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Pesquisa : D12.776.543.750.695.160.500.750 [Categoria DeCS]
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[PMID]:27312995
[Au] Autor:Nakanishi M; Morita Y; Hata K; Muragaki Y
[Ad] Endereço:Department of Pathology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan. Electronic address: n-masako@wakayama-med.ac.jp.
[Ti] Título:Acidic microenvironments induce lymphangiogenesis and IL-8 production via TRPV1 activation in human lymphatic endothelial cells.
[So] Source:Exp Cell Res;345(2):180-9, 2016 Jul 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Local acidosis is one of the characteristic features of the cancer microenvironment. Many reports indicate that acidosis accelerates the proliferation and invasiveness of cancer cells. However, whether acidic conditions affect lymphatic metastasis is currently unknown. In the present study, we focused on the effects of acidosis on lymphatic endothelial cells (LECs) to assess the relationship between acidic microenvironments and lymph node metastasis. We demonstrated that normal human LECs express various acid receptors by immunohistochemistry and reverse transcriptase-polymerase chain reaction (PCR). Acidic stimulation with low pH medium induced morphological changes in LECs to a spindle shape, and significantly promoted cellular growth and tube formation. Moreover, real-time PCR revealed that acidic conditions increased the mRNA expression of interleukin (IL)-8. Acidic stimulation increased IL-8 production in LECs, whereas a selective transient receptor potential vanilloid subtype 1 (TRPV1) antagonist, 5'-iodoresiniferatoxin, decreased IL-8 production. IL-8 accelerated the proliferation of LECs, and inhibition of IL-8 diminished tube formation and cell migration. In addition, phosphorylation of nuclear factor (NF)-κB was induced by acidic conditions, and inhibition of NF-κB activation reduced acid-induced IL-8 expression. These results suggest that acidic microenvironments in tumors induce lymphangiogenesis via TRPV1 activation in LECs, which in turn may promote lymphatic metastasis.
[Mh] Termos MeSH primário: Ácidos/farmacologia
Microambiente Celular/efeitos dos fármacos
Células Endoteliais/metabolismo
Linfangiogênese/efeitos dos fármacos
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Forma Celular/efeitos dos fármacos
Células Endoteliais/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
Concentração de Íons de Hidrogênio
Interleucina-8/biossíntese
Interleucina-8/genética
Interleucina-8/secreção
NF-kappa B/metabolismo
Neovascularização Fisiológica/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Superfície Celular/metabolismo
Receptores de Interleucina-8/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acids); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (Receptors, Interleukin-8); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170519
[Lr] Data última revisão:
170519
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160618
[St] Status:MEDLINE


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[PMID]:26801304
[Au] Autor:Giordano S; Zhao X; Xing D; Hage F; Oparil S; Cooke JP; Lee J; Nakayama KH; Huang NF; Chen YF
[Ad] Endereço:Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
[Ti] Título:Targeted delivery of human iPS-ECs overexpressing IL-8 receptors inhibits neointimal and inflammatory responses to vascular injury in the rat.
[So] Source:Am J Physiol Heart Circ Physiol;310(6):H705-15, 2016 Mar 15.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-8 (IL8) is highly expressed by injured arteries in a variety of diseases and is a chemoattractant for neutrophils which express IL8 receptors IL8RA and RB (IL8RA/B) on their membranes. Neutrophils interact with the damaged endothelium and initiate an inflammatory cascade at the site of injury. We have generated a novel translational targeted cell therapy for acute vascular injury using adenoviral vectors to overexpress IL8RA/B and green fluorescent protein (GFP) on the surface of endothelial cells (ECs) derived from human induced pluripotent stem cells (HiPS-IL8RA/B-ECs). We hypothesize that HiPS-IL8RA/B-ECs transfused intravenously into rats with balloon injury of the carotid artery will target to the injured site and compete with neutrophils, thus inhibiting inflammation and neointima formation. Young adult male Sprague-Dawley rats underwent balloon injury of the right carotid artery and received intravenous transfusion of saline vehicle, 1.5 × 10(6) HiPS-ECs, 1.5 × 10(6) HiPS-Null-ECs, or 1.5 × 10(6) HiPS-IL8RA/B-ECs immediately after endoluminal injury. Tissue distribution of HiPS-IL8RA/B-ECs was analyzed by a novel GFP DNA qPCR method. Cytokine and chemokine expression and leukocyte infiltration were measured in injured and uninjured arteries at 24 h postinjury by ELISA and immunohistochemistry, respectively. Neointimal, medial areas, and reendothelialization were measured 14 days postinjury. HiPS-IL8RA/B-ECs homed to injured arteries, inhibited inflammatory mediator expression and inflammatory cell infiltration, accelerated reendothelialization, and attenuated neointima formation after endoluminal injury while control HiPS-ECs and HiPS-Null-ECs did not. HiPS-IL8RA/B-ECs transfused into rats with endoluminal carotid artery injury target to the injured artery and provide a novel strategy to treat vascular injury.
[Mh] Termos MeSH primário: Artérias Carótidas/patologia
Lesões das Artérias Carótidas/terapia
Terapia Baseada em Transplante de Células e Tecidos/métodos
Células-Tronco Pluripotentes Induzidas/transplante
Neointima/prevenção & controle
Receptores de Interleucina-8/imunologia
[Mh] Termos MeSH secundário: Animais
Artérias Carótidas/imunologia
Lesões das Artérias Carótidas/imunologia
Lesões das Artérias Carótidas/patologia
Células Endoteliais
Ensaio de Imunoadsorção Enzimática
Proteínas de Fluorescência Verde/genética
Seres Humanos
Imuno-Histoquímica
Células-Tronco Pluripotentes Induzidas/imunologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Inflamação
Masculino
Neointima/imunologia
Neointima/patologia
Reação em Cadeia da Polimerase
Ratos
Ratos Sprague-Dawley
Receptores de Interleucina-8/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Receptors, Interleukin-8); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170315
[Lr] Data última revisão:
170315
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160124
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00587.2015


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[PMID]:26751209
[Au] Autor:D JJ; Dhanraj M; Solaiappan S; Sivanesan S; Kron M; Dhanasekaran A
[Ad] Endereço:Center for Biotechnology, Anna University, Chennai-25, Tamil Nadu, India.
[Ti] Título:Brugia malayi Asparaginyl-tRNA Synthetase Stimulates Endothelial Cell Proliferation, Vasodilation and Angiogenesis.
[So] Source:PLoS One;11(1):e0146132, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A hallmark of chronic infection with lymphatic filarial parasites is the development of lymphatic disease which often results in permanent vasodilation and lymphedema, but all of the mechanisms by which filarial parasites induce pathology are not known. Prior work showed that the asparaginyl-tRNA synthetase (BmAsnRS) of Brugia malayi, an etiological agent of lymphatic filariasis, acts as a physiocrine that binds specifically to interleukin-8 (IL-8) chemokine receptors. Endothelial cells are one of the many cell types that express IL-8 receptors. IL-8 also has been reported previously to induce angiogenesis and vasodilation, however, the effect of BmAsnRS on endothelial cells has not been reported. Therefore, we tested the hypothesis that BmAsnRS might produce physiological changes in endothelial by studying the in vitro effects of BmAsnRS using a human umbilical vein cell line EA.hy926 and six different endothelial cell assays. Our results demonstrated that BmAsnRS produces consistent and statistically significant effects on endothelial cells that are identical to the effects of VEGF, vascular endothelial growth factor. This study supports the idea that new drugs or immunotherapies that counteract the adverse effects of parasite-derived physiocrines may prevent or ameliorate the vascular pathology observed in patients with lymphatic filariasis.
[Mh] Termos MeSH primário: Aspartato-tRNA Ligase/farmacologia
Brugia Malayi/química
Proliferação Celular/efeitos dos fármacos
Proteínas de Helminto/farmacologia
Neovascularização Patológica/induzido quimicamente
Aminoacil-RNA de Transferência/farmacologia
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aspartato-tRNA Ligase/genética
Aspartato-tRNA Ligase/metabolismo
Brugia Malayi/enzimologia
Linhagem Celular Transformada
Quimiotaxia
Embrião de Galinha
Membrana Corioalantoide/irrigação sanguínea
Membrana Corioalantoide/efeitos dos fármacos
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Proteínas de Helminto/genética
Proteínas de Helminto/metabolismo
Interações Hospedeiro-Parasita
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Ligação Proteica
Aminoacil-RNA de Transferência/genética
Aminoacil-RNA de Transferência/metabolismo
Receptores de Interleucina-8/genética
Receptores de Interleucina-8/metabolismo
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/farmacologia
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Helminth Proteins); 0 (RNA, Transfer, Amino Acyl); 0 (Receptors, Interleukin-8); 0 (Recombinant Proteins); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); EC 6.1.1.12 (Aspartate-tRNA Ligase); EC 6.1.1.22 (asparaginyl-tRNA synthetase)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170202
[Lr] Data última revisão:
170202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0146132


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[PMID]:26742712
[Au] Autor:Harada R; Furumoto S; Yoshikawa T; Ishikawa Y; Shibuya K; Okamura N; Ishiwata K; Iwata R; Yanai K
[Ad] Endereço:Division of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
[Ti] Título:Synthesis and Characterization of ¹8F-Interleukin-8 Using a Cell-Free Translation System and 4-¹8F-Fluoro-L-Proline.
[So] Source:J Nucl Med;57(4):634-9, 2016 Apr.
[Is] ISSN:1535-5667
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Macromolecules such as proteins are attracting increasing interest for molecular imaging. We previously proposed a novel strategy for preparing macromolecules labeled with a PET radionuclide, (11)C, using a cell-free translation system with (11)C-methionine. However, macromolecules tend to exhibit slower kinetics, thus requiring a longer scanning time. Here, we expand our strategy using (18)F, which has a longer half-life, with the cell-free translation system with 4-(18)F-fluoro-L-proline ((18)F-FPro). We evaluated (18)F-interleukin-8 ((18)F-IL-8) produced by this method in vitro and in vivo to provide a proof of concept of our strategy. METHODS: We tested some fluorinated amino acids to be incorporated into a protein. Trans-(18)F-FPro was radiolabeled from the corresponding precursor. (18)F-IL-8 was produced using the cell-free translation system with trans-(18)F-FPro instead of natural L-proline with incubation at 37°C for 120 min. An in vitro binding assay of (18)F-IL-8 was performed using IL-8 receptor-expressing cells. After intravenous administration of (18)F-IL-8, in vivo PET imaging of IL-8 receptor-expressing xenograft-bearing mice was performed using a small-animal PET system. RESULTS: FPro was identified as an amino acid incorporated into the protein. (18)F-IL-8 was successfully prepared using the cell-free translation system and trans-(18)F-FPro with the radiochemical yield of 1.5% (decay-corrected) based on trans-(18)F-FPro. In vitro binding assays of (18)F-IL-8 demonstrated its binding to IL-8 receptor. In vivo PET imaging demonstrated that (18)F-IL-8 clearly accumulated in IL-8 receptor-expressing xenografts in mice, unlike trans-(18)F-FPro. CONCLUSION: (18)F-IL-8 produced by this method binds to IL-8 receptors in vitro, and (18)F-IL-8 PET clearly visualizes its target receptor-expressing xenograft in vivo. Therefore, this technique might be useful for labeling macromolecules and performing preclinical evaluations of proteins of interest in vitro and in vivo.
[Mh] Termos MeSH primário: Interleucina-8/química
Prolina/análogos & derivados
Compostos Radiofarmacêuticos/síntese química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Aminoácidos/química
Animais
Ligação Competitiva
Sistema Livre de Células
Radioisótopos de Flúor
Células HEK293
Seres Humanos
Interleucina-8/farmacocinética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos ICR
Modelos Moleculares
Dados de Sequência Molecular
Transplante de Neoplasias
Neoplasias Experimentais/diagnóstico por imagem
Prolina/química
Prolina/farmacocinética
Cintilografia
Receptores de Interleucina-8/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acids); 0 (Fluorine Radioisotopes); 0 (Interleukin-8); 0 (Radiopharmaceuticals); 0 (Receptors, Interleukin-8); 0 (fluoro-proline); 9DLQ4CIU6V (Proline)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160109
[St] Status:MEDLINE
[do] DOI:10.2967/jnumed.115.162602


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[PMID]:26613766
[Au] Autor:Wigerblad G; Bas DB; Fernades-Cerqueira C; Krishnamurthy A; Nandakumar KS; Rogoz K; Kato J; Sandor K; Su J; Jimenez-Andrade JM; Finn A; Bersellini Farinotti A; Amara K; Lundberg K; Holmdahl R; Jakobsson PJ; Malmström V; Catrina AI; Klareskog L; Svensson CI
[Ad] Endereço:Molecular Pain Research, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism.
[So] Source:Ann Rheum Dis;75(4):730-8, 2016 Apr.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: An interesting and so far unexplained feature of chronic pain in autoimmune disease is the frequent disconnect between pain and inflammation. This is illustrated well in rheumatoid arthritis (RA) where pain in joints (arthralgia) may precede joint inflammation and persist even after successful anti-inflammatory treatment. In the present study, we have addressed the possibility that autoantibodies against citrullinated proteins (ACPA), present in RA, may be directly responsible for the induction of pain, independent of inflammation. METHODS: Antibodies purified from human patients with RA, healthy donors and murinised monoclonal ACPA were injected into mice. Pain-like behaviour was monitored for up to 28 days, and tissues were analysed for signs of pathology. Mouse osteoclasts were cultured and stimulated with antibodies, and supernatants analysed for release of factors. Mice were treated with CXCR1/2 (interleukin (IL) 8 receptor) antagonist reparixin. RESULTS: Mice injected with either human or murinised ACPA developed long-lasting pronounced pain-like behaviour in the absence of inflammation, while non-ACPA IgG from patients with RA or control monoclonal IgG were without pronociceptive effect. This effect was coupled to ACPA-mediated activation of osteoclasts and release of the nociceptive chemokine CXCL1 (analogue to human IL-8). ACPA-induced pain-like behaviour was reversed with reparixin. CONCLUSIONS: The data suggest that CXCL1/IL-8, released from osteoclasts in an autoantibody-dependent manner, produces pain by activating sensory neurons. The identification of this new pain pathway may open new avenues for pain treatment in RA and also in other painful diseases associated with autoantibody production and/or osteoclast activation.
[Mh] Termos MeSH primário: Artralgia/imunologia
Autoanticorpos/imunologia
Quimiocina CXCL1/imunologia
Citrulina/imunologia
Interleucina-8/imunologia
Nociceptividade/fisiologia
Osteoclastos/imunologia
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/farmacologia
Comportamento Animal/efeitos dos fármacos
Estudos de Casos e Controles
Quimiocina CXCL1/efeitos dos fármacos
Quimiocinas
Inflamação
Interleucina-8/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Nociceptividade/efeitos dos fármacos
Osteoclastos/efeitos dos fármacos
Receptores de Interleucina-8/antagonistas & inibidores
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(4-isobutylphenyl)propionylmethanesulfonamide); 0 (Autoantibodies); 0 (Chemokine CXCL1); 0 (Chemokines); 0 (Cxcl1 protein, mouse); 0 (Interleukin-8); 0 (Receptors, Interleukin-8); 0 (Sulfonamides); 29VT07BGDA (Citrulline)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160420
[Lr] Data última revisão:
160420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151129
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2015-208094


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[PMID]:26612338
[Au] Autor:Krishnamurthy A; Joshua V; Haj Hensvold A; Jin T; Sun M; Vivar N; Ytterberg AJ; Engström M; Fernandes-Cerqueira C; Amara K; Magnusson M; Wigerblad G; Kato J; Jiménez-Andrade JM; Tyson K; Rapecki S; Lundberg K; Catrina SB; Jakobsson PJ; Svensson C; Malmström V; Klareskog L; Wähämaa H; Catrina AI
[Ad] Endereço:Rheumatology Unit, Department of Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Identification of a novel chemokine-dependent molecular mechanism underlying rheumatoid arthritis-associated autoantibody-mediated bone loss.
[So] Source:Ann Rheum Dis;75(4):721-9, 2016 Apr.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Rheumatoid arthritis (RA)-specific anti-citrullinated protein/peptide antibodies (ACPAs) appear before disease onset and are associated with bone destruction. We aimed to dissect the role of ACPAs in osteoclast (OC) activation and to identify key cellular mediators in this process. METHODS: Polyclonal ACPA were isolated from the synovial fluid (SF) and peripheral blood of patients with RA. Monoclonal ACPAs were isolated from single SF B-cells of patients with RA. OCs were developed from blood cell precursors with or without ACPAs. We analysed expression of citrullinated targets and peptidylarginine deiminases (PAD) enzymes by immunohistochemistry and cell supernatants by cytometric bead array. The effect of an anti-interleukin (IL)-8 neutralising antibody and a pan-PAD inhibitor was tested in the OC cultures. Monoclonal ACPAs were injected into mice and bone structure was analysed by micro-CT before and after CXCR1/2 blocking with reparixin. RESULTS: Protein citrullination by PADs is essential for OC differentiation. Polyclonal ACPAs enhance OC differentiation through a PAD-dependent IL-8-mediated autocrine loop that is completely abolished by IL-8 neutralisation. Some, but not all, human monoclonal ACPAs derived from single SF B-cells of patients with RA and exhibiting distinct epitope specificities promote OC differentiation in cell cultures. Transfer of the monoclonal ACPAs into mice induced bone loss that was completely reversed by the IL-8 antagonist reparixin. CONCLUSIONS: We provide novel insights into the key role of citrullination and PAD enzymes during OC differentiation and ACPA-induced OC activation. Our findings suggest that IL8-dependent OC activation may constitute an early event in the initiation of the joint specific inflammation in ACPA-positive RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Autoanticorpos/imunologia
Reabsorção Óssea/imunologia
Osso e Ossos/imunologia
Citrulina/imunologia
Hidrolases/metabolismo
Interleucina-8/imunologia
Osteoclastos/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Reabsorção Óssea/diagnóstico por imagem
Osso e Ossos/diagnóstico por imagem
Osso e Ossos/efeitos dos fármacos
Técnicas de Cultura de Células
Quimiocinas/imunologia
Feminino
Seres Humanos
Hidrolases/antagonistas & inibidores
Imuno-Histoquímica
Interleucina-8/antagonistas & inibidores
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Meia-Idade
Osteoclastos/efeitos dos fármacos
Desiminases de Arginina em Proteínas
Receptores de Interleucina-8/antagonistas & inibidores
Sulfonamidas/farmacologia
Líquido Sinovial
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(4-isobutylphenyl)propionylmethanesulfonamide); 0 (Autoantibodies); 0 (Chemokines); 0 (Interleukin-8); 0 (Receptors, Interleukin-8); 0 (Sulfonamides); 29VT07BGDA (Citrulline); EC 3.- (Hydrolases); EC 3.5.3.15 (Protein-Arginine Deiminases)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151128
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2015-208093


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[PMID]:26343219
[Au] Autor:Diaz-Valencia JD; Pérez-Yépez EA; Ayala-Sumuano JT; Franco E; Meza I
[Ad] Endereço:Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México, DF 07630, Mexico.
[Ti] Título:A surface membrane protein of Entamoeba histolytica functions as a receptor for human chemokine IL-8: its role in the attraction of trophozoites to inflammation sites.
[So] Source:Int J Parasitol;45(14):915-23, 2015 Dec.
[Is] ISSN:1879-0135
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Entamoeba histolytica trophozoites respond to the presence of IL-8, moving by chemotaxis towards the source of the chemokine. IL-8 binds to the trophozoite membrane and triggers a response that activates signaling pathways that in turn regulate actin/myosin cytoskeleton organisation to initiate migration towards the chemokine, suggesting the presence of a receptor for IL-8 in the parasite. Antibodies directed to the human IL-8 receptor (CXCR1) specifically recognised a 29 kDa protein in trophozoite membrane fractions. The same protein was immunoprecipitated by this antibody from total amebic extracts. Peptide analysis of the immunoprecipitated protein revealed a sequence with high homology to a previously identified amebic outer membrane peroxiredoxin and a motif within the third loop of human CXCR1, which is an important site for IL-8 binding and activation of signaling processes. Immunodetection assays demonstrated that the anti-human CXCR1 antibody binds to the 29 kDa protein in a different but close site to where IL-8 binds to the trophozoite surface membrane, suggesting that human and amebic receptors for this chemokine share common epitopes. In the context of the human intestinal environment, a receptor for IL-8 could be a great advantage for E. histolytica trophozoite survival, as they could reach an inflammatory milieu containing abundant nutrients. In addition, it has been suggested that the high content of accessible thiol groups of the protein and its peroxidase activity could provide protection in the oxygen rich milieu of colonic lesions, allowing trophozoite invasion of other tissues and escape from the host immune response.
[Mh] Termos MeSH primário: Quimiotaxia
Entamoeba histolytica/fisiologia
Interações Hospedeiro-Patógeno
Interleucina-8/metabolismo
Proteínas de Membrana/metabolismo
Receptores de Interleucina-8/metabolismo
[Mh] Termos MeSH secundário: Movimento Celular
Entamoeba histolytica/efeitos dos fármacos
Seres Humanos
Inflamação/parasitologia
Inflamação/patologia
Trofozoítos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-8); 0 (Membrane Proteins); 0 (Receptors, Interleukin-8)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150908
[St] Status:MEDLINE


  8 / 69 MEDLINE  
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[PMID]:26199092
[Au] Autor:Chen L; Min L; Wang X; Zhao J; Chen H; Qin J; Chen W; Shen Z; Tang Z; Gan Q; Ruan Y; Sun Y; Qin X; Gu J
[Ad] Endereço:Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
[Ti] Título:Loss of RACK1 Promotes Metastasis of Gastric Cancer by Inducing a miR-302c/IL8 Signaling Loop.
[So] Source:Cancer Res;75(18):3832-41, 2015 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gastric cancer remains the third leading cause of cancer-related mortality worldwide, and invasion and metastasis of gastric cancer represent the major reason for its poor prognosis. In this study, we found that loss of the receptor for activated C-kinase 1 (RACK1) promoted the metastasis of gastric cancer by enhancing the autocrine expression of IL8 in vitro and in vivo. microRNA (miRNA; miR) array identified that RACK1 modulated the expression of a series of miRNAs, including the miR-302 cluster, and RACK1 modulated the IL8 expression and tumor invasion through miRNA-302c. Moreover, upregulation of IL8 in turn decreased the level of miRNA-302c and induced IL8 expression in a feedback manner. Tissue microarray also indicated that RACK1 was correlated with invasion/metastasis phenotype, IL8 expression, as well as 5-year survival in clinical cases of gastric cancer. Together, our results imply that loss of RACK1 in gastric cancer links epigenetics to inflammatory cytokines to promote tumor metastasis.
[Mh] Termos MeSH primário: Proteínas de Ligação ao GTP/fisiologia
Interleucina-8/fisiologia
MicroRNAs/genética
Metástase Neoplásica/genética
Proteínas de Neoplasias/fisiologia
Receptores de Superfície Celular/fisiologia
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Comunicação Autócrina
Feminino
Proteínas de Ligação ao GTP/deficiência
Proteínas de Ligação ao GTP/genética
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Interleucina-8/biossíntese
Interleucina-8/genética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Meia-Idade
Invasividade Neoplásica
Proteínas de Neoplasias/deficiência
Proteínas de Neoplasias/genética
Neoplasias Peritoneais/secundário
RNA Interferente Pequeno/farmacologia
Receptores de Quinase C Ativada
Receptores de Superfície Celular/deficiência
Receptores de Superfície Celular/genética
Receptores de Interleucina-8/biossíntese
Receptores de Interleucina-8/genética
Transdução de Sinais
Neoplasias Gástricas/genética
Neoplasias Gástricas/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-8); 0 (MIRN302 microRNA, mouse); 0 (MicroRNAs); 0 (Neoplasm Proteins); 0 (RACK1 protein, human); 0 (RNA, Small Interfering); 0 (Receptors for Activated C Kinase); 0 (Receptors, Cell Surface); 0 (Receptors, Interleukin-8); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150723
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-14-3690


  9 / 69 MEDLINE  
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[PMID]:26084289
[Au] Autor:Selitrennik M; Lev S
[Ad] Endereço:Molecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
[Ti] Título:PYK2 integrates growth factor and cytokine receptors signaling and potentiates breast cancer invasion via a positive feedback loop.
[So] Source:Oncotarget;6(26):22214-26, 2015 Sep 08.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The involvement of ErbB family members in breast cancer progression and metastasis has been demonstrated by many studies. However, the downstream effectors that mediate their migratory and invasive responses have not been fully explored. In this study, we show that the non-receptor tyrosine kinase PYK2 is a key effector of EGFR and HER2 signaling in human breast carcinoma. We found that PYK2 is activated by both EGF and heregulin (HRG) in breast cancer cells, and positively regulates EGF/HRG-induced cell spreading, migration and invasion. PYK2 depletion markedly affects ERK1/2 and STAT3 phosphorylation in response to EGF/HRG as well as to IL8 treatment. Importantly, PYK2 depletion also reduced EGF/HRG-induced MMP9 and IL8 transcription, while IL8 inhibition abrogated EGF-induced MMP9 transcription and attenuated cell invasion. IL8, which is transcriptionally regulated by STAT3 and induces PYK2 activation, prolonged EGF-induced PYK2, STAT3 and ERK1/2 phosphorylation suggesting that IL8 acts through an autocrine loop to reinforce EGF-induced signals. Collectively our studies suggest that PYK2 is a common downstream effector of ErbB and IL8 receptors, and that PYK2 integrates their signaling pathways through a positive feedback loop to potentiate breast cancer invasion. Hence, PYK2 could be a potential therapeutic target for a subset of breast cancer patients.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Quinase 1 de Adesão Focal/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptores de Interleucina-8/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Fator de Crescimento Epidérmico/farmacologia
Feminino
Quinase 1 de Adesão Focal/deficiência
Quinase 1 de Adesão Focal/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Células MCF-7
Invasividade Neoplásica
Neuregulina-1/farmacologia
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuregulin-1); 0 (Receptors, Interleukin-8); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150619
[St] Status:MEDLINE


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[PMID]:25973893
[Au] Autor:Nakajima A; Masaki Y; Nakamura T; Kawanami T; Ishigaki Y; Takegami T; Kawano M; Yamada K; Tsukamoto N; Matsui S; Saeki T; Okazaki K; Kamisawa T; Miyashita T; Yakushijin Y; Fujikawa K; Yamamoto M; Hamano H; Origuchi T; Hirata S; Tsuboi H; Sumida T; Morimoto H; Sato T; Iwao H; Miki M; Sakai T; Fujita Y; Tanaka M; Fukushima T; Okazaki T; Umehara H
[Ad] Endereço:Hematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
[Ti] Título:Decreased Expression of Innate Immunity-Related Genes in Peripheral Blood Mononuclear Cells from Patients with IgG4-Related Disease.
[So] Source:PLoS One;10(5):e0126582, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: IgG4-related disease (IgG4-RD) is a new clinical entity of unknown etiology characterized by elevated serum IgG4 and tissue infiltration by IgG4-positive plasma cells. Although aberrancies in acquired immune system functions, including increases in Th2 and Treg cytokines observed in patients with IgG4-RD, its true etiology remains unclear. To investigate the pathogenesis of IgG4-RD, this study compared the expression of genes related to innate immunity in patients with IgG4-RD and healthy controls. MATERIALS AND METHODS: Peripheral blood mononuclear cells (PBMCs) were obtained from patients with IgG4-RD before and after steroid therapy and from healthy controls. Total RNA was extracted and DNA microarray analysis was performed in two IgG4-RD patients to screen for genes showing changes in expression. Candidate genes were validated by real-time RT-PCR in 27 patients with IgG4-RD and 13 healthy controls. RESULTS: DNA microarray analysis identified 21 genes that showed a greater than 3-fold difference in expression between IgG4-RD patients and healthy controls and 30 genes that showed a greater than 3-fold change in IgG4-RD patients following steroid therapy. Candidate genes related to innate immunity, including those encoding Charcot-Leyden crystal protein (CLC), membrane-spanning 4-domain subfamily A member 3 (MS4A3), defensin alpha (DEFA) 3 and 4, and interleukin-8 receptors (IL8R), were validated by real-time RT-PCR. Expression of all genes was significantly lower in IgG4-RD patients than in healthy controls. Steroid therapy significantly increased the expression of DEFA3, DEFA4 and MS4A3, but had no effect on the expression of CLC, IL8RA and IL8RB. CONCLUSIONS: The expression of genes related to allergy or innate immunity, including CLC, MS4A3, DEFA3, DEFA4, IL8RA and IL8RB, was lower in PBMCs from patients with IgG4-RD than from healthy controls. Although there is the limitation in the number of patients applied in DNA microarray, impaired expression of genes related to innate immunity may be involved in the pathogenesis of IgG4-RD as well as in abnormalities of acquired immunity.
[Mh] Termos MeSH primário: Imunoglobulina G/sangue
Leucócitos Mononucleares/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Doenças Autoimunes/imunologia
Doenças Autoimunes/patologia
Estudos de Casos e Controles
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Regulação para Baixo
Feminino
Glicoproteínas/genética
Glicoproteínas/metabolismo
Seres Humanos
Imunidade Inata/genética
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/imunologia
Lisofosfolipase/genética
Lisofosfolipase/metabolismo
Masculino
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Meia-Idade
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Interleucina-8/genética
Receptores de Interleucina-8/metabolismo
Células Th2/citologia
Células Th2/imunologia
Regulação para Cima
alfa-Defensinas/genética
alfa-Defensinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Glycoproteins); 0 (Immunoglobulin G); 0 (MS4A3 protein, human); 0 (Membrane Proteins); 0 (Receptors, Interleukin-8); 0 (alpha-Defensins); 0 (human neutrophil peptide 3); 0 (human neutrophil peptide 4); EC 3.1.1.5 (Lysophospholipase); EC 3.1.1.5 (lysolecithin acylhydrolase)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150515
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0126582



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