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Pesquisa : D12.776.543.750.705.408.200 [Categoria DeCS]
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  1 / 909 MEDLINE  
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[PMID]:28893948
[Au] Autor:Abnave P; Aboukhatwa E; Kosaka N; Thompson J; Hill MA; Aboobaker AA
[Ad] Endereço:Department of Zoology, Tinbergen Building, South Parks Road, University of Oxford, Oxford OX1 3PS, UK.
[Ti] Título:Epithelial-mesenchymal transition transcription factors control pluripotent adult stem cell migration in planarians.
[So] Source:Development;144(19):3440-3453, 2017 10 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Migration of stem cells underpins the physiology of metazoan animals. For tissues to be maintained, stem cells and their progeny must migrate and differentiate in the correct positions. This need is even more acute after tissue damage by wounding or pathogenic infection. Inappropriate migration also underpins metastasis. Despite this, few mechanistic studies address stem cell migration during repair or homeostasis in adult tissues. Here, we present a shielded X-ray irradiation assay that allows us to follow stem cell migration in planarians. We demonstrate the use of this system to study the molecular control of stem cell migration and show that , and EMT transcription factor homologs are necessary for cell migration to wound sites and for the establishment of migratory cell morphology. We also observed that stem cells undergo homeostatic migration to anterior regions that lack local stem cells, in the absence of injury, maintaining tissue homeostasis. This requires the polarity determinant Our work establishes planarians as a suitable model for further in-depth study of the processes controlling stem cell migration .
[Mh] Termos MeSH primário: Células-Tronco Adultas/citologia
Movimento Celular
Transição Epitelial-Mesenquimal
Planárias/citologia
Planárias/metabolismo
Células-Tronco Pluripotentes/citologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Células-Tronco Adultas/metabolismo
Células-Tronco Adultas/efeitos da radiação
Animais
Linhagem da Célula/efeitos da radiação
Movimento Celular/efeitos da radiação
Forma Celular/efeitos da radiação
Sequência Conservada
Epiderme/citologia
Transição Epitelial-Mesenquimal/efeitos da radiação
Cadeias beta de Integrinas/metabolismo
Metaloproteinases da Matriz/metabolismo
Planárias/genética
Células-Tronco Pluripotentes/efeitos da radiação
Fatores de Transcrição da Família Snail/metabolismo
Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin beta Chains); 0 (Snail Family Transcription Factors); 0 (Transcription Factors); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1242/dev.154971


  2 / 909 MEDLINE  
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[PMID]:28736941
[Au] Autor:Sharma P; Sharma A; Srivastava M
[Ad] Endereço:Parasitology Division, CSIR-Central Drug Research Institute, Lucknow, India.
[Ti] Título:In vivo neutralization of α4 and ß7 integrins inhibits eosinophil trafficking and prevents lung injury during tropical pulmonary eosinophilia in mice.
[So] Source:Eur J Immunol;47(9):1501-1512, 2017 Sep.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Integrins regulate leukocyte trafficking during homeostasis and inflammatory conditions. However, the role of α4 and ß7 integrins in guiding eosinophil transmigration into the lungs during filarial manifestation of Tropical Pulmonary Eosinophilia (TPE) has not been explored. In this study, mice exhibiting TPE manifestations were administered with in vivo neutralizing antibodies against integrins α4 and ß7 or their combination and immuno-pathological parameters were evaluated. Results show an intact lung barrier, significantly lower lung inflammation and reduced eosinophil counts in the Bronchoalveolar lavage fluid and lungs of mice receiving anti-α4 ß7 treatment. Reduced eosinophil peroxidase and ß-hexosaminidase activity, downregulation of inflammatory genes, lower production of inflammatory lipid intermediates like prostaglandins E2 and D2, leukotriene B4 and cysteinyl leukotrienes were also noted in anti-α4 ß7 treated mice. Reduced accumulation of central memory, effector memory, regulatory T cells and lower production of IL-4, IL-5, and TGF-ß were other cardinal features of anti-α4 ß7 treated mice lungs. Flow cytometry-sorted lung eosinophils from anti-α4 ß7 treated mice showed higher apoptotic potential, downregulated anti-apoptotic gene Bcl-2, and exhibited reduced F-actin polymerization and calcium influx as compared to IgG controls. In summary, neutralization of α4 ß7 integrins impairs the transmigration, activation and survival of eosinophils and reduces TPE induced pathology in mice lungs.
[Mh] Termos MeSH primário: Anticorpos Neutralizantes/uso terapêutico
Brugia Malayi/imunologia
Filariose Linfática/terapia
Eosinófilos/imunologia
Imunoterapia/métodos
Lesão Pulmonar/prevenção & controle
Eosinofilia Pulmonar/terapia
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Células Cultivadas
Citocinas/metabolismo
Filariose Linfática/imunologia
Seres Humanos
Mediadores da Inflamação/metabolismo
Integrina alfa4/imunologia
Cadeias beta de Integrinas/imunologia
Lesão Pulmonar/etiologia
Lesão Pulmonar/imunologia
Camundongos
Camundongos Endogâmicos
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Eosinofilia Pulmonar/complicações
Eosinofilia Pulmonar/imunologia
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Integrin beta Chains); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (integrin beta7); 143198-26-9 (Integrin alpha4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747086


  3 / 909 MEDLINE  
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[PMID]:28717031
[Au] Autor:Killpack TL; Ballesteros M; Bunnell SC; Bedugnis A; Kobzik L; Hu LT; Petnicki-Ocwieja T
[Ad] Endereço:Department of Biological Sciences, Wellesley College, Wellesley, Massachusetts, USA.
[Ti] Título:Phagocytic Receptors Activate Syk and Src Signaling during Borrelia burgdorferi Phagocytosis.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phagocytosis of the Lyme disease-causing pathogen has been shown to be important for generating an inflammatory response to the pathogen. As a result, understanding the mechanisms of phagocytosis has been an area of great interest in the field of Lyme disease. Several cell surface receptors that participate in phagocytosis have been reported, including the scavenger receptor MARCO and integrin α3ß1. We sought to define the mechanisms by which these receptors mediate phagocytosis and to identify signaling pathways activated downstream of these receptors upon contact with We identified both Syk and Src signaling pathways as ones that participate in phagocytosis and the resulting cytokine activation. In our studies, we found that both MARCO and integrin ß1 play a role in the activation of the Src kinase pathway. However, only integrin ß1 participates in the activation of Syk. Interestingly, the integrin activates Syk without the help of the signaling adaptor Dap12 or FcRγ. Thus, we report that multiple pathways participate in internalization and that different cell surface receptors act simultaneously in cooperation and independently to mediate phagocytosis.
[Mh] Termos MeSH primário: Borrelia burgdorferi/imunologia
Cadeias beta de Integrinas/metabolismo
Fagocitose
Receptores Imunológicos/metabolismo
Transdução de Sinais
Quinase Syk/metabolismo
Quinases da Família src/metabolismo
[Mh] Termos MeSH secundário: Animais
Borrelia burgdorferi/fisiologia
Doença de Lyme/imunologia
Doença de Lyme/microbiologia
Camundongos
Receptores Imunológicos/imunologia
Receptores Depuradores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta Chains); 0 (Marco protein, mouse); 0 (Receptors, Immunologic); 0 (Receptors, Scavenger); EC 2.7.10.2 (Syk Kinase); EC 2.7.10.2 (Syk protein, mouse); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE


  4 / 909 MEDLINE  
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[PMID]:28622453
[Au] Autor:Mei HE; Hahne S; Redlin A; Hoyer BF; Wu K; Baganz L; Lisney AR; Alexander T; Rudolph B; Dörner T
[Ad] Endereço:Charité University Medicine Berlin and German Rheumatism Research Center Berlin, Berlin, Germany.
[Ti] Título:Plasmablasts With a Mucosal Phenotype Contribute to Plasmacytosis in Systemic Lupus Erythematosus.
[So] Source:Arthritis Rheumatol;69(10):2018-2028, 2017 Oct.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To analyze the composition of known plasmacytosis in systemic lupus erythematosus (SLE) to obtain further insight into the nature of underlying mechanisms. METHODS: Plasmablasts from patients with active SLE, patients with inactive/treated SLE, and healthy controls were characterized by flow cytometry, enzyme-linked immunospot assay, and Transwell migration assays and compared to vaccination-induced plasmablasts. Serum cytokine levels were analyzed by Luminex assay, and histologic analysis of kidney biopsy specimens was performed. RESULTS: Circulating plasmablasts in SLE expressed markers of mucosal immune reactions. IgA, CCR10, and ß7 integrin were expressed by 48%, 40%, and 38% of plasmablasts, respectively, with varying coexpression patterns. Consistent with mucosal homing, some SLE plasmablasts migrated toward the mucosal chemokine CCL28 and secreted polymeric IgA. SLE plasmablasts shared phenotypic characteristics with antigen-specific plasmablasts induced by oral, but not parenteral, vaccinations. Autoreactive antibody-secreting cells of the IgG and IgA isotypes were detectable, but only the emergence of phenotypically mucosal plasmablasts was positively associated with serum interleukin-2 and platelet-derived growth factor BB levels. CONCLUSION: Our data suggest that distinct plasmablast differentiation pathways jointly contribute to peripheral plasmacytosis in SLE, i.e., a cytokine-amplified mucosal "steady-state" plasmablast response, and an autoreactive plasmablast response, representing conventional autoimmunity. Our results indicate an overly activated mucosal immune system in patients with SLE, with both immunologic and clinical implications.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Citocinas/imunologia
Rim/patologia
Lúpus Eritematoso Sistêmico/imunologia
Nefrite Lúpica/imunologia
Membrana Mucosa/imunologia
Plasmócitos/imunologia
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
Diferenciação Celular/imunologia
Movimento Celular/imunologia
Quimiocinas CC/imunologia
Ensaio de Imunoadsorção Enzimática
ELISPOT
Feminino
Citometria de Fluxo
Seres Humanos
Imunoglobulina A/imunologia
Imunoglobulina G/imunologia
Técnicas In Vitro
Cadeias beta de Integrinas/imunologia
Interleucina-2/imunologia
Rim/imunologia
Lúpus Eritematoso Sistêmico/patologia
Nefrite Lúpica/patologia
Masculino
Meia-Idade
Fenótipo
Proteínas Proto-Oncogênicas c-sis/imunologia
Receptores CCR10/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (CCL28 protein, human); 0 (CCR10 protein, human); 0 (Chemokines, CC); 0 (Cytokines); 0 (IL2 protein, human); 0 (Immunoglobulin A); 0 (Immunoglobulin G); 0 (Integrin beta Chains); 0 (Interleukin-2); 0 (Proto-Oncogene Proteins c-sis); 0 (Receptors, CCR10); 0 (integrin beta7); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1002/art.40181


  5 / 909 MEDLINE  
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[PMID]:28606226
[Au] Autor:Kong QL; An XZ; Guan XM; Ma YM; Li PF; Liang SY; Hu YN; Cui YH; Yu J
[Ad] Endereço:Department of Hematology, Children's Hospital of Chongqing Medical University/Ministry of Education Key Laboratory of Child Development and Disorders/Chongqing Key Laboratory of Pediatrics/China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, China. 1808106657@qq.com.
[Ti] Título:[Expression of ß-integrin family members in children with T-cell acute lymphoblastic leukemia].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(6):620-626, 2017 Jun.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To study the expression of ß-integrin family members in children with T-cell acute lymphoblastic leukemia (T-ALL) and their significance. METHODS: Quantitative real-time PCR analyses were performed to assess the expression levels of ß-integrin family members in bone marrow samples from 22 children with newly-diagnosed T-ALL and 21 controls (16 children with non-malignant hematologic disease and 5 healthy donors with bone marrow transplantation). Jurkat cells were treated with integrin inhibitor arginine-glycine-aspartate (Arg-Gly-Asp, RGD) peptide. The cell viability and apoptosis rate were determined by CCK8 assay and flow cytometry respectively. RESULTS: The mRNA levels of integrins ß , ß , and ß were significantly lower in children with T-ALL than in controls (P<0.05). In T-ALL patients, high integrin ß expression was associated with lower white blood cell counts (<100×10 /L), minimal residual disease (MRD) positivity, and day 33 bone marrow negative remission (P<0.05). In T-ALL patients, higher integrin ß expression was associated with relapse of T-ALL (P<0.05). Based on survival curve analysis, higher integrin ß expression was related to lower event-free survival and overall survival rates. RGD peptide treatment inhibited the proliferation of Jurkat cells and increased their apoptosis rate (P<0.05). CONCLUSIONS: ß-Integrin may play a role in the occurrence and development of T-ALL by affecting cell proliferation and apoptosis. The expression of integrin ß5 is closely related to the risk of relapse of T-ALL. The expression of integrin ß3 is closely related the treatment response and prognosis of T-ALL.
[Mh] Termos MeSH primário: Cadeias beta de Integrinas/fisiologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/mortalidade
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Feminino
Seres Humanos
Cadeias beta de Integrinas/genética
Células Jurkat
Masculino
Leucemia-Linfoma Linfoblástico de Células T Precursoras/etiologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
RNA Mensageiro/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta Chains); 0 (RNA, Messenger)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


  6 / 909 MEDLINE  
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[PMID]:28572000
[Au] Autor:Wang P; Zhuo XR; Tang L; Liu XS; Wang YF; Wang GX; Yu XQ; Wang JL
[Ad] Endereço:Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, China.
[Ti] Título:C-type lectin interacting with ß-integrin enhances hemocytic encapsulation in the cotton bollworm, Helicoverpa armigera.
[So] Source:Insect Biochem Mol Biol;86:29-40, 2017 Jul.
[Is] ISSN:1879-0240
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The encapsulation reaction in invertebrates is analogous to granuloma formation in vertebrates, and this reaction is severely compromised when ecdysone signaling is blocked. However, the molecular mechanism underlying the encapsulation reaction and its regulation by ecdysone remains obscure. In our previous study, we found that the C-type lectin HaCTL3, from the cotton bollworm Helicoverpa armigera, is involved in anti-bacterial immune response, acting as a pattern recognition receptor (PRR). In the current study, we demonstrate that HaCTL3 is involved in defense against parasites and directly binds to the surface of nematodes. Our in vitro and in vivo studies indicate that HaCTL3 enhances hemocytic encapsulation and melanization, whereas H. armigera ß-integrin (Haß-integrin), located on the surface of hemocytes, participates in encapsulation. Additionally, co-immunoprecipitation experiments reveal HaCTL3 interacts with Haß-integrin, and knockdown of Haß-integrin leads to reduced encapsulation of HaCTL3-coated beads. These results indicate that Haß-integrin serves as a hemocytic receptor of HaCTL3 during the encapsulation reaction. Furthermore, we demonstrate that 20-hydroxyecdysone (20E) treatment dramatically induces the expression of HaCTL3, and knockdown of the 20E receptor (EcR)/ultraspiracle (USP), abrogates this response. Overall, this study provides the first evidence of the presence of a hemocytic receptor (Haß-integrin), that interacts with the PRR HaCTL3 to facilitate encapsulation reaction in insects and demonstrates the regulation of this process by the steroid hormone ecdysone.
[Mh] Termos MeSH primário: Interações Hospedeiro-Parasita/imunologia
Cadeias beta de Integrinas/metabolismo
Lectinas Tipo C/metabolismo
Mariposas/imunologia
Nematoides/imunologia
[Mh] Termos MeSH secundário: Animais
Ecdisterona
Hemócitos/metabolismo
Melaninas/metabolismo
Mariposas/metabolismo
Mariposas/parasitologia
Coelhos
Receptores de Esteroides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta Chains); 0 (Lectins, C-Type); 0 (Melanins); 0 (Receptors, Steroid); 0 (ecdysone receptor); 5289-74-7 (Ecdysterone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE


  7 / 909 MEDLINE  
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[PMID]:28535372
[Au] Autor:Ma S; Santhosh D; Kumar T P; Huang Z
[Ad] Endereço:Departments of Neuroscience and Neurology, University of Wisconsin-Madison, Madison, WI, 53705, USA; Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, WI53706, USA.
[Ti] Título:A Brain-Region-Specific Neural Pathway Regulating Germinal Matrix Angiogenesis.
[So] Source:Dev Cell;41(4):366-381.e4, 2017 May 22.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intimate communication between neural and vascular cells is critical for normal brain development and function. Germinal matrix (GM), a key primordium for the brain reward circuitry, is unique among brain regions for its distinct pace of angiogenesis and selective vulnerability to hemorrhage during development. A major neonatal condition, GM hemorrhage can lead to cerebral palsy, hydrocephalus, and mental retardation. Here we identify a brain-region-specific neural progenitor-based signaling pathway dedicated to regulating GM vessel development. This pathway consists of cell-surface sphingosine-1-phosphate receptors, an intracellular cascade including Gα co-factor Ric8a and p38 MAPK, and target gene integrin ß8, which in turn regulates vascular TGF-ß signaling. These findings provide insights into region-specific specialization of neurovascular communication, with special implications for deciphering potent early-life endocrine, as well as potential gut microbiota impacts on brain reward circuitry. They also identify tissue-specific molecular targets for GM hemorrhage intervention.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Encéfalo/metabolismo
Neovascularização Fisiológica
Vias Neurais/metabolismo
[Mh] Termos MeSH secundário: Embrião de Mamíferos/irrigação sanguínea
Embrião de Mamíferos/metabolismo
Embrião de Mamíferos/patologia
Ativação Enzimática/efeitos dos fármacos
Cloridrato de Fingolimode/farmacologia
Fatores de Troca do Nucleotídeo Guanina/genética
Hemorragia/patologia
Seres Humanos
Cadeias beta de Integrinas/metabolismo
Lisofosfolipídeos/metabolismo
Mutação/genética
Neostriado/efeitos dos fármacos
Neostriado/patologia
Neovascularização Fisiológica/efeitos dos fármacos
Vias Neurais/efeitos dos fármacos
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/metabolismo
Especificidade de Órgãos/efeitos dos fármacos
Fenótipo
Receptores de Lisoesfingolipídeo/metabolismo
Recompensa
Transdução de Sinais/efeitos dos fármacos
Esfingosina/análogos & derivados
Esfingosina/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Guanine Nucleotide Exchange Factors); 0 (Integrin beta Chains); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (Ric8 protein, mouse); 0 (Transforming Growth Factor beta); 0 (integrin beta8); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); G926EC510T (Fingolimod Hydrochloride); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


  8 / 909 MEDLINE  
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[PMID]:28483911
[Au] Autor:Lee KJ; Kim Y; Yoo YH; Kim MS; Lee SH; Kim CG; Park K; Jeoung D; Lee H; Ko IY; Hahn JH
[Ad] Endereço:Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon, Republic of Korea.
[Ti] Título:CD99-Derived Agonist Ligands Inhibit Fibronectin-Induced Activation of ß1 Integrin through the Protein Kinase A/SHP2/Extracellular Signal-Regulated Kinase/PTPN12/Focal Adhesion Kinase Signaling Pathway.
[So] Source:Mol Cell Biol;37(14), 2017 Jul 15.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human CD99 protein is a 32-kDa glycosylated transmembrane protein that regulates various cellular responses, including cell adhesion and leukocyte extravasation. We previously reported that CD99 activation suppresses ß1 integrin activity through dephosphorylation of focal adhesion kinase (FAK) at Y397. We explored a molecular mechanism underlying the suppression of ß1 integrin activity by CD99 agonists and its relevance to tumor growth CD99-Fc fusion proteins or a series of CD99-derived peptides suppressed ß1 integrin activity by specifically interacting with three conserved motifs of the CD99 extracellular domain. CD99CRIII3, a representative CD99-derived 3-mer peptide, facilitated protein kinase A-SHP2 interaction and subsequent activation of the HRAS/RAF1/MEK/ERK signaling pathway. Subsequently, CD99CRIII3 induced FAK phosphorylation at S910, which led to the recruitment of PTPN12 and PIN1 to FAK, followed by FAK dephosphorylation at Y397. Taken together, these results indicate that CD99-derived agonist ligands inhibit fibronectin-mediated ß1 integrin activation through the SHP2/ERK/PTPN12/FAK signaling pathway.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Movimento Celular/fisiologia
Fibronectinas/metabolismo
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Cadeias beta de Integrinas/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Antígeno 12E7/metabolismo
Linhagem Celular Tumoral
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Ligantes
Fosforilação
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 12/metabolismo
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (12E7 Antigen); 0 (CD99 protein, human); 0 (Fibronectins); 0 (Integrin beta Chains); 0 (Ligands); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.1.3.48 (PTPN12 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 12)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE


  9 / 909 MEDLINE  
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[PMID]:28423181
[Au] Autor:Shiokawa A; Kotaki R; Takano T; Nakajima-Adachi H; Hachimura S
[Ad] Endereço:Research Center for Food Safety, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
[Ti] Título:Mesenteric lymph node CD11b CD103 PD-L1 dendritic cells highly induce regulatory T cells.
[So] Source:Immunology;152(1):52-64, 2017 Sep.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs) in mesenteric lymph nodes (MLNs) induce Foxp3 regulatory T cells to regulate immune responses to beneficial or non-harmful agents in the intestine, such as commensal bacteria and foods. Several studies in MLN DCs have revealed that the CD103 DC subset highly induces regulatory T cells, and another study has reported that MLN DCs from programmed death ligand 1 (PD-L1) -deficient mice could not induce regulatory T cells. Hence, the present study investigated the expression of these molecules on MLN CD11c cells. Four distinct subsets expressing CD103 and/or PD-L1 were identified, namely CD11b CD103 PD-L1 , CD11b CD103 PD-L1 , CD11b CD103 PD-L1 and CD11b CD103 PD-L1 . Among them, the CD11b CD103 PD-L1 DC subset highly induced Foxp3 T cells. This subset expressed Aldh1a2 and Itgb8 genes, which are involved in retinoic acid metabolism and transforming growth factor-ß (TGF-ß) activation, respectively. Exogenous TGF-ß supplementation equalized the level of Foxp3 T-cell induction by the four subsets whereas retinoic acid did not, which suggests that high ability to activate TGF-ß is determinant for the high Foxp3 T-cell induction by CD11b CD103 PD-L1 DC subset. Finally, this subset exhibited a migratory DC phenotype and could take up and present orally administered antigens. Collectively, the MLN CD11b CD103 PD-L1 DC subset probably takes up luminal antigens in the intestine, migrates to MLNs, and highly induces regulatory T cells through TGF-ß activation.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Antígeno B7-H1/imunologia
Antígeno CD11b/imunologia
Comunicação Celular
Células Dendríticas/imunologia
Cadeias alfa de Integrinas/imunologia
Intestinos/imunologia
Linfonodos/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Administração Oral
Aldeído Desidrogenase/imunologia
Aldeído Desidrogenase/metabolismo
Animais
Antígenos CD/metabolismo
Antígeno B7-H1/metabolismo
Antígeno CD11b/metabolismo
Comunicação Celular/efeitos dos fármacos
Movimento Celular
Células Cultivadas
Técnicas de Cocultura
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Imunidade nas Mucosas
Cadeias alfa de Integrinas/metabolismo
Cadeias beta de Integrinas/imunologia
Cadeias beta de Integrinas/metabolismo
Intestinos/citologia
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Linfonodos/citologia
Linfonodos/efeitos dos fármacos
Linfonodos/metabolismo
Mesentério
Camundongos Endogâmicos BALB C
Ovalbumina/administração & dosagem
Ovalbumina/imunologia
Fenótipo
Transdução de Sinais
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/metabolismo
Fator de Crescimento Transformador beta/imunologia
Fator de Crescimento Transformador beta/metabolismo
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (B7-H1 Antigen); 0 (CD11b Antigen); 0 (Cd274 protein, mouse); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Integrin alpha Chains); 0 (Integrin beta Chains); 0 (Transforming Growth Factor beta); 0 (alpha E integrins); 0 (integrin beta8); 5688UTC01R (Tretinoin); 9006-59-1 (Ovalbumin); EC 1.14.13.- (Aldh1a2 protein, mouse); EC 1.2.1.3 (Aldehyde Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12747


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[PMID]:28246016
[Au] Autor:Hong CP; Park A; Yang BG; Yun CH; Kwak MJ; Lee GW; Kim JH; Jang MS; Lee EJ; Jeun EJ; You G; Kim KS; Choi Y; Park JH; Hwang D; Im SH; Kim JF; Kim YK; Seoh JY; Surh CD; Kim YM; Jang MH
[Ad] Endereço:Academy of Immunology and Microbiology, Institute for Basic Science, Pohang, Republic of Korea; Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea; Department of Microbiology, Graduate School of Medicine, Ewha Womans Universi
[Ti] Título:Gut-Specific Delivery of T-Helper 17 Cells Reduces Obesity and Insulin Resistance in Mice.
[So] Source:Gastroenterology;152(8):1998-2010, 2017 Jun.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Obesity and metabolic syndrome have been associated with alterations to the intestinal microbiota. However, few studies examined the effects of obesity on the intestinal immune system. We investigated changes in subsets of intestinal CD4 T-helper (T ) cells with obesity and the effects of gut-tropic T 17 cells in mice on a high-fat diet (HFD). METHODS: We isolated immune cells from small intestine and adipose tissue of C57BL/6 mice fed a normal chow diet or a HFD for 10 weeks and analyzed the cells by flow cytometry. Mice fed a vitamin A-deficient HFD were compared with mice fed a vitamin A-sufficient HFD. Obese RAG1-deficient mice were given injections of only regulatory T cells or a combination of regulatory T cells and T 17 cells (wild type or deficient in integrin ß7 subunit or interleukin 17 [IL17]). Mice were examined for weight gain, fat mass, fatty liver, glucose tolerance, and insulin resistance. Fecal samples were collected before and after T cell transfer and analyzed for microbiota composition by metagenomic DNA sequencing and quantitative polymerase chain reaction. RESULTS: Mice placed on a HFD became obese, which affected the distribution of small intestinal CD4 T cells. Intestinal tissues from obese mice had significant reductions in the proportion of T 17 cells but increased proportion of T 1 cells, compared with intestinal tissues from nonobese mice. Depletion of vitamin A in obese mice further reduced the proportion of T 17 cells in small intestine; this reduction correlated with more weight gain and worsening of glucose intolerance and insulin resistance. Adoptive transfer of in vitro-differentiated gut-tropic T 17 cells to obese mice reduced these metabolic defects, which required the integrin ß7 subunit and IL17. Delivery of T 17 cells to intestines of mice led to expansion of commensal microbes associated with leanness. CONCLUSIONS: In mice, intestinal T 17 cells contribute to development of a microbiota that maintains metabolic homeostasis, via IL17. Gut-homing T 17 cells might be used to reduce metabolic disorders in obese individuals.
[Mh] Termos MeSH primário: Transferência Adotiva
Imunidade nas Mucosas
Resistência à Insulina
Intestino Delgado/imunologia
Síndrome Metabólica/prevenção & controle
Obesidade/prevenção & controle
Células Th17/transplante
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Dieta Hiperlipídica
Modelos Animais de Doenças
Fezes/microbiologia
Microbioma Gastrointestinal/imunologia
Genótipo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Interações Hospedeiro-Patógeno
Cadeias beta de Integrinas/genética
Cadeias beta de Integrinas/metabolismo
Interleucina-17/deficiência
Interleucina-17/genética
Intestino Delgado/metabolismo
Intestino Delgado/microbiologia
Masculino
Síndrome Metabólica/genética
Síndrome Metabólica/imunologia
Síndrome Metabólica/microbiologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/genética
Obesidade/imunologia
Obesidade/microbiologia
Fenótipo
Células Th17/imunologia
Células Th17/microbiologia
Fatores de Tempo
Deficiência de Vitamina A/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Integrin beta Chains); 0 (Interleukin-17); 0 (integrin beta7); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE



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