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Pesquisa : D12.776.543.750.705.852.760.345 [Categoria DeCS]
Referências encontradas : 2237 [refinar]
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  1 / 2237 MEDLINE  
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[PMID]:29025654
[Au] Autor:Cheng Z; Landish B; Chi Z; Nannan C; Jingyu D; Sen L; Xiangjin L
[Ad] Endereço:Department of Orthopaedic Orthopaedics, First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou 310003, People's Republic of China; The Sport Medicine Center of the First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou
[Ti] Título:3D printing hydrogel with graphene oxide is functional in cartilage protection by influencing the signal pathway of Rank/Rankl/OPG.
[So] Source:Mater Sci Eng C Mater Biol Appl;82:244-252, 2018 Jan 01.
[Is] ISSN:1873-0191
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:3Dprinting is defined as the use of printing technology to deposit living cells, and biomaterials on a given /a substrate. Graphene oxide nanoparticles (GO-np) have been used as a delivery vehicle for small molecule drugs in order to investigate the state of GO-np within 3D tissue constructs in terms of a composite 3D printing scaffold, which in turn is relevant to the protection of cartilage. We transplanted rats with hydrogel/GO-np and hydrogel, which in turn showed that hydrogel/GO-np protected the tissue of cartilage by the signal pathway of Rank/Rankl/OPG. Those findings indicated that GO-np may be potentially used to control the release of carrier materials and influence the signal pathway of Rank/Rankl/OPG.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Cartilagem/metabolismo
Grafite/química
Hidrogéis/química
Osteoprotegerina/metabolismo
Ligante RANK/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis/farmacologia
Proteína Morfogenética Óssea 7/química
Proteína Morfogenética Óssea 7/metabolismo
Proteína Morfogenética Óssea 7/farmacologia
Cartilagem/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Portadores de Fármacos/química
Seres Humanos
Masculino
Nanopartículas/química
Óxidos/química
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Tecidos Suporte/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Bone Morphogenetic Protein 7); 0 (Drug Carriers); 0 (Hydrogels); 0 (Osteoprotegerin); 0 (Oxides); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B); 7782-42-5 (Graphite)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  2 / 2237 MEDLINE  
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[PMID]:28464271
[Au] Autor:Yang X; Gao W; Wang B; Wang X; Guo H; Xiao Y; Kong L; Hao D
[Ad] Endereço:Hong-Hui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, 710054, China.
[Ti] Título:Picroside II Inhibits RANKL-Mediated Osteoclastogenesis by Attenuating the NF-κB and MAPKs Signaling Pathway In Vitro and Prevents Bone Loss in Lipopolysaccharide Treatment Mice.
[So] Source:J Cell Biochem;118(12):4479-4486, 2017 Dec.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Picroside II, one of the major components isolated from the seed of natural plant picrorhiza, is widely used in traditional Chinese medicine. The present study was performed to define effects of picroside II on nuclear factor-kappaB ligand (RANKL)-stimulated osteoclast differentiation in vitro and on lipopolysaccharide (LPS)-induced bone loss in vivo. The bone marrow cells (BMMs) were harvested and induced with RANKL followed by treatment with picroside II at several doses, and the differentiation of osteoclasts from these cells was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and resorption pit formation assay. The effects of picroside II on osteoclastogenesis were studied by examining RANKL-induced osteoclast F-actin ring formation and osteoclast bone resorption. Moreover, we explored the mechanisms of these downregulation effects by performed Western blotting and quantitative RT-PCR examination. Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. Moreover, picroside II markedly decreased the phosphorylation of p38, ERK, JNK, p65, and I-κB degradation, and significantly suppressed c-Fos and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), both the key transcription factors during osteoclastogenesis. Furthermore, in vivo studies verified the bone protection effects of picroside II. These results collectively suggested that picroside II acted as an anti-resorption agent by blocking osteoclast activation. J. Cell. Biochem. 118: 4479-4486, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Cinamatos/farmacologia
Glucosídeos Iridoides/farmacologia
Lipopolissacarídeos/toxicidade
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
NF-kappa B/metabolismo
Osteoclastos/metabolismo
Osteólise
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos
Osteoclastos/patologia
Osteólise/induzido quimicamente
Osteólise/metabolismo
Osteólise/patologia
Osteólise/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cinnamates); 0 (Iridoid Glucosides); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tnfrsf11a protein, mouse); 39012-20-9 (picroside II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.26105


  3 / 2237 MEDLINE  
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[PMID]:29025596
[Au] Autor:Papanastasiou AD; Sirinian C; Plakoula E; Zolota V; Zarkadis IK; Kalofonos HP
[Ad] Endereço:Clinical and Molecular Oncology Laboratory, Division of Oncology, School of Medicine, University of Patras, 26504, Greece. Electronic address: apapanasta@gmail.com.
[Ti] Título:RANK and EGFR in invasive breast carcinoma.
[So] Source:Cancer Genet;216-217:61-66, 2017 Oct.
[Is] ISSN:2210-7762
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Breast cancer is the most common malignancy, affecting one in eight women in North America and Europe. The human epidermal growth factor receptor (EGFR) protein comprises a major determinant of normal development but also cancer. RANK receptor (Receptor Activator of Nuclear factor-κB) is a tumor necrosis superfamily member and a binding partner for RANKL, which was recently implicated in breast cancer initiation, progression and metastasis. Here we provide preliminary evidence of a possible interplay between RANK and EGFR signaling in breast cancer. TCGA (cancergenome.nih.gov) publicly available data for EGFR and TNFRSF11A (RANK) genes from breast cancer patients and breast cancer cell lines were retrieved and analyzed. RANK mRNA showed a statistically significant positive correlation (p <0.001) with the mRNA and protein expression of EGFR, but not with ERBB2/3/4. Further analyses of survival data of a group of breast cancer patients (n = 248) from TCGA, revealed an EGFR /RANK subpopulation that showed a statistically significant (p = 0.001) reduced overall survival when compared to EGFR /RANK group of patients. Finally, EGFR and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT and ERK signaling after EGF stimulation in cell lines and also an increase of breast cancer cell invasiveness.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Receptor Ativador de Fator Nuclear kappa-B/genética
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Invasividade Neoplásica
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (TNFRSF11A protein, human); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  4 / 2237 MEDLINE  
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[PMID]:28885764
[Au] Autor:Chypre M; Madel MB; Chaloin O; Blin-Wakkach C; Morice C; Mueller CG
[Ad] Endereço:Prestwick Chemical, PC SAS, 67400, Illkirch-Graffenstaden, France.
[Ti] Título:Porphyrin Derivatives Inhibit the Interaction between Receptor Activator of NF-κB and Its Ligand.
[So] Source:ChemMedChem;12(20):1697-1702, 2017 Oct 20.
[Is] ISSN:1860-7187
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Receptor activator of NF-κB (RANK), a member of the TNF-receptor superfamily, plays an important role in bone resorption and stimulates immune and epithelial cell activation. Denosumab, a human monoclonal antibody that blocks the RANK ligand (RANKL), is approved for the treatment of osteoporosis and bone metastasis. However, a small molecule that inhibits the RANK-RANKL interaction would be beneficial to decrease cost and to facilitate treatments with orally available therapeutic agents. Herein we report the discovery of the first nonpeptidic inhibitors of RANK-RANKL interactions. In screening a chemical library by competitive ELISA, the porphyrin verteporfin was identified as a hit. Derivatives were screened, and the chlorin-macrocycle-containing pheophorbide A and purpurin 18 were found to bind recombinant RANKL, to inhibit RANK-RANKL interactions in the ELISA, and to suppress the RANKL-dependent activation of model cells and the differentiation of RANK-expressing precursors into osteoclasts. This discovery of a family of small molecules that inhibit RANK activation presents an initial basis for further development of nonpeptidic therapeutic agents targeting the interaction between RANK and RANKL.
[Mh] Termos MeSH primário: Porfirinas/farmacologia
Ligante RANK/antagonistas & inibidores
Receptor Ativador de Fator Nuclear kappa-B/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular
Seres Humanos
Células Jurkat
Camundongos
Estrutura Molecular
Osteogênese/efeitos dos fármacos
Porfirinas/química
Ligação Proteica
Ligante RANK/química
Ligante RANK/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/química
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Porphyrins); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1002/cmdc.201700462


  5 / 2237 MEDLINE  
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[PMID]:28882590
[Au] Autor:Nagashima K; Sawa S; Nitta T; Prados A; Koliaraki V; Kollias G; Nakashima T; Takayanagi H
[Ad] Endereço:Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113-0033, Japan.
[Ti] Título:Targeted deletion of RANKL in M cell inducer cells by the Col6a1-Cre driver.
[So] Source:Biochem Biophys Res Commun;493(1):437-443, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gut-associated lymphoid tissues (GALTs), including Peyer's patches (PPs), cryptopatches (CPs) and isolated lymphoid follicles (ILFs), establish a host-microbe symbiosis by the promotion of immune reactions against gut microbes. Microfold cell inducer (MCi) cells in GALTs are the recently identified mesenchymal cells that express the cytokine RANKL and initiate bacteria-specific immunoglobulin A (IgA) production via induction of microfold (M) cell differentiation. In the previous study, the Twist2-Cre driver was utilized for gene deletion in mesenchymal cells including MCi cells. In order to investigate MCi cells more extensively, it will be necessary to develop experimental tools in addition to the Twist2-Cre driver mice and characterize such drivers in specificity and efficiency. Here we show that M cell differentiation and IgA production are impaired in the targeted deletion of RANKL by the Col6a1-Cre driver. We compared Col6a1-Cre with Twist2-Cre in terms of the specificity for mesenchymal cells in GALTs. Col6a1-Cre CAG-CAT-EGFP mice exhibited EGFP expression in podoplanin CD31 cells including MCi cells, while Twist2-Cre mice were shown to target endothelial cells and podoplanin CD31 cells. Tnfsf11 Col6a1-Cre mice exhibited the absence of M cells and severe IgA reduction together with an alteration in gut microbial composition. Moreover, we analyzed germ free mice to test whether changes in the microbiota are the cause of M cell deficiency. M cell differentiation was normal in the CPs/ILFs of germ free mice, indicating that MCi cells induce M cells independently of microbial colonization. This study demonstrates that Col6a1-Cre driver mice are as useful as Twist2-Cre driver mice for functional analyses of GALT-resident mesenchymal cells, including MCi cells.
[Mh] Termos MeSH primário: Colágeno Tipo VI/genética
Integrases/genética
Mucosa Intestinal/imunologia
Receptor Ativador de Fator Nuclear kappa-B/genética
Receptor Ativador de Fator Nuclear kappa-B/imunologia
Linfócitos T Auxiliares-Indutores/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Deleção de Genes
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Col6a1 protein, mouse); 0 (Collagen Type VI); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tnfrsf11a protein, mouse); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  6 / 2237 MEDLINE  
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[PMID]:28847008
[Au] Autor:Araújo AA; Pereira ASBF; Medeiros CACX; Brito GAC; Leitão RFC; Araújo LS; Guedes PMM; Hiyari S; Pirih FQ; Araújo Júnior RF
[Ad] Endereço:Department of Biophysics and Pharmacology, Post Graduation Program Public Health / Post Graduation Program in Pharmaceutical Science, UFRN, Natal, RN, Brazil.
[Ti] Título:Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis.
[So] Source:PLoS One;12(8):e0183506, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To evaluate the effects of metformin (Met) on inflammation, oxidative stress, and bone loss in a rat model of ligature-induced periodontitis. MATERIALS & METHODS: Male albino Wistar rats were divided randomly into five groups of twenty-one rats each, and given the following treatments for 10 days: (1) no ligature + water, (2) ligature + water, (3) ligature + 50 mg/kg Met, (4) ligature + 100 mg/kg Met, and (5) ligature + 200 mg/kg Met. Water or Met was administered orally. Maxillae were fixed and scanned using Micro-computed Tomography (µCT) to quantitate linear and bone volume/tissue volume (BV/TV) volumetric bone loss. Histopathological characteristics were assessed through immunohistochemical staining for MMP-9, COX-2, the RANKL/RANK/OPG pathway, SOD-1, and GPx-1. Additionally, confocal microscopy was used to analyze osteocalcin fluorescence. UV-VIS analysis was used to examine the levels of malondialdehyde, glutathione, IL-1ß and TNF-α from gingival tissues. Quantitative RT-PCR reaction was used to gene expression of AMPK, NF-κB (p65), and Hmgb1 from gingival tissues. Significance among groups were analysed using a one-way ANOVA. A p-value of p<0.05 indicated a significant difference. RESULTS: Treatment with 50 mg/kg Met significantly reduced concentrations of malondialdehyde, IL-1ß, and TNF-α (p < 0.05). Additionally, weak staining was observed for COX-2, MMP-9, RANK, RANKL, SOD-1, and GPx-1 after 50 mg/kg Met. OPG and Osteocalcin showed strong staining in the same group. Radiographically, linear measurements showed a statistically significant reduction in bone loss after 50 mg/kg Met compared to the ligature and Met 200 mg/kg groups. The same pattern was observed volumetrically in BV/TV and decreased osteoclast number (p<0.05). RT-PCR showed increased AMPK expression and decreased expression of NF-κB (p65) and HMGB1 after 50 mg/kg Met. CONCLUSIONS: Metformin, at a concentration of 50 mg/kg, decreases the inflammatory response, oxidative stress and bone loss in ligature-induced periodontitis in rats.
[Mh] Termos MeSH primário: Perda do Osso Alveolar/tratamento farmacológico
Metformina/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Periodontite/tratamento farmacológico
[Mh] Termos MeSH secundário: Perda do Osso Alveolar/diagnóstico por imagem
Perda do Osso Alveolar/metabolismo
Perda do Osso Alveolar/patologia
Animais
Modelos Animais de Doenças
Gengiva/metabolismo
Glutationa Peroxidase/metabolismo
Inflamação/diagnóstico por imagem
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Inflamação/patologia
Interleucina-1beta/metabolismo
Masculino
Malondialdeído/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Metformina/uso terapêutico
NF-kappa B/metabolismo
Periodontite/diagnóstico por imagem
Periodontite/metabolismo
Periodontite/patologia
Ligante RANK/metabolismo
Ratos
Ratos Wistar
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (NF-kappa B); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tumor Necrosis Factor-alpha); 4Y8F71G49Q (Malondialdehyde); 9100L32L2N (Metformin); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.9 (Glutathione Peroxidase); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183506


  7 / 2237 MEDLINE  
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[PMID]:28832712
[Au] Autor:Lin M; Hu Y; Wang Y; Kawai T; Wang Z; Han X
[Ad] Endereço:Beijing ChaoYang Hospital affiliated with Capital Medical University, Department of Stomatology, Beijing, China.
[Ti] Título:Different engagement of TLR2 and TLR4 in Porphyromonas gingivalis vs. ligature-induced periodontal bone loss.
[So] Source:Braz Oral Res;31:e63, 2017 Aug 21.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study was conducted to investigate the roles of different Toll-like receptor (TLR) signaling in Porphyromonas gingivalis (P. gingivalis)-induced and ligature-induced experimental periodontal bone resorption in mice. Wild-type (WT), TLR2 knockout (KO), TLR4KO, and TLR2&4 KO mice with C57/BL6 background were divided into three groups: control, P. gingivalis infection, and ligation. Live P. gingivalis or silk ligatures were placed in the sulcus around maxillary second molars over a 2-week period. Images were captured by digital stereomicroscopy, and the bone resorption area was measured with ImageJ software. The protein expression level of gingival RANKL was measured by ELISA. The gingival mRNA levels of RANKL, IL-1ß, TNF-α, and IL-10 were detected by RT-qPCR. The results showed that P. gingivalis induced significant periodontal bone resorption in WT mice and TLR2 KO mice but not in TLR4 KO mice or TLR2&4 KO mice. For all four types of mice, ligation induced significant bone loss compared with that in control groups, and this bone loss was significantly higher than that in the P. gingivalis infection group. RANKL protein expression was significantly increased in the ligation group compared with that in the control group for all four types of mice, and in the P. gingivalis infection group of WT, TLR2 KO, and TLR4 KO mice. Expression patterns of RANKL, IL-1ß, TNF-α, and IL-10 mRNA were different in the P. gingivalis infection group and the ligation group in different types of mice. In summary, P. gingivalis-induced periodontal bone resorption is TLR4-dependent, whereas ligation-induced periodontal bone resorption is neither TLR2- nor TLR4-dependent.
[Mh] Termos MeSH primário: Perda do Osso Alveolar/etiologia
Modelos Animais de Doenças
Periodontite/microbiologia
Porphyromonas gingivalis/patogenicidade
Receptor 2 Toll-Like/fisiologia
Receptor 4 Toll-Like/fisiologia
[Mh] Termos MeSH secundário: Perda do Osso Alveolar/microbiologia
Animais
Ensaio de Imunoadsorção Enzimática
Interleucina-10/metabolismo
Interleucina-1beta/metabolismo
Ligadura
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Reprodutibilidade dos Testes
Fatores de Tempo
Receptor 2 Toll-Like/análise
Receptor 2 Toll-Like/genética
Receptor 4 Toll-Like/análise
Receptor 4 Toll-Like/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tlr2 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Tnfrsf11a protein, mouse); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


  8 / 2237 MEDLINE  
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[PMID]:28814613
[Au] Autor:Okamoto K; Nakashima T; Shinohara M; Negishi-Koga T; Komatsu N; Terashima A; Sawa S; Nitta T; Takayanagi H
[Ad] Endereço:Department of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan; Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan; Japan Science and Technology Agency (JST), Precu
[Ti] Título:Osteoimmunology: The Conceptual Framework Unifying the Immune and Skeletal Systems.
[So] Source:Physiol Rev;97(4):1295-1349, 2017 Oct 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The immune and skeletal systems share a variety of molecules, including cytokines, chemokines, hormones, receptors, and transcription factors. Bone cells interact with immune cells under physiological and pathological conditions. Osteoimmunology was created as a new interdisciplinary field in large part to highlight the shared molecules and reciprocal interactions between the two systems in both heath and disease. Receptor activator of NF-κB ligand (RANKL) plays an essential role not only in the development of immune organs and bones, but also in autoimmune diseases affecting bone, thus effectively comprising the molecule that links the two systems. Here we review the function, gene regulation, and signal transduction of osteoimmune molecules, including RANKL, in the context of osteoclastogenesis as well as multiple other regulatory functions. Osteoimmunology has become indispensable for understanding the pathogenesis of a number of diseases such as rheumatoid arthritis (RA). We review the various osteoimmune pathologies, including the bone destruction in RA, in which pathogenic helper T cell subsets [such as IL-17-expressing helper T (Th17) cells] induce bone erosion through aberrant RANKL expression. We also focus on cellular interactions and the identification of the communication factors in the bone marrow, discussing the contribution of bone cells to the maintenance and regulation of hematopoietic stem and progenitors cells. Thus the time has come for a basic reappraisal of the framework for understanding both the immune and bone systems. The concept of a unified osteoimmune system will be absolutely indispensable for basic and translational approaches to diseases related to bone and/or the immune system.
[Mh] Termos MeSH primário: Imunidade
Esqueleto/imunologia
[Mh] Termos MeSH secundário: Alergia e Imunologia
Animais
Artrite Reumatoide/imunologia
Comunicação Celular
Células-Tronco Hematopoéticas/fisiologia
Seres Humanos
Osteoclastos/metabolismo
Osteologia
Osteoprotegerina/metabolismo
Ligante RANK/imunologia
Ligante RANK/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/imunologia
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Transdução de Sinais
Esqueleto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Osteoprotegerin); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (TNFRSF11A protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00036.2016


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[PMID]:28709801
[Au] Autor:Onder L; Mörbe U; Pikor N; Novkovic M; Cheng HW; Hehlgans T; Pfeffer K; Becher B; Waisman A; Rülicke T; Gommerman J; Mueller CG; Sawa S; Scandella E; Ludewig B
[Ad] Endereço:Institute of Immunobiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
[Ti] Título:Lymphatic Endothelial Cells Control Initiation of Lymph Node Organogenesis.
[So] Source:Immunity;47(1):80-92.e4, 2017 Jul 18.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymph nodes (LNs) are strategically situated throughout the body at junctures of the blood vascular and lymphatic systems to direct immune responses against antigens draining from peripheral tissues. The current paradigm describes LN development as a programmed process that is governed through the interaction between mesenchymal lymphoid tissue organizer (LTo) cells and hematopoietic lymphoid tissue inducer (LTi) cells. Using cell-type-specific ablation of key molecules involved in lymphoid organogenesis, we found that initiation of LN development is dependent on LTi-cell-mediated activation of lymphatic endothelial cells (LECs) and that engagement of mesenchymal stromal cells is a succeeding event. LEC activation was mediated mainly by signaling through receptor activator of NF-κB (RANK) and the non-canonical NF-κB pathway and was steered by sphingosine-1-phosphate-receptor-dependent retention of LTi cells in the LN anlage. Finally, the finding that pharmacologically enforced interaction between LTi cells and LECs promotes ectopic LN formation underscores the central LTo function of LECs.
[Mh] Termos MeSH primário: Células Endoteliais/fisiologia
Linfonodos/fisiologia
Células Mesenquimais Estromais/fisiologia
Organogênese
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Coristoma
Embrião de Mamíferos
Receptor beta de Linfotoxina/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
NF-kappa B/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ltbr protein, mouse); 0 (Lymphotoxin beta Receptor); 0 (NF-kappa B); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Receptors, Lysosphingolipid); 0 (Tnfrsf11a protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


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[PMID]:28682542
[Au] Autor:Zhu C; Lingkai S
[Ad] Endereço:Dept. of Conservative Dentistry and Endodontics, Guiyang Hospital of Stomatology, Affiliated Guiyang Hospital of Stomatology, Zunyi Medical University, Guiyang 550002, China.
[Ti] Título:[Effects of paeonol on the function of bone marrow-derived macrophage from Porphyromonas gingivalis-induced mice].
[So] Source:Hua Xi Kou Qiang Yi Xue Za Zhi;35(2):139-144, 2017 Apr 01.
[Is] ISSN:1000-1182
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: This work aims to examine the effects of paeonol treatment on the ability of bone marrow-derived macrophage (BMM) to excrete inflammatory factors and to differentiate into osteoclasts upon induction with Porphyromonas gingivalis (P. gingivalis). This work also aims to investigate the underlying mechanisms of these abilities. METHODS: BMM culture was treated with different paeonol concentrations at for 1 h and then stimulated with P. gingivalis for 24 h before programmed death-ligand 1 (PD-L1) was quantified with flow cytometry. Tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA). The BMM culture was treated with the receptor activator for nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF), and then with paeonol for 1 h prior to induction with P. gingivalis. Then, osteoclast formation was assessed using tartrate resistant acid phosphatase (TRAP) staining. The osteoclast-related proteins TRAP and receptor activator of nuclear factor-κB (RANK) were quantified by Western blotting. RESULTS: Paeonol was nontoxic to BMM within a range of 10-50 µmol·L⁻¹. Flow cytometry showed that paeonol inhibited PD-L1 expression in P. gingivalis-induced BMM in a dose-dependent manner. ELISA indicated that paeonol dose-dependently inhibited the excretion of TNF-α, IL-1ß, and IL-6 by P. gingivalis-induced BMM (P<0.01). TRAP staining revealed that paenol treatment inhibited the differentiation of P. gingivalis-induced BMM into osteoclasts. Western blot results suggested that paeonol decreased the expression of TRAP and RANK in BMM. CONCLUSIONS: Paeonol dose-dependently inhibited the excretion of the inflammatory factors TNF-α, IL-1ß, and IL-6 by P. gingivalis-induced BMM in a dose-dependent manner. Moreover, paenol treatment prevented the differentiation of P. gingivalis-induced BMM differentiation into osteoclasts.
.
[Mh] Termos MeSH primário: Acetofenonas/farmacologia
Diferenciação Celular
Macrófagos
Osteoclastos
Porphyromonas gingivalis
[Mh] Termos MeSH secundário: Fosfatase Ácida
Animais
Proteínas de Transporte
Interleucina-1beta
Interleucina-6
Isoenzimas
Fator Estimulador de Colônias de Macrófagos
Glicoproteínas de Membrana
Camundongos
Ligante RANK
Receptor Ativador de Fator Nuclear kappa-B
Fator de Necrose Tumoral alfa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Carrier Proteins); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Isoenzymes); 0 (Membrane Glycoproteins); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Tumor Necrosis Factor-alpha); 3R834EPI82 (paeonol); 81627-83-0 (Macrophage Colony-Stimulating Factor); EC 3.1.3.2 (Acid Phosphatase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.7518/hxkq.2017.02.006



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