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Pesquisa : D12.776.395.550.200.625.347 [Categoria DeCS]
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[PMID]:29348537
[Au] Autor:Kotagiri N; Cooper ML; Rettig M; Egbulefu C; Prior J; Cui G; Karmakar P; Zhou M; Yang X; Sudlow G; Marsala L; Chanswangphuwana C; Lu L; Habimana-Griffin L; Shokeen M; Xu X; Weilbaecher K; Tomasson M; Lanza G; DiPersio JF; Achilefu S
[Ad] Endereço:Department of Radiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
[Ti] Título:Radionuclides transform chemotherapeutics into phototherapeutics for precise treatment of disseminated cancer.
[So] Source:Nat Commun;9(1):275, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most cancer patients succumb to disseminated disease because conventional systemic therapies lack spatiotemporal control of their toxic effects in vivo, particularly in a complicated milieu such as bone marrow where progenitor stem cells reside. Here, we demonstrate the treatment of disseminated cancer by photoactivatable drugs using radiopharmaceuticals. An orthogonal-targeting strategy and a contact-facilitated nanomicelle technology enabled highly selective delivery and co-localization of titanocene and radiolabelled fluorodeoxyglucose in disseminated multiple myeloma cells. Selective ablation of the cancer cells was achieved without significant off-target toxicity to the resident stem cells. Genomic, proteomic and multimodal imaging analyses revealed that the downregulation of CD49d, one of the dimeric protein targets of the nanomicelles, caused therapy resistance in small clusters of cancer cells. Similar treatment of a highly metastatic breast cancer model using human serum albumin-titanocene formulation significantly inhibited cancer growth. This strategy expands the use of phototherapy for treating previously inaccessible metastatic disease.
[Mh] Termos MeSH primário: Neoplasias Mamárias Experimentais/terapia
Mieloma Múltiplo/terapia
Compostos Organometálicos/administração & dosagem
Fotoquimioterapia
Compostos Radiofarmacêuticos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Resistência a Medicamentos Antineoplásicos
Feminino
Integrina alfa4beta1
Camundongos Endogâmicos C57BL
Camundongos SCID
Micelas
Terapia de Alvo Molecular
Nanopartículas
Ratos
Albumina Sérica Humana
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (Micelles); 0 (Organometallic Compounds); 0 (Radiopharmaceuticals); 1271-29-0 (titanocene); ZIF514RVZR (Serum Albumin, Human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02758-9


  2 / 1584 MEDLINE  
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[PMID]:28939758
[Au] Autor:Sorcini D; Bruscoli S; Frammartino T; Cimino M; Mazzon E; Galuppo M; Bramanti P; Al-Banchaabouchi M; Farley D; Ermakova O; Britanova O; Izraelson M; Chudakov D; Biagioli M; Sportoletti P; Flamini S; Raspa M; Scavizzi F; Nerlov C; Migliorati G; Riccardi C; Bereshchenko O
[Ad] Endereço:Department of Medicine, University of Perugia, Perugia 06132, Italy.
[Ti] Título:Wnt/ß-Catenin Signaling Induces Integrin α4ß1 in T Cells and Promotes a Progressive Neuroinflammatory Disease in Mice.
[So] Source:J Immunol;199(9):3031-3041, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanisms leading to autoimmune and inflammatory diseases in the CNS have not been elucidated. The environmental triggers of the aberrant presence of CD4 T cells in the CNS are not known. In this article, we report that abnormal ß-catenin expression in T cells drives a fatal neuroinflammatory disease in mice that is characterized by CNS infiltration of T cells, glial activation, and progressive loss of motor function. We show that enhanced ß-catenin expression in T cells leads to aberrant and Th1-biased T cell activation, enhanced expression of integrin α4ß1, and infiltration of activated T cells into the spinal cord, without affecting regulatory T cell function. Importantly, expression of ß-catenin in mature naive T cells was sufficient to drive integrin α4ß1 expression and CNS migration, whereas pharmacologic inhibition of integrin α4ß1 reduced the abnormal T cell presence in the CNS of ß-catenin-expressing mice. Together, these results implicate deregulation of the Wnt/ß-catenin pathway in CNS inflammation and suggest novel therapeutic strategies for neuroinflammatory disorders.
[Mh] Termos MeSH primário: Integrina alfa4beta1/imunologia
Doenças da Medula Espinal/imunologia
Medula Espinal/imunologia
Células Th1/imunologia
Via de Sinalização Wnt/imunologia
beta Catenina/imunologia
[Mh] Termos MeSH secundário: Animais
Inflamação/genética
Inflamação/imunologia
Inflamação/patologia
Integrina alfa4beta1/genética
Camundongos
Camundongos Knockout
Medula Espinal/patologia
Doenças da Medula Espinal/genética
Doenças da Medula Espinal/patologia
Células Th1/patologia
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (beta Catenin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700247


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[PMID]:28739875
[Au] Autor:Resheq YJ; Menzner AK; Bosch J; Tickle J; Li KK; Wilhelm A; Hepburn E; Murihead G; Ward ST; Curbishley SM; Zimmermann HW; Bruns T; Gilbert DF; Tripal P; Mackensen A; Adams DH; Weston CJ
[Ad] Endereço:Institute of Immunology and Immunotherapy, Centre for Liver Research and National Institute for Health Research Birmingham Liver Biomedical Research Centre, College of Medicine and Dentistry, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom; yazid.resheq@uk-erlangen.de.
[Ti] Título:Impaired Transmigration of Myeloid-Derived Suppressor Cells across Human Sinusoidal Endothelium Is Associated with Decreased Expression of CD13.
[So] Source:J Immunol;199(5):1672-1681, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human monocytic myeloid-derived suppressor cells (MO-MDSCs) within the hepatic compartment suppress inflammation and impair immune surveillance in liver cancer. It is currently not known whether recruitment of MO-MDSCs from blood via hepatic sinusoidal endothelium (HSEC) contributes to their enrichment within the hepatic compartment. We compared the transmigratory potential of MO-MDSCs and monocytes after adhesion to hepatic endothelial monolayers in flow-based assays that mimic in vivo shear stress in the sinusoids. Despite comparable binding to HSEC monolayers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating that the final steps of extravasation, where actin polymerization plays an important role, are impaired in MO-MDSCs. In this article, we found reduced levels of CD13 on MO-MDSCs, which has recently been reported to control cell motility in monocytes, alongside reduced VLA-4 expression, an integrin predominantly involved in adherence to the apical side of the endothelium. CD13 and VLA-4 blocking and activating Abs were used in flow-based adhesion assays, live-cell imaging of motility, and actin polymerization studies to confirm a role for CD13 in impaired MO-MDSC transmigration. These findings indicate that CD13 significantly contributes to tissue infiltration by MO-MDSCs and monocytes, thereby contributing to the pathogenesis of hepatic inflammation.
[Mh] Termos MeSH primário: Antígenos CD13/metabolismo
Epitélio Posterior/fisiologia
Hemocromatose/imunologia
Hepatite/imunologia
Fígado/imunologia
Células Supressoras Mieloides/imunologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Actinas/metabolismo
Anticorpos Bloqueadores/farmacologia
Antígenos CD13/genética
Antígenos CD13/imunologia
Adesão Celular
Movimento Celular
Células Cultivadas
Regulação para Baixo
Seres Humanos
Integrina alfa4beta1/genética
Integrina alfa4beta1/imunologia
Integrina alfa4beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antibodies, Blocking); 0 (Integrin alpha4beta1); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600466


  4 / 1584 MEDLINE  
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[PMID]:28637896
[Au] Autor:Stewart-Hutchinson PJ; Szasz TP; Jaeger ER; Onken MD; Cooper JA; Morley SC
[Ad] Endereço:Division of Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA.
[Ti] Título:Technical Advance: New in vitro method for assaying the migration of primary B cells using an endothelial monolayer as substrate.
[So] Source:J Leukoc Biol;102(3):941-948, 2017 Sep.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Migration of B cells supports their development and recruitment into functional niches. Therefore, defining factors that control B cell migration will lead to a better understanding of adaptive immunity. In vitro cell migration assays with B cells have been limited by poor adhesion of cells to glass coated with adhesion molecules. We have developed a technique using monolayers of endothelial cells as the substrate for B cell migration and used this technique to establish a robust in vitro assay for B cell migration. We use TNF-α to up-regulate surface expression of the adhesion molecule VCAM-1 on endothelial cells. The ligand VLA-4 is expressed on B cells, allowing them to interact with the endothelial monolayer and migrate on its surface. We tested our new method by examining the role of L-plastin (LPL), an F-actin-bundling protein, in B cell migration. LPL-deficient (LPL ) B cells displayed decreased speed and increased arrest coefficient compared with wild-type (WT) B cells, following chemokine stimulation. However, the confinement ratios for WT and LPL B cells were similar. Thus, we demonstrate how the use of endothelial monolayers as a substrate will support future interrogation of molecular pathways essential to B cell migration.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Movimento Celular/imunologia
Células Endoteliais/imunologia
Integrina alfa4beta1/imunologia
Fosfoproteínas/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Movimento Celular/genética
Técnicas de Cocultura/métodos
Células Endoteliais/citologia
Integrina alfa4beta1/genética
Camundongos
Camundongos Knockout
Fosfoproteínas/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (Phosphoproteins); 0 (Tumor Necrosis Factor-alpha); 128868-76-8 (Lcp1 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.1TA0117-008R


  5 / 1584 MEDLINE  
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[PMID]:28592427
[Au] Autor:Mattila JT; Beaino W; Maiello P; Coleman MT; White AG; Scanga CA; Flynn JL; Anderson CJ
[Ad] Endereço:Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA 15213.
[Ti] Título:Positron Emission Tomography Imaging of Macaques with Tuberculosis Identifies Temporal Changes in Granuloma Glucose Metabolism and Integrin α4ß1-Expressing Immune Cells.
[So] Source:J Immunol;199(2):806-815, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Positron emission tomography and computed tomography imaging (PET/CT) is an increasingly valuable tool for diagnosing tuberculosis (TB). The glucose analog [ F]fluoro-2-deoxy-2-d-glucose ([ F]-FDG) is commonly used in PET/CT that is retained by metabolically active inflammatory cells in granulomas, but lacks specificity for particular cell types. A PET probe that could identify recruitment and differentiation of different cell populations in granulomas would be a useful research tool and could improve TB diagnosis and treatment. We used the -antigen murine inflammation model and macaques with TB to identify [ Cu]-labeled CB-TE1A1P-PEG -LLP2A ([ Cu]-LLP2A), a high affinity peptidomimetic ligand for very late Ag-4 (VLA-4; also called integrin α4ß1) binding cells in granulomas, and compared [ Cu]-LLP2A with [ F]-FDG over the course of infection. We found that [ Cu]-LLP2A retention was driven by macrophages and T cells, with less contribution from neutrophils and B cells. In macaques, granulomas had higher [ Cu]-LLP2A uptake than uninfected tissues, and immunohistochemical analysis of granulomas with known [ Cu]-LLP2A uptake identified significant correlations between LLP2A signal and macrophage and T cell numbers. The same cells coexpressed integrin α4 and ß1, further supporting that macrophages and T cells drive [ Cu]-LLP2A avidity in granulomas. Over the course of infection, granulomas and thoracic lymph nodes experienced dynamic changes in affinity for both probes, suggesting metabolic changes and cell differentiation or recruitment occurs throughout granuloma development. These results indicate [ Cu]-LLP2A is a PET probe for VLA-4, which when used in conjunction with [ F]-FDG, may be a useful tool for understanding granuloma biology in TB.
[Mh] Termos MeSH primário: Glucose/metabolismo
Granuloma/imunologia
Integrina alfa4beta1/genética
Tuberculose/diagnóstico por imagem
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Movimento Celular
Granuloma/diagnóstico por imagem
Granuloma/metabolismo
Granuloma/fisiopatologia
Compostos Heterocíclicos com 2 Anéis/química
Integrina alfa4beta1/imunologia
Linfonodos/citologia
Linfonodos/imunologia
Macaca
Macrófagos/imunologia
Neutrófilos/imunologia
Organofosfonatos/química
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos
Linfócitos T/imunologia
Tuberculose/diagnóstico
Tuberculose/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,4,8,11-tetraazacyclotetradecane-1-(methanephosphonic acid)-8-(methane carboxylic acid)); 0 (Heterocyclic Compounds, 2-Ring); 0 (Integrin alpha4beta1); 0 (Organophosphonates); 0 (Radiopharmaceuticals); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700231


  6 / 1584 MEDLINE  
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[PMID]:28495929
[Au] Autor:Rothmeier AS; Marchese P; Langer F; Kamikubo Y; Schaffner F; Cantor J; Ginsberg MH; Ruggeri ZM; Ruf W
[Ad] Endereço:From the Department of Immunology and Microbiology (A.S.R., F.S., W.R.) and Molecular Medicine (P.M., Y.K., Z.M.R.), The Scripps Research Institute, La Jolla, CA; II. Medical Clinic and Polyclinic, University Medical Center Eppendorf, Hamburg, Germany (F.L.); Department of Medicine, University of Ca
[Ti] Título:Tissue Factor Prothrombotic Activity Is Regulated by Integrin-arf6 Trafficking.
[So] Source:Arterioscler Thromb Vasc Biol;37(7):1323-1331, 2017 Jul.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Coagulation initiation by tissue factor (TF) is regulated by cellular inhibitors, cell surface availability of procoagulant phosphatidylserine, and thiol-disulfide exchange. How these mechanisms contribute to keeping TF in a noncoagulant state and to generating prothrombotic TF remain incompletely understood. APPROACH AND RESULTS: Here, we study the activation of TF in primary macrophages by a combination of pharmacological, genetic, and biochemical approaches. We demonstrate that primed macrophages effectively control TF cell surface activity by receptor internalization. After cell injury, ATP signals through the purinergic receptor P2rx7 induce release of TF microvesicles. TF cell surface availability for release onto microvesicles is regulated by the GTPase arf6 associated with integrin α4ß1. Furthermore, microvesicles proteome analysis identifies activation of Gα as a participating factor in the release of microvesicles with prothrombotic activity in flowing blood. ATP not only prevents TF and phosphatidylserine internalization but also induces TF conversion to a conformation with high affinity for its ligand, coagulation factor VII. Although inhibition of dynamin-dependent internalization also exposes outer membrane procoagulant phosphatidylserine, the resulting TF microvesicles distinctly lack protein disulfide isomerase and high affinity TF and fail to produce fibrin strands typical for microvesicles generated by thrombo-inflammatory P2rx7 activation. CONCLUSIONS: These data show that procoagulant phospholipid exposure is not sufficient and that TF affinity maturation is required to generate prothrombotic microvesicles from a variety of cell types. These findings are significant for understanding TF-initiated thrombosis and should be considered in designing functional microvesicles-based diagnostic approaches.
[Mh] Termos MeSH primário: Fatores de Ribosilação do ADP/metabolismo
Coagulação Sanguínea
Integrina alfa4/metabolismo
Integrina alfa4beta1/metabolismo
Macrófagos/metabolismo
Tromboplastina/metabolismo
Trombose/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Linhagem Celular Tumoral
Micropartículas Derivadas de Células/metabolismo
Fator VIIa/metabolismo
Técnicas de Introdução de Genes
Genótipo
Seres Humanos
Integrina alfa4/genética
Integrina alfa4beta1/genética
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Fosfolipídeos/metabolismo
Transporte Proteico
Receptores Purinérgicos P2X7/metabolismo
Transdução de Sinais
Trombose/sangue
Trombose/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (P2RX7 protein, human); 0 (P2rx7 protein, mouse); 0 (Phospholipids); 0 (Receptors, Purinergic P2X7); 143198-26-9 (Integrin alpha4); 8L70Q75FXE (Adenosine Triphosphate); 9035-58-9 (Thromboplastin); EC 3.4.21.21 (Factor VIIa); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (ADP-ribosylation factor 6)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309315


  7 / 1584 MEDLINE  
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[PMID]:28325836
[Au] Autor:Sens C; Huck K; Pettera S; Uebel S; Wabnitz G; Moser M; Nakchbandi IA
[Ad] Endereço:From the Max-Planck Institute of Biochemistry, 82152 Martinsried and.
[Ti] Título:Fibronectins containing extradomain A or B enhance osteoblast differentiation via distinct integrins.
[So] Source:J Biol Chem;292(19):7745-7760, 2017 May 12.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fibronectin is a multidomain protein secreted by various cell types. It forms a network of fibers within the extracellular matrix and impacts intracellular processes by binding to various molecules, primarily integrin receptors on the cells. Both the presence of several isoforms and the ability of the various domains and isoforms to bind to a variety of integrins result in a wide range of effects. findings suggest that fibronectin isoforms produced by the osteoblasts enhance their differentiation. Here we report that the isoform characterized by the presence of extradomain A activates α4ß1 integrin and augments osteoblast differentiation. In addition, the isoform containing extradomain B enhances the binding of fibronectin through the RGD sequence to ß3-containing integrin, resulting in increased mineralization by and differentiation of osteoblasts. Our study thus reveals novel functions for two fibronectin isoforms and the mediating receptors in osteoblast differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular
Fibronectinas/metabolismo
Integrina alfa4beta1/metabolismo
Integrina alfaVbeta3/metabolismo
Osteoblastos/citologia
[Mh] Termos MeSH secundário: Células 3T3
Animais
Animais Recém-Nascidos
Adesão Celular
DNA Complementar/metabolismo
Ensaio de Imunoadsorção Enzimática
Matriz Extracelular/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Seres Humanos
Camundongos
Oligopeptídeos/metabolismo
Osteoblastos/metabolismo
Osteogênese
Ligação Proteica
Domínios Proteicos
Isoformas de Proteínas
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (FN1 protein, human); 0 (Fibronectins); 0 (Integrin alpha4beta1); 0 (Integrin alphaVbeta3); 0 (Oligopeptides); 0 (Protein Isoforms); 0 (RNA, Small Interfering); 147336-22-9 (Green Fluorescent Proteins); 78VO7F77PN (arginyl-glycyl-aspartic acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.739987


  8 / 1584 MEDLINE  
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[PMID]:28235946
[Au] Autor:Labrousse-Arias D; Martínez-Alonso E; Corral-Escariz M; Bienes-Martínez R; Berridy J; Serrano-Oviedo L; Conde E; García-Bermejo ML; Giménez-Bachs JM; Salinas-Sánchez AS; Sánchez-Prieto R; Yao M; Lasa M; Calzada MJ
[Ad] Endereço:Department of Medicine, Instituto de Investigación Sanitaria Princesa, School of Medicine, Universidad Autónoma de Madrid, 28049 Madrid, Spain.
[Ti] Título:VHL promotes immune response against renal cell carcinoma via NF-κB-dependent regulation of VCAM-1.
[So] Source:J Cell Biol;216(3):835-847, 2017 Mar 06.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular cell adhesion molecule 1 (VCAM-1) is an adhesion molecule assigned to the activated endothelium mediating immune cells adhesion and extravasation. However, its expression in renal carcinomas inversely correlates with tumor malignancy. Our experiments in clear cell renal cell carcinoma (ccRCC) cell lines demonstrated that von Hippel Lindau (VHL) loss, hypoxia, or PHD (for prolyl hydroxylase domain-containing proteins) inactivation decreased VCAM-1 levels through a transcriptional mechanism that was independent of the hypoxia-inducible factor and dependent on the nuclear factor κB signaling pathway. Conversely, VHL expression leads to high VCAM-1 levels in ccRCC, which in turn leads to better outcomes, possibly by favoring antitumor immunity through VCAM-1 interaction with the α4ß1 integrin expressed in immune cells. Remarkably, in ccRCC human samples with VHL nonmissense mutations, we observed a negative correlation between VCAM-1 levels and ccRCC stage, microvascular invasion, and symptom presentation, pointing out the clinical value of VCAM-1 levels as a marker of ccRCC progression.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/imunologia
Neoplasias Renais/genética
Neoplasias Renais/imunologia
NF-kappa B/genética
Molécula 1 de Adesão de Célula Vascular/genética
Doença de von Hippel-Lindau/imunologia
[Mh] Termos MeSH secundário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/imunologia
Biomarcadores Tumorais/genética
Biomarcadores Tumorais/imunologia
Carcinoma de Células Renais/genética
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica/genética
Regulação Neoplásica da Expressão Gênica/imunologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/imunologia
Integrina alfa4beta1/genética
Integrina alfa4beta1/imunologia
Mutação/genética
Mutação/imunologia
NF-kappa B/imunologia
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Transcrição Genética/genética
Transcrição Genética/imunologia
Molécula 1 de Adesão de Célula Vascular/imunologia
Proteína Supressora de Tumor Von Hippel-Lindau/genética
Proteína Supressora de Tumor Von Hippel-Lindau/imunologia
Doença de von Hippel-Lindau/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Biomarkers, Tumor); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Integrin alpha4beta1); 0 (NF-kappa B); 0 (Vascular Cell Adhesion Molecule-1); EC 2.3.2.27 (Von Hippel-Lindau Tumor Suppressor Protein)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170226
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201608024


  9 / 1584 MEDLINE  
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[PMID]:28096298
[Au] Autor:Hirano Y; Yang WL; Aziz M; Zhang F; Sherry B; Wang P
[Ad] Endereço:Center for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
[Ti] Título:MFG-E8-derived peptide attenuates adhesion and migration of immune cells to endothelial cells.
[So] Source:J Leukoc Biol;101(5):1201-1209, 2017 May.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Milk fat globule-epidermal growth factor-factor 8 (MFG-E8) plays an immunomodulatory role in inflammatory diseases. MFG-E8-derived short peptide (MSP68) greatly reduces neutrophil infiltration and injury in the lung during sepsis. In this study, we examined the effect of MSP68 on chemotaxis of various immune cells and its regulatory mechanism. Bone marrow-derived neutrophils (BMDNs) from C57BL/6 mice, human monocyte THP-1 cell line, and human T lymphocyte Jurkat cell line were used for adhesion and migration assays using a Transwell method in the presence of MSP68. Treatment with MSP68 significantly inhibited the BMDN and THP-1 cell but not Jurkat cell adhesion on the TNF-α-stimulated pulmonary artery endothelial cell (PAEC) monolayer dose-dependently. MSP68 also significantly reduced BMDN adhesion on VCAM-1-coated wells dose dependently. Surface plasmon resonance (SPR) analysis revealed that MSP68 efficiently recognized integrin α ß (receptor for VCAM-1) at the dissociation constant (K ) of 1.53 × 10 M. These findings implicate that MSP68 prevents neutrophil adhesion to the activated endothelial cells by interfering with the binding between integrin α ß on neutrophils and VCAM-1 on endothelial cells. Moreover, MSP68 significantly attenuated the migration of BMDN and THP-1 cells but not Jurkat cells to their chemoattractants. Pretreatment with MSP68 inhibited the transmigration of BMDNs across the PAECs toward chemoattractants, fMLP, MIP-2, and complement fragment 5a (C5a) dose-dependently. Finally, we identified that the activation of p38 MAPK in BMDNs by fMLP was inhibited by MSP68. Thus, MSP68 attenuates extravasation of immune cells through the endothelial cell lining into inflamed tissue, implicating MSP68 to be a novel, therapeutic agent for inflammatory diseases caused by excessive immune cell infiltration.
[Mh] Termos MeSH primário: Antígenos de Superfície/química
Células Endoteliais/efeitos dos fármacos
Proteínas do Leite/química
Monócitos/efeitos dos fármacos
Neutrófilos/efeitos dos fármacos
Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Superfície/imunologia
Adesão Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Técnicas de Cocultura
Complemento C5a/genética
Complemento C5a/imunologia
Cultura em Câmaras de Difusão
Células Endoteliais/citologia
Células Endoteliais/imunologia
Regulação da Expressão Gênica
Seres Humanos
Integrina alfa4beta1/genética
Integrina alfa4beta1/imunologia
Células Jurkat
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas do Leite/imunologia
Monócitos/citologia
Monócitos/imunologia
Neutrófilos/citologia
Neutrófilos/imunologia
Peptídeos/síntese química
Cultura Primária de Células
Transdução de Sinais
Fator de Necrose Tumoral alfa/farmacologia
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Surface); 0 (Integrin alpha4beta1); 0 (MFGE8 protein, human); 0 (Milk Proteins); 0 (Peptides); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 80295-54-1 (Complement C5a)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3A0416-184RR


  10 / 1584 MEDLINE  
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[PMID]:28088473
[Au] Autor:de Sousa J; Sousa Aarão TL; Rodrigues de Sousa J; Hirai KE; Silva LM; Dias LB; Oliveira Carneiro FR; Fuzii HT; Quaresma JA
[Ad] Endereço:Centro de Ciencias Biologicas e da Saude, Universidade do Estado do Para, Belem, Para, Brazil.
[Ti] Título:Endothelium adhesion molecules ICAM-1, ICAM-2, VCAM-1 and VLA-4 expression in leprosy.
[So] Source:Microb Pathog;104:116-124, 2017 Mar.
[Is] ISSN:1096-1208
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Leprosy triggers a complex relationship between the pathogen and host immune response. Endothelium plays an important role in this immune response by directly influencing cell migration to infected tissues. The objective of this work is to investigate the possible role of endothelium in M. leprae infection, correlating the characteristics of endothelial markers with the expression pattern of cytokines. Thirty-six skin biopsy samples were cut into 5-µm thick sections and stained with hematoxylin-eosin and Ziehl-Neelsen for morphological analysis and then submitted to immunohistochemical analysis using monoclonal antibodies against ICAM-1, ICAM-2, VCAM-1, and VLA-4. Immunostaining for ICAM-1 showed a significantly larger number of stained endothelial cells in the tuberculoid leprosy (9.92 ± 1.11 cells/mm ) when compared to lepromatous samples (5.87 ± 1.01 cells/mm ) and ICAM-2 revealed no significant difference in the number of endothelial cells expressing this marker between the tuberculoid (13.21 ± 1.27 cells/mm ) and lepromatous leprosy (14.3 ± 1.02 cells/mm ). VCAM-1-immunostained showed 18.28 ± 1.46/mm cells in tuberculoid leprosy and 10.67 ± 1.25 cells/mm in the lepromatous leprosy. VLA-4 exhibited 22.46 ± 1.38 cells/mm in the tuberculoid leprosy 16.04 ± 1.56 cells/mm in the lepromatous leprosy. Samples with characteristics of the tuberculoid leprosy exhibited a larger number of cells stained with ICAM-1, VCAM-1 and VLA-4, demonstrating the importance of these molecules in the migration and selection of cells that reach the inflamed tissue.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Endotélio Vascular/metabolismo
Hanseníase/etiologia
Hanseníase/metabolismo
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/metabolismo
Moléculas de Adesão Celular/genética
Expressão Gênica
Seres Humanos
Integrina alfa4beta1/genética
Integrina alfa4beta1/metabolismo
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
Hanseníase/patologia
Pele/metabolismo
Pele/microbiologia
Pele/patologia
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cell Adhesion Molecules); 0 (ICAM2 protein, human); 0 (Integrin alpha4beta1); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170116
[St] Status:MEDLINE



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