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[PMID]:28236856
[Au] Autor:Souza MM; de Paula FM; Hsieh R; Macedo MC; Corral MA; Nunes TB; De Paula F; Lourenço SV
[Ad] Endereço:Department of Dermatology, School of Medicine, University of São Paulo, 255, Dr. Enéas de Carvalho Aguiar Avenue, 3° Floor, 05403-900, Cerqueira Cesar, São Paulo, Brazil. Electronic address: milenamsouza@usp.br.
[Ti] Título:Could mucin 16 and colony-stimulating factor 2-receptor beta possible graft versus host disease biomarkers? Medical hypotheses.
[So] Source:Med Hypotheses;100:89-93, 2017 Mar.
[Is] ISSN:1532-2777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Graft versus host disease (GVHD) occurs after bone marrow transplantation and is one of the most important causes of death worldwide. Reviews demonstrated GVHD patients with involvement of various tissues and organs, such as salivary glands. The diagnosis of acute GVHD has been the biopsies and the histopathologic evaluation of tissue from an involved organ. These procedures are invasive. Saliva proteins as possible biomarker for GVHD could facilitate the management and diagnosis accuracy. For support the proposed hypotheses, in this pilot study we collected whole saliva samples from patients with undergoing allogeneic hematopoietic cell transplantation (HCT) and from healthy subjects. Samples were collected prospectively between pre-transplant, thirty days, one hundred and, two hundred days after transplant. The proteomic profile was analyzed using SDS-PAGE and LCMS-ESI-IT-TOF mass spectrometry. The relevant personal data, past medical history were also recorded. The most relevant proteins found exclusively in GVHD patients were: CSF2RB, Protocadherin (Pcdh) Fat 2 precursor, protein capicua homolog isoform CIC-S, MUC16 and RGPD8_HUMAN RANBP2. This study aims to conduct an initial evaluation of the possible presence of such biomarkers in saliva from GVHD patients, and suggested a potential application of proteomics analysis as a alternative method to diagnose GVHD.
[Mh] Termos MeSH primário: Biomarcadores/análise
Antígeno Ca-125/análise
Subunidade beta Comum dos Receptores de Citocinas/análise
Doença Enxerto-Hospedeiro/diagnóstico
Proteínas de Membrana/análise
[Mh] Termos MeSH secundário: Adulto
Feminino
Voluntários Saudáveis
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Leucemia Mieloide Aguda/terapia
Masculino
Modelos Teóricos
Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia
Proteômica
Saliva/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CA-125 Antigen); 0 (CSF2RB protein, human); 0 (Cytokine Receptor Common beta Subunit); 0 (MUC16 protein, human); 0 (Membrane Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE


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[PMID]:28130045
[Au] Autor:Salter BM; Sehmi R
[Ad] Endereço:CardioRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON, Canada.
[Ti] Título:Hematopoietic Processes in Eosinophilic Asthma.
[So] Source:Chest;152(2):410-416, 2017 Aug.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Airway eosinophilia is a hallmark of allergic asthma, and understanding mechanisms that promote increases in lung eosinophil numbers is important for effective pharmacotherapeutic development. It has become evident that expansion of hematopoietic compartments in the bone marrow (BM) promotes differentiation and trafficking of mature eosinophils to the airways. Hematopoietic progenitor cells egress the BM and home to the lungs, where in situ differentiation within the tissue provides an ongoing source of proinflammatory cells. In addition, hematopoietic progenitor cells in the airways can respond to locally derived alarmins to produce a panoply of cytokines, thereby themselves acting as effector proinflammatory cells that potentiate type 2 responses in eosinophilic asthma. In this review, we provide evidence for these findings and discuss novel targets for modulating eosinophilopoietic processes, migration, and effector function of precursor cells.
[Mh] Termos MeSH primário: Asma/etiologia
Hematopoese/fisiologia
Eosinofilia Pulmonar/etiologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/uso terapêutico
Asma/tratamento farmacológico
Asma/fisiopatologia
Linfócitos T CD4-Positivos/fisiologia
Diferenciação Celular/fisiologia
Subunidade beta Comum dos Receptores de Citocinas/antagonistas & inibidores
Citocinas/antagonistas & inibidores
Citocinas/fisiologia
Eosinófilos/citologia
Eosinófilos/fisiologia
Células-Tronco Hematopoéticas/fisiologia
Seres Humanos
Proteínas de Membrana/antagonistas & inibidores
Eosinofilia Pulmonar/tratamento farmacológico
Eosinofilia Pulmonar/fisiopatologia
Hipersensibilidade Respiratória/etiologia
Hipersensibilidade Respiratória/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Cytokine Receptor Common beta Subunit); 0 (Cytokines); 0 (Membrane Proteins); 0 (TMEM102 protein, human); 0 (thymic stromal lymphopoietin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE


  3 / 109 MEDLINE  
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[PMID]:27634443
[Au] Autor:Zhang C; Yang C; Zhu T
[Ad] Endereço:Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China and Shanghai Key Laboratory of Organ Transplantation, Shanghai, 200032. China.
[Ti] Título:From Erythropoietin to Its Peptide Derivatives: Smaller but Stronger.
[So] Source:Curr Protein Pept Sci;18(12):1191-1194, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Erythropoietin (EPO), recognized early as a tissue protective agent, can trigger antiinflammatory and anti-apoptotic processes to delimit injury and promote repair by binding tissueprotective receptor (TPR). However, only at a high dosage can EPO exert tissue protective effect, which may elicit severe side-effects at the meantime. Helix B surface peptide (HBSP), a 11-amnio acid sequence derived from the non-erythropoietic helix B of EPO, not only shows higher affinity to TPR but also plays a more specific and powerful role in tissue protection without erythropoietic side-effects. While it has obvious merits, the 2-min plasma half-life of HBSP restricts its application in vivo. Therefore, based on the amino acid sequence of HBSP, we originally designed and synthesized thioethercyclized helix B peptide (CHBP) for an increased resistance to proteolytic degradation as well as an improved tissue protective potency, implying a brighter prospective for translational application. In this review, we will mainly discuss the development from EPO to CHBP, the merits and limitation of CHBP and the probable mechanism mediating tissue protection.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Eritropoetina/farmacologia
Fragmentos de Peptídeos/farmacologia
Peptídeos Cíclicos/farmacologia
Substâncias Protetoras/farmacologia
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacocinética
Apoptose/efeitos dos fármacos
Ciclização
Subunidade beta Comum dos Receptores de Citocinas/genética
Subunidade beta Comum dos Receptores de Citocinas/metabolismo
Modelos Animais de Doenças
Eritropoetina/efeitos adversos
Eritropoetina/farmacocinética
Regulação da Expressão Gênica
Meia-Vida
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Estresse Oxidativo/efeitos dos fármacos
Fragmentos de Peptídeos/farmacocinética
Peptídeos Cíclicos/síntese química
Peptídeos Cíclicos/farmacocinética
Substâncias Protetoras/farmacocinética
Receptores da Eritropoetina/genética
Receptores da Eritropoetina/metabolismo
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokine Receptor Common beta Subunit); 0 (EPO protein, human); 0 (Peptide Fragments); 0 (Peptides, Cyclic); 0 (Protective Agents); 0 (Receptors, Erythropoietin); 0 (glutaminyl-glutamyl-glutaminyl-leucyl-glutamyl-arginyl-alanyl-leucyl-asparagyl-seryl-serine); 11096-26-7 (Erythropoietin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160917
[St] Status:MEDLINE
[do] DOI:10.2174/1389203717666160909130006


  4 / 109 MEDLINE  
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[PMID]:27634442
[Au] Autor:Zhang Y; Chen W; Wu Y; Yang B
[Ad] Endereço:Renal Group, Basic Medical Research Centre, Medical College of Nantong University, Nantong, Jiangsu. China.
[Ti] Título:Renoprotection and Mechanisms of Erythropoietin and Its Derivatives Helix B Surface Peptide in Kidney Injuries.
[So] Source:Curr Protein Pept Sci;18(12):1183-1190, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The renoprotection of erythropoietin (EPO) and its derivatives such as helix B surface peptide (HBSP) have attracted a great deal of attention from scientists and clinicians alike. The evolutional achievement in the dissociation of tissue protection and erythropoiesis is obtained through HBSP characterisation and synthesis. We performed a series of studies using EPO, as well as HBSP, in a variety of biological models subjected to transplant-related renal injuries such as ischemia reperfusion injury (IRI) and/or immunosuppressant nephrotoxicity. In this short review, we would like to address the effects of EPO in different formats, and its underlying mechanisms with focuses on apoptosis and inflammation in in vitro, ex vivo and in vivo renal injury models, and to further explore potential applications and challenges in humans.
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Anti-Inflamatórios/farmacologia
Eritropoetina/farmacologia
Fragmentos de Peptídeos/farmacologia
Substâncias Protetoras/farmacologia
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Animais
Apoptose/efeitos dos fármacos
Subunidade beta Comum dos Receptores de Citocinas/genética
Subunidade beta Comum dos Receptores de Citocinas/metabolismo
Modelos Animais de Doenças
Regulação da Expressão Gênica
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Estresse Oxidativo/efeitos dos fármacos
Receptores da Eritropoetina/genética
Receptores da Eritropoetina/metabolismo
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokine Receptor Common beta Subunit); 0 (EPO protein, human); 0 (Peptide Fragments); 0 (Protective Agents); 0 (Receptors, Erythropoietin); 0 (glutaminyl-glutamyl-glutaminyl-leucyl-glutamyl-arginyl-alanyl-leucyl-asparagyl-seryl-serine); 11096-26-7 (Erythropoietin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160917
[St] Status:MEDLINE
[do] DOI:10.2174/1389203717666160909144436


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[PMID]:27377463
[Au] Autor:Chuang LS; Villaverde N; Hui KY; Mortha A; Rahman A; Levine AP; Haritunians T; Evelyn Ng SM; Zhang W; Hsu NY; Facey JA; Luong T; Fernandez-Hernandez H; Li D; Rivas M; Schiff ER; Gusev A; Schumm LP; Bowen BM; Sharma Y; Ning K; Remark R; Gnjatic S; Legnani P; George J; Sands BE; Stempak JM; Datta LW; Lipka S; Katz S; Cheifetz AS; Barzilai N; Pontikos N; Abraham C; Dubinsky MJ; Targan S; Taylor K; Rotter JI; Scherl EJ; Desnick RJ; Abreu MT; Zhao H; Atzmon G; Pe'er I; Kugathasan S; Hakonarson H; McCauley JL; Lencz T; Darvasi A; Plagnol V
[Ad] Endereço:Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
[Ti] Título:A Frameshift in CSF2RB Predominant Among Ashkenazi Jews Increases Risk for Crohn's Disease and Reduces Monocyte Signaling via GM-CSF.
[So] Source:Gastroenterology;151(4):710-723.e2, 2016 Oct.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Crohn's disease (CD) has the highest prevalence in Ashkenazi Jewish populations. We sought to identify rare, CD-associated frameshift variants of high functional and statistical effects. METHODS: We performed exome sequencing and array-based genotype analyses of 1477 Ashkenazi Jewish individuals with CD and 2614 Ashkenazi Jewish individuals without CD (controls). To validate our findings, we performed genotype analyses of an additional 1515 CD cases and 7052 controls for frameshift mutations in the colony-stimulating factor 2-receptor ß common subunit gene (CSF2RB). Intestinal tissues and blood samples were collected from patients with CD; lamina propria leukocytes were isolated and expression of CSF2RB and granulocyte-macrophage colony-stimulating factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cytometry (CyTOF analysis). Variants of CSF2RB were transfected into HEK293 cells and the expression and functions of gene products were compared. RESULTS: In the discovery cohort, we associated CD with a frameshift mutation in CSF2RB (P = 8.52 × 10(-4)); the finding was validated in the replication cohort (combined P = 3.42 × 10(-6)). Incubation of intestinal lamina propria leukocytes with granulocyte-macrophage colony-stimulating factor resulted in high levels of phosphorylation of signal transducer and activator of transcription (STAT5) and lesser increases in phosphorylation of extracellular signal-regulated kinase and AK straining transforming (AKT). Cells co-transfected with full-length and mutant forms of CSF2RB had reduced pSTAT5 after stimulation with granulocyte-macrophage colony-stimulating factor, compared with cells transfected with control CSF2RB, indicating a dominant-negative effect of the mutant gene. Monocytes from patients with CD who were heterozygous for the frameshift mutation (6% of CD cases analyzed) had reduced responses to granulocyte-macrophage colony-stimulating factor and markedly decreased activity of aldehyde dehydrogenase; activity of this enzyme has been associated with immune tolerance. CONCLUSIONS: In a genetic analysis of Ashkenazi Jewish individuals, we associated CD with a frameshift mutation in CSF2RB. Intestinal monocytes from carriers of this mutation had reduced responses to granulocyte-macrophage colony-stimulating factor, providing an additional mechanism for alterations to the innate immune response in individuals with CD.
[Mh] Termos MeSH primário: Doença de Crohn/genética
Subunidade beta Comum dos Receptores de Citocinas/genética
Mutação da Fase de Leitura
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Judeus/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Doença de Crohn/etnologia
Doença de Crohn/patologia
Feminino
Seres Humanos
Intestinos/citologia
Intestinos/patologia
Masculino
Monócitos/metabolismo
Fatores de Risco
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CSF2RB protein, human); 0 (Cytokine Receptor Common beta Subunit); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160706
[St] Status:MEDLINE


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[PMID]:27373512
[Au] Autor:Levine AP; Pontikos N; Schiff ER; Jostins L; Speed D; Lovat LB; Barrett JC; Grasberger H; Plagnol V; Segal AW; NIDDK Inflammatory Bowel Disease Genetics Consortium
[Ad] Endereço:Division of Medicine, University College London (UCL), London, United Kingdom.
[Ti] Título:Genetic Complexity of Crohn's Disease in Two Large Ashkenazi Jewish Families.
[So] Source:Gastroenterology;151(4):698-709, 2016 Oct.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Crohn's disease (CD) is a highly heritable disease that is particularly common in the Ashkenazi Jewish population. We studied 2 large Ashkenazi Jewish families with a high prevalence of CD in an attempt to identify novel genetic risk variants. METHODS: Ashkenazi Jewish patients with CD and a positive family history were recruited from the University College London Hospital. We used genome-wide, single-nucleotide polymorphism data to assess the burden of common CD-associated risk variants and for linkage analysis. Exome sequencing was performed and rare variants that were predicted to be deleterious and were observed at a high frequency in cases were prioritized. We undertook within-family association analysis after imputation and assessed candidate variants for evidence of association with CD in an independent cohort of Ashkenazi Jewish individuals. We examined the effects of a variant in DUOX2 on hydrogen peroxide production in HEK293 cells. RESULTS: We identified 2 families (1 with >800 members and 1 with >200 members) containing 54 and 26 cases of CD or colitis, respectively. Both families had a significant enrichment of previously described common CD-associated risk variants. No genome-wide significant linkage was observed. Exome sequencing identified candidate variants, including a missense mutation in DUOX2 that impaired its function and a frameshift mutation in CSF2RB that was associated with CD in an independent cohort of Ashkenazi Jewish individuals. CONCLUSIONS: In a study of 2 large Ashkenazi Jewish with multiple cases of CD, we found the genetic basis of the disease to be complex, with a role for common and rare genetic variants. We identified a frameshift mutation in CSF2RB that was replicated in an independent cohort. These findings show the value of family studies and the importance of the innate immune system in the pathogenesis of CD.
[Mh] Termos MeSH primário: Doença de Crohn/genética
Subunidade beta Comum dos Receptores de Citocinas/genética
Judeus/genética
NADPH Oxidases/genética
Linhagem
[Mh] Termos MeSH secundário: Adolescente
Idade de Início
Doença de Crohn/etnologia
Oxidases Duais
Exoma
Feminino
Mutação da Fase de Leitura
Ligação Genética
Predisposição Genética para Doença
Células HEK293/metabolismo
Seres Humanos
Masculino
Dados de Sequência Molecular
Mutação de Sentido Incorreto
Polimorfismo de Nucleotídeo Único
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CSF2RB protein, human); 0 (Cytokine Receptor Common beta Subunit); EC 1.11.1.- (Dual Oxidases); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (DUOX2 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160705
[St] Status:MEDLINE


  7 / 109 MEDLINE  
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[PMID]:27365391
[Au] Autor:Schmidt T; Ye F; Situ AJ; An W; Ginsberg MH; Ulmer TS
[Ad] Endereço:From the Department of Biochemistry & Molecular Biology and Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033.
[Ti] Título:A Conserved Ectodomain-Transmembrane Domain Linker Motif Tunes the Allosteric Regulation of Cell Surface Receptors.
[So] Source:J Biol Chem;291(34):17536-46, 2016 08 19.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In many families of cell surface receptors, a single transmembrane (TM) α-helix separates ecto- and cytosolic domains. A defined coupling of ecto- and TM domains must be essential to allosteric receptor regulation but remains little understood. Here, we characterize the linker structure, dynamics, and resulting ecto-TM domain coupling of integrin αIIb in model constructs and relate it to other integrin α subunits by mutagenesis. Cellular integrin activation assays subsequently validate the findings in intact receptors. Our results indicate a flexible yet carefully tuned ecto-TM coupling that modulates the signaling threshold of integrin receptors. Interestingly, a proline at the N-terminal TM helix border, termed NBP, is critical to linker flexibility in integrins. NBP is further predicted in 21% of human single-pass TM proteins and validated in cytokine receptors by the TM domain structure of the cytokine receptor common subunit ß and its P441A-substituted variant. Thus, NBP is a conserved uncoupling motif of the ecto-TM domain transition and the degree of ecto-TM domain coupling represents an important parameter in the allosteric regulation of diverse cell surface receptors.
[Mh] Termos MeSH primário: Subunidade beta Comum dos Receptores de Citocinas/química
Cadeias beta de Integrinas/química
[Mh] Termos MeSH secundário: Regulação Alostérica/fisiologia
Animais
Células CHO
Cricetinae
Cricetulus
Subunidade beta Comum dos Receptores de Citocinas/genética
Subunidade beta Comum dos Receptores de Citocinas/metabolismo
Seres Humanos
Cadeias beta de Integrinas/genética
Cadeias beta de Integrinas/metabolismo
Domínios Proteicos
Estrutura Secundária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cytokine Receptor Common beta Subunit); 0 (Integrin beta Chains)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.733683


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[PMID]:26992565
[Au] Autor:van de Laar L; Saelens W; De Prijck S; Martens L; Scott CL; Van Isterdael G; Hoffmann E; Beyaert R; Saeys Y; Lambrecht BN; Guilliams M
[Ad] Endereço:Unit of Immunoregulation and Mucosal Immunology, VIB Inflammation Research Center, Ghent 9052, Belgium; Department of Internal Medicine, Ghent University, Ghent 9000, Belgium.
[Ti] Título:Yolk Sac Macrophages, Fetal Liver, and Adult Monocytes Can Colonize an Empty Niche and Develop into Functional Tissue-Resident Macrophages.
[So] Source:Immunity;44(4):755-68, 2016 Apr 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident macrophages can derive from yolk sac macrophages (YS-Macs), fetal liver monocytes (FL-MOs), or adult bone-marrow monocytes (BM-MOs). The relative capacity of these precursors to colonize a niche, self-maintain, and perform tissue-specific functions is unknown. We simultaneously transferred traceable YS-Macs, FL-MOs, and BM-MOs into the empty alveolar macrophage (AM) niche of neonatal Csf2rb(-/-) mice. All subsets produced AMs, but in competition preferential outgrowth of FL-MOs was observed, correlating with their superior granulocyte macrophage-colony stimulating factor (GM-CSF) reactivity and proliferation capacity. When transferred separately, however, all precursors efficiently colonized the alveolar niche and generated AMs that were transcriptionally almost identical, self-maintained, and durably prevented alveolar proteinosis. Mature liver, peritoneal, or colon macrophages could not efficiently colonize the empty AM niche, whereas mature AMs could. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages and the plasticity of the mononuclear phagocyte system is largest at the precursor stage.
[Mh] Termos MeSH primário: Células da Medula Óssea/citologia
Diferenciação Celular/imunologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Fígado/citologia
Macrófagos Alveolares/citologia
Saco Vitelino/citologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Subunidade beta Comum dos Receptores de Citocinas/genética
Fígado/embriologia
Fígado/imunologia
Macrófagos Alveolares/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Transcriptoma/imunologia
Saco Vitelino/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokine Receptor Common beta Subunit); 144715-98-0 (Csf2rb1 protein, mouse); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160421
[Lr] Data última revisão:
160421
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160320
[St] Status:MEDLINE


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[PMID]:26926469
[Au] Autor:Sarrazy V; Viaud M; Westerterp M; Ivanov S; Giorgetti-Peraldi S; Guinamard R; Gautier EL; Thorp EB; De Vivo DC; Yvan-Charvet L
[Ad] Endereço:From the Institut National de la Santé et de la Recherche Médicale (INSERM) U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France (V.S., M.V., S.I., S.G.-P., R.G., L.Y.-C.); Division of Molecular Medicine, Department of Medicine (M.W.) and Department of Neurology (D.C.D.V.), Columb
[Ti] Título:Disruption of Glut1 in Hematopoietic Stem Cells Prevents Myelopoiesis and Enhanced Glucose Flux in Atheromatous Plaques of ApoE(-/-) Mice.
[So] Source:Circ Res;118(7):1062-77, 2016 Apr 01.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Inflamed atherosclerotic plaques can be visualized by noninvasive positron emission and computed tomographic imaging with (18)F-fluorodeoxyglucose, a glucose analog, but the underlying mechanisms are poorly understood. OBJECTIVE: Here, we directly investigated the role of Glut1-mediated glucose uptake in apolipoprotein E-deficient (ApoE(-/-)) mouse model of atherosclerosis. METHODS AND RESULTS: We first showed that the enhanced glycolytic flux in atheromatous plaques of ApoE(-/-) mice was associated with the enhanced metabolic activity of hematopoietic stem and multipotential progenitor cells and higher Glut1 expression in these cells. Mechanistically, the regulation of Glut1 in ApoE(-/-) hematopoietic stem and multipotential progenitor cells was not because of alterations in hypoxia-inducible factor 1α signaling or the oxygenation status of the bone marrow but was the consequence of the activation of the common ß subunit of the granulocyte-macrophage colony-stimulating factor/interleukin-3 receptor driving glycolytic substrate utilization by mitochondria. By transplanting bone marrow from WT, Glut1(+/-), ApoE(-/-), and ApoE(-/-)Glut1(+/-) mice into hypercholesterolemic ApoE-deficient mice, we found that Glut1 deficiency reversed ApoE(-/-) hematopoietic stem and multipotential progenitor cell proliferation and expansion, which prevented the myelopoiesis and accelerated atherosclerosis of ApoE(-/-) mice transplanted with ApoE(-/-) bone marrow and resulted in reduced glucose uptake in the spleen and aortic arch of these mice. CONCLUSIONS: We identified that Glut1 connects the enhanced glucose uptake in atheromatous plaques of ApoE(-/-) mice with their myelopoiesis through regulation of hematopoietic stem and multipotential progenitor cell maintenance and myelomonocytic fate and suggests Glut1 as potential drug target for atherosclerosis.
[Mh] Termos MeSH primário: Transportador de Glucose Tipo 1/fisiologia
Glucose/metabolismo
Células-Tronco Hematopoéticas/metabolismo
Hipercolesterolemia/metabolismo
Mielopoese/fisiologia
Placa Aterosclerótica/metabolismo
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/metabolismo
Apolipoproteínas E/deficiência
Transplante de Medula Óssea
Divisão Celular
Subunidade beta Comum dos Receptores de Citocinas/fisiologia
Progressão da Doença
Metabolismo Energético
Regulação da Expressão Gênica
Transportador de Glucose Tipo 1/deficiência
Glicólise
Hipercolesterolemia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/deficiência
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Metformina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células-Tronco Multipotentes/metabolismo
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Receptores de Interleucina-3/antagonistas & inibidores
Receptores de Interleucina-3/fisiologia
Baço/metabolismo
Tirfostinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Cytokine Receptor Common beta Subunit); 0 (Glucose Transporter Type 1); 0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Messenger); 0 (Receptors, Interleukin-3); 0 (Slc2a1 protein, mouse); 0 (Tyrphostins); 0 (alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide); 9100L32L2N (Metformin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.115.307599


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[PMID]:26748017
[Au] Autor:Gao C; Leyton JV; Schimmer AD; Minden M; Reilly RM
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Toronto, Ontario, Canada.
[Ti] Título:Auger electron-emitting (111)In-DTPA-NLS-CSL360 radioimmunoconjugates are cytotoxic to human acute myeloid leukemia (AML) cells displaying the CD123(+)/CD131(-) phenotype of leukemia stem cells.
[So] Source:Appl Radiat Isot;110:1-7, 2016 Apr.
[Is] ISSN:1872-9800
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chimeric IgG1 monoclonal antibody CSL360 recognizes the CD123(+)/CD131(-) phenotype expressed by leukemic stem cells (LSC). Auger electron-emitting (111)In-DTPA-NLS-CSL360 radioimmunoconjugates incorporating nuclear translocation sequence (NLS) peptides bound specifically to Raji cells transfected with CD123 and exhibited a KD of 11nmols/L in a competition receptor-binding assay using CD123-transfected CHO cells. (111)In-DTPA-NLS-CSL360 was bound, internalized and transported to the nucleus of human AML-5 myeloid leukemia cells. The clonogenic survival of AML-5 cells was reduced by (111)In-DTPA-NLS-CSL360 up to 3.7-fold. Isotype control (111)In-DTPA-chIgG1 was 2-fold less cytotoxic, and unlabeled CSL360, DTPA-NLS-CSL360 or free (111)In acetate did not decrease cell survival. These results are promising for further evaluation of (111)In-DTPA-NLS-CSL360 for Auger electron radioimmunotherapy of AML targeting the critical LSC subpopulation.
[Mh] Termos MeSH primário: Leucemia Mieloide Aguda/radioterapia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Linhagem Celular Tumoral
Subunidade beta Comum dos Receptores de Citocinas/metabolismo
Seres Humanos
Imunoconjugados/uso terapêutico
Radioisótopos de Índio/uso terapêutico
Subunidade alfa de Receptor de Interleucina-3/metabolismo
Leucemia Mieloide Aguda/imunologia
Células-Tronco Neoplásicas/imunologia
Células-Tronco Neoplásicas/efeitos da radiação
Ácido Pentético/uso terapêutico
Radioimunoterapia
Compostos Radiofarmacêuticos
Ensaio Tumoral de Célula-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (CSF2RB protein, human); 0 (CSL360); 0 (Cytokine Receptor Common beta Subunit); 0 (IL3RA protein, human); 0 (Immunoconjugates); 0 (Indium Radioisotopes); 0 (Interleukin-3 Receptor alpha Subunit); 0 (Radiopharmaceuticals); 7A314HQM0I (Pentetic Acid)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160110
[St] Status:MEDLINE



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