/metabolismo
Sítios de Ligação
Feminino
Seres Humanos
Masculino
Meia-Idade
Monoaminoxidase/metabolismo
Tomografia por Emissão de Pósitrons
Ensaio Radioligante
Membrana Sinovial/metabolismo
Sinovite/metabolismo
Trítio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Monoamine Oxidase Inhibitors); 10028-17-8 (Tritium); 2K1V7GP655 (Selegiline); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:29237438
[Au] Autor:Khansai M; Phitak T; Klangjorhor J; Udomrak S; Fanhchaksai K; Pothacharoen P; Kongtawelert P
[Ad] Endereço:Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
[Ti] Título:Effects of sesamin on primary human synovial fibroblasts and SW982 cell line induced by tumor necrosis factor-alpha as a synovitis-like model.
[So] Source:BMC Complement Altern Med;17(1):532, 2017 Dec 13.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovitis, cartilage degradation and bone deformities. Synovitis is the term for inflammation of the synovial membrane, an early stage of RA. The pathogenesis of the disease occurs through cytokine induction. The major cytokine that increases the severity of RA is TNF-α. Thus, inhibition of the TNF-α cascade is an effective way to diminish the progression of the disease. We are interested in investigating the difference between primary human synovial fibroblast (hSF) cells and SW982 as synovitis models induced by TNF-α and in monitoring their responses to sesamin as an anti-inflammatory phytochemical. METHOD: The designed experiments were performed in hSF cells or the SW982 cell line treated with 10 ng/ml TNF-α with or without 0.25, 0.5 or 1 µM sesamin. Subsequently, pro-inflammatory cytokine genes and proteins were measured in parallel with a study of associated signalling transduction involved in inflammatory processes, including NF-κB and MAPK pathways. RESULTS: The results demonstrated that although hSF and SW982 cells responded to TNF-α induction in the same fashion, they reacted at different levels. TNF-α could induce IL-6, IL-8 and IL-1ß in both cell types, but the levels in SW982 cells were much higher than in hSF cells. This characteristic was due to the different induction of MAPKs in each cell type. Both cell types reacted to sesamin in almost the same fashion. However, hSF cells were more sensitive to sesamin than SW982 cells in terms of the anti-RA effect. CONCLUSIONS: The responses of TNF-α-induced hSF and SW982 were different at the signal transduction level. However, the two cell types showed almost the same reaction to sesamin treatment in terms of the end point of the response.
[Mh] Termos MeSH primário: Dioxóis/farmacologia
Fibroblastos/efeitos dos fármacos
Lignanas/farmacologia
Membrana Sinovial/citologia
Sinovite/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Artrite Reumatoide
Linhagem Celular
Citocinas/metabolismo
Seres Humanos
Modelos Biológicos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Dioxoles); 0 (Lignans); 0 (Tumor Necrosis Factor-alpha); S7946O4P76 (sesamin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2035-2


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[PMID]:29255213
[Au] Autor:Donahue HJ; Qu RW; Genetos DC
[Ad] Endereço:Department of Biomedical Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, Virginia 23284, USA.
[Ti] Título:Joint diseases: from connexins to gap junctions.
[So] Source:Nat Rev Rheumatol;14(1):42-51, 2017 Dec 19.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexons form the basis of hemichannels and gap junctions. They are composed of six tetraspan proteins called connexins. Connexons can function as individual hemichannels, releasing cytosolic factors (such as ATP) into the pericellular environment. Alternatively, two hemichannel connexons from neighbouring cells can come together to form gap junctions, membrane-spanning channels that facilitate cell-cell communication by enabling signalling molecules of approximately 1 kDa to pass from one cell to an adjacent cell. Connexins are expressed in joint tissues including bone, cartilage, skeletal muscle and the synovium. Indicative of their importance as gap junction components, connexins are also known as gap junction proteins, but individual connexin proteins are gaining recognition for their channel-independent roles, which include scaffolding and signalling functions. Considerable evidence indicates that connexons contribute to the function of bone and muscle, but less is known about the function of connexons in other joint tissues. However, the implication that connexins and gap junctional channels might be involved in joint disease, including age-related bone loss, osteoarthritis and rheumatoid arthritis, emphasizes the need for further research into these areas and highlights the therapeutic potential of connexins.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Conexinas/metabolismo
Junções Comunicantes/metabolismo
Artropatias/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/metabolismo
Osso e Ossos/metabolismo
Cartilagem/metabolismo
Comunicação Celular/fisiologia
Diferenciação Celular/fisiologia
Conexinas/fisiologia
Conexinas/uso terapêutico
Junções Comunicantes/fisiologia
Seres Humanos
Ativação do Canal Iônico/fisiologia
Canais Iônicos/fisiologia
Camundongos
Camundongos Knockout
Sistema Musculoesquelético/metabolismo
Sistema Musculoesquelético/patologia
Osteoartrite/metabolismo
Osteoporose/metabolismo
Membrana Sinovial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (Ion Channels)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.204


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[PMID]:28957567
[Au] Autor:Favero M; El-Hadi H; Belluzzi E; Granzotto M; Porzionato A; Sarasin G; Rambaldo A; Iacobellis C; Cigolotti A; Fontanella CG; Natali A; Ramonda R; Ruggieri P; De Caro R; Vettor R; Rossato M; Macchi V
[Ad] Endereço:Rheumatology Unit, Department of Medicine - DIMED, University Hospital of Padova, Padova.
[Ti] Título:Infrapatellar fat pad features in osteoarthritis: a histopathological and molecular study.
[So] Source:Rheumatology (Oxford);56(10):1784-1793, 2017 Oct 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objective: The infrapatellar fat pad (IFP) is considered a local producer of adipocytokines, suggesting a potential role in OA. The objective of this study was to evaluate the histopathological and molecular characteristics of OA IFPs compared with controls. Methods: The histopathological characteristics of IFPs were evaluated in patients undergoing total knee replacements and in control patients (without OA), considering the following parameters: presence of inflammatory cells, vascularization, adipose lobules dimension and thickness of the interlobular septa. Immunohistochemistry was performed to evaluate VEGF, monocyte chemotactic protein 1 (MCP-1) and IL-6 proteins. Quantitative real time PCR was performed to evaluate the expression levels of adipocytokines in the OA IFPs. Results: OA IFPs showed an increase in inflammatory infiltration, vascularization and thickness of the interlobular septa compared with controls. VEGF, MCP-1 and IL-6 proteins were higher in OA IFPs compared with in controls. Inflammatory infiltration, hyperplasia, vascularization and fibrosis were increased in OA IFP synovial membranes compared with in those of controls. VEGF protein levels were associated with an increased number of vessels in the OA IFPs, while MCP-1 and IL-6 protein levels were associated with higher grades of inflammatory infiltration. Leptin levels were positively correlated with adiponectin and MCP-1expression, while adiponectin positively correlated with peroxisome proliferative activated receptor gamma, MCP-1 and IFP vascularity. MCP-1 showed a positive correlation with peroxisome proliferative activated receptor gamma. IFP lobules dimensions were positively correlated with IL-6 expression and negatively with thickness of interlobular septa. VEGF mRNA levels were positively correlated with increased synovial vascularity. Conclusions: OA IFPs and synovial membranes are more inflamed, vascularized and fibrous compared with those of control patients (without OA).
[Mh] Termos MeSH primário: Tecido Adiposo/patologia
Osteoartrite do Joelho/patologia
Patela/patologia
[Mh] Termos MeSH secundário: Adipocinas/análise
Adiponectina/análise
Tecido Adiposo/irrigação sanguínea
Tecido Adiposo/metabolismo
Idoso
Idoso de 80 Anos ou mais
Artroplastia do Joelho
Estudos de Casos e Controles
Quimiocina CCL2/análise
Feminino
Seres Humanos
Interleucina-6/análise
Articulação do Joelho/irrigação sanguínea
Articulação do Joelho/metabolismo
Articulação do Joelho/patologia
Masculino
Meia-Idade
Osteoartrite do Joelho/metabolismo
Osteoartrite do Joelho/cirurgia
Patela/irrigação sanguínea
Patela/metabolismo
Membrana Sinovial/irrigação sanguínea
Membrana Sinovial/metabolismo
Membrana Sinovial/patologia
Fator A de Crescimento do Endotélio Vascular/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adipokines); 0 (Adiponectin); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[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/kex287


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[PMID]:28898718
[Au] Autor:Ganesan R; Rasool M
[Ad] Endereço:Immunopathology Lab, School of Bio Sciences and Technology, VIT University, Vellore 632 014, Tamilnadu, India.
[Ti] Título:Interleukin 17 regulates SHP-2 and IL-17RA/STAT-3 dependent Cyr61, IL-23 and GM-CSF expression and RANKL mediated osteoclastogenesis by fibroblast-like synoviocytes in rheumatoid arthritis.
[So] Source:Mol Immunol;91:134-144, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-17 predominately produced by the Th17 cells, plays a crucial role in the fibroblast-like synoviocytes (FLS) mediated disease process of rheumatoid arthritis (RA). IL-17 exerts its pathogenic effects in RA-FLS by IL-17/IL-17RA/STAT-3 signaling. Recent studies have shown that RA-FLS produces SHP-2, Cyr61, IL-23, GM-CSF and RANKL which results in worsening of the disease. However, whether IL-17/IL-17RA/STAT-3 signaling regulates SHP-2, Cyr61, IL-23, GM-CSF and RANKL expressions in RA-FLS remains unknown. In this study, IL-17 treatment dramatically induced the production of Cyr61, IL-23 and GM-CSF in FLS isolated from adjuvant induced arthritis (AA) rats. Conversely, IL-17 mediated production of Cyr61, IL-23 and GM-CSF was abrogated by knockdown of IL-17RA using a small interfering RNA or blockade of STAT-3 activation with S3I-201 in AA-FLS. Interestingly, IL-17 treatment noticeably increased the expression of IL-17RA and SHP-2 in AA-FLS. However, silencing of IL-17RA reversed the effect of IL-17 on the expression of IL-17RA and SHP-2 in AA-FLS. In addition, an increased number of TRAP-positive multinucleated cells were observed in a coculture system consisting of IL-17 treated AA-FLS and rat bone marrow derived monocytes/macrophages. Further, mechanistically we found that IL-17 upregulated RANKL expression in AA-FLS that was dependent on the IL-17/IL-17RA/STAT-3 signaling cascade. Knockdown of IL-17RA or inhibition of STAT-3 activation decreased the IL- 17 induced RANKL expression by AA-FLS and their osteoclastogenic potential. Taken together, our findings demonstrate that IL-17 regulates SHP-2 expression and IL-17RA/STAT-3 dependent production of Cyr61, IL-23, GM-CSF and RANKL in AA-FLS and may reveal a new insight into the pathogenesis of RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Proteína Rica em Cisteína 61/imunologia
Fibroblastos/imunologia
Regulação da Expressão Gênica/imunologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Interleucina-17/imunologia
Interleucina-23/imunologia
Osteoclastos/imunologia
Proteína Tirosina Fosfatase não Receptora Tipo 11/imunologia
Ligante RANK/imunologia
Receptores de Interleucina-17/imunologia
Fator de Transcrição STAT3/imunologia
Transdução de Sinais/imunologia
Membrana Sinovial/imunologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/patologia
Fibroblastos/patologia
Osteoclastos/patologia
Ratos
Ratos Wistar
Membrana Sinovial/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyr61 protein, rat); 0 (Cysteine-Rich Protein 61); 0 (Interleukin-17); 0 (Interleukin-23); 0 (RANK Ligand); 0 (Receptors, Interleukin-17); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE


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[PMID]:28865311
[Au] Autor:Liu YR; Yan X; Yu HX; Yao Y; Wang JQ; Li XF; Chen RN; Xu QQ; Ma TT; Huang C; Li J
[Ad] Endereço:Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China; The Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, China.
[Ti] Título:NLRC5 promotes cell proliferation via regulating the NF-κB signaling pathway in Rheumatoid arthritis.
[So] Source:Mol Immunol;91:24-34, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease and the pathogenesis remains unclear. Previous studies suggested that fibroblast-like synoviocytes (FLSs) play an important role in RA pathogenesis, including the injury of cartilage, the hyperplasia of the synovium and the release of inflammatory cytokines. We used complete Freund's adjuvant (CFA) induced rats as animal models for studying the RA pathogenesis. NLRC5 as the largest member of the NLR family has been reported to play a critical role in regulating immune responses. Increasing evidence suggests that NLRC5 is an pivotal negative modulator of inflammatory pathways. We investigated the mechanisms and signaling pathways of NLRC5 in RA progression. Significantly increased expression of NLRC5 was found in AA rats synovial tissues and cells. And high expression of inflammatory cytokine and cell proliferation of FLSs accompanied with NLRC5 overexpression, but inhibited in cells with NLRC5 silencing treatment. Interestingly, we found that overexpression of NLRC5 also coordinated the activation of NF-κB signaling pathway. These results suggested that NLRC5 promotes RA progression via the NF-κB signaling pathway potentially.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Proliferação Celular
Regulação da Expressão Gênica/imunologia
Peptídeos e Proteínas de Sinalização Intracelular/imunologia
NF-kappa B/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/induzido quimicamente
Artrite Reumatoide/genética
Citocinas/genética
Citocinas/imunologia
Feminino
Adjuvante de Freund/efeitos adversos
Adjuvante de Freund/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
NF-kappa B/genética
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Membrana Sinovial/imunologia
Membrana Sinovial/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Intracellular Signaling Peptides and Proteins); 0 (NF-kappa B); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE


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[PMID]:28863153
[Au] Autor:Walsh AM; Wechalekar MD; Guo Y; Yin X; Weedon H; Proudman SM; Smith MD; Nagpal S
[Ad] Endereço:Immunology, Janssen Research and Development, LLC., Spring House, Pennsylvania, United States of America.
[Ti] Título:Triple DMARD treatment in early rheumatoid arthritis modulates synovial T cell activation and plasmablast/plasma cell differentiation pathways.
[So] Source:PLoS One;12(9):e0183928, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This study sought to investigate the genome-wide transcriptional effects of a combination of disease modifying anti-rheumatic drugs (tDMARD; methotrexate, sulfasalazine and hydroxychloroquine) in synovial tissues obtained from early rheumatoid arthritis (RA) patients. While combination DMARD strategies have been investigated for clinical efficacy, very little data exists on the potential molecular mechanism of action. We hypothesized that tDMARD would impact multiple biological pathways, but the specific pathways were unknown. METHODS: Paired synovial biopsy samples from early RA patients before and after 6 months of tDMARD therapy were collected by arthroscopy (n = 19). These biopsies as well as those from subjects with normal synovium (n = 28) were profiled by total RNA sequencing. RESULTS: Large differences in gene expression between RA and control biopsies (over 5000 genes) were identified. Despite clinical efficacy, the expression of a restricted set of less than 300 genes was reversed after 6 months of treatment. Many genes remained elevated, even in patients who achieved low disease activity. Interestingly, tDMARD downregulated genes included those involved in T cell activation and signaling and plasmablast/plasma cell differentiation and function. CONCLUSIONS: We have identified transcriptomic signatures that characterize synovial tissue from RA patients with early disease. Analysis after 6 months of tDMARD treatment highlight consistent alterations in expression of genes related to T cell activation and plasmablast/plasma cell differentiation. These results provide novel insight into the biology of early RA and the mechanism of tDMARD action and may help identify novel drug targets to improve rates of treatment-induced disease remission.
[Mh] Termos MeSH primário: Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Membrana Sinovial/efeitos dos fármacos
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Artroscopia
Biópsia
Estudos de Casos e Controles
Diferenciação Celular
Regulação para Baixo
Quimioterapia Combinada
Feminino
Seres Humanos
Hidroxicloroquina/uso terapêutico
Ativação Linfocitária/efeitos dos fármacos
Masculino
Metotrexato/uso terapêutico
Meia-Idade
Plasmócitos/citologia
Análise de Componente Principal
Indução de Remissão
Análise de Sequência de RNA
Sulfassalazina/uso terapêutico
Membrana Sinovial/metabolismo
Linfócitos T/efeitos dos fármacos
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 3XC8GUZ6CB (Sulfasalazine); 4QWG6N8QKH (Hydroxychloroquine); YL5FZ2Y5U1 (Methotrexate)
[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:170902
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183928



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