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  1 / 7004 MEDLINE  
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[PMID]:29381400
[Au] Autor:Song ZY; Wang F; Cui SX; Qu XJ
[Ad] Endereço:a Department of Pharmacology, School of Basic Medical Sciences , Capital Medical University , Beijing , China.
[Ti] Título:Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/ß-Catenin Pathways.
[So] Source:Cancer Invest;36(1):10-18, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CXCL12 is an extracellular chemokine binding to cell surface receptor CXCR4. We found that activation of CXCL12/CXCR4 axis stimulated angiogenesis in endothelial cells. Knockdown of CXCR4 in endothelial cells prevented the branch points of angiogenesis. Endothelial cells exposed to CXCL12 presented high level of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase MMP-2, but not in CXCR4 knockdown cells. Further studies revealed that activation of CXCL12/CXCR4 axis in vascular endothelial cells stimulates the angiogenesis through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/ß-catenin pathways. Conclusion, downregulation of CXCR4 could inhibit angiogenesis in cancer tissues.
[Mh] Termos MeSH primário: Quimiocina CXCL12/genética
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica/genética
Neovascularização Patológica/genética
Receptores CXCR4/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Metaloproteinase 2 da Matriz/genética
Proteínas Quinases Ativadas por Mitógeno/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Receptor do Fator de Crescimento Epidérmico/genética
Regulação para Cima/genética
Fator A de Crescimento do Endotélio Vascular/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1422512


  2 / 7004 MEDLINE  
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[PMID]:29275565
[Au] Autor:Li P; Li WL; Qi JX
[Ad] Endereço:Department of Head Neck and Thyroid, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou 450008, China.
[Ti] Título:[Expression of integrin αvß3, CXC chemokine receptor 4 and CXC chemokine receptor 7 and their relationship with lymph node metastasis in squamous cell carcinoma of head and neck].
[So] Source:Zhonghua Kou Qiang Yi Xue Za Zhi;52(12):723-729, 2017 Dec 09.
[Is] ISSN:1002-0098
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the expression of integrin αvß3, CXC chemokine receptor (CXCR)4 and CXCR7 and their relationship with lymph node metastasis in squamous cell carcinoma of head and neck (SCCHN). The expression of integrin αvß3, CXCR4 and CXCR7 was detected by immunohistochemistry SABC in 92 cases of primary SCCHN, metastatic lymph node, normal oral mucosa tissues and normal lymph nodes. The positive rate of the expression of integrin αvß3, CXCR4 and CXCR7 was 75% (69/92), 81%(75/92) and 76%(70/92), respectively in primary SCCHN, and was 82%(75/92), 76%(70/92) and 65%(60/92), respectively in metastatic lymph node. The expression of integrin αvß3 and CXCR4 in primary SCCHN ( 0.813, 0.05) and lymph node metastasis ( 0.541, 0.05) was positively correlated. Integrin αvß3 and CXCR7 expression in primary SCCHN ( 0.683, 0.05) and lymph node metastasis ( 0.708, 0.05) was positively correlated. CXCR4 and CXCR7 expression in primary SCCHN ( 0.644, 0.05) and lymph node metastasis ( 0.707, 0.05) had a positive correlation. The expression level was associated with tumor size ( 0.040, 0.001, 0.009), lymph node metastasis ( 0.001, 0.000, 0.000) and surrounding tissue invasion ( 0.046, 0.002, 0.001), but not related to age ( 0.097, 0.274, 0.162), gender ( 0.103, 0.309, 0.187). The overexpression of integrin αvß3, CXCR4 and CXCR7 in primary head and neck squamous carcinoma and metastatic lymph nodes was related to lymph node metastasis. The co-expression of integrin αvß3, CXCR4 and CXCR7 may play a synergistic role in lymphatic metastasis of SCCHN.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/secundário
Neoplasias de Cabeça e Pescoço/metabolismo
Neoplasias de Cabeça e Pescoço/patologia
Integrina alfaVbeta3/metabolismo
Receptores CXCR4/metabolismo
Receptores CXCR/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Imuno-Histoquímica
Metástase Linfática
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, human); 0 (CXCR7 protein, human); 0 (Integrin alphaVbeta3); 0 (RNA, Messenger); 0 (Receptors, CXCR); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171226
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1002-0098.2017.12.003


  3 / 7004 MEDLINE  
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[PMID]:28450349
[Au] Autor:Döring Y; Noels H; van der Vorst EPC; Neideck C; Egea V; Drechsler M; Mandl M; Pawig L; Jansen Y; Schröder K; Bidzhekov K; Megens RTA; Theelen W; Klinkhammer BM; Boor P; Schurgers L; van Gorp R; Ries C; Kusters PJH; van der Wal A; Hackeng TM; Gäbel G; Brandes RP; Soehnlein O; Lutgens E; Vestweber D; Teupser D; Holdt LM; Rader DJ; Saleheen D; Weber C
[Ti] Título:Vascular CXCR4 Limits Atherosclerosis by Maintaining Arterial Integrity: Evidence From Mouse and Human Studies.
[So] Source:Circulation;136(4):388-403, 2017 Jul 25.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The CXCL12/CXCR4 chemokine ligand/receptor axis controls (progenitor) cell homeostasis and trafficking. So far, an atheroprotective role of CXCL12/CXCR4 has only been implied through pharmacological intervention, in particular, because the somatic deletion of the gene in mice is embryonically lethal. Moreover, cell-specific effects of CXCR4 in the arterial wall and underlying mechanisms remain elusive, prompting us to investigate the relevance of CXCR4 in vascular cell types for atheroprotection. METHODS: We examined the role of vascular CXCR4 in atherosclerosis and plaque composition by inducing an endothelial cell (BmxCreER -driven)-specific or smooth muscle cell (SMC, SmmhcCreER - or TaglnCre-driven)-specific deficiency of in an apolipoprotein E-deficient mouse model. To identify underlying mechanisms for effects of CXCR4, we studied endothelial permeability, intravital leukocyte adhesion, involvement of the Akt/WNT/ß-catenin signaling pathway and relevant phosphatases in VE-cadherin expression and function, vascular tone in aortic rings, cholesterol efflux from macrophages, and expression of SMC phenotypic markers. Finally, we analyzed associations of common genetic variants at the locus with the risk for coronary heart disease, along with transcript expression in human atherosclerotic plaques. RESULTS: The cell-specific deletion of in arterial endothelial cells (n=12-15) or SMCs (n=13-24) markedly increased atherosclerotic lesion formation in hyperlipidemic mice. Endothelial barrier function was promoted by CXCL12/CXCR4, which triggered Akt/WNT/ß-catenin signaling to drive VE-cadherin expression and stabilized junctional VE-cadherin complexes through associated phosphatases. Conversely, endothelial deficiency caused arterial leakage and inflammatory leukocyte recruitment during atherogenesis. In arterial SMCs, CXCR4 sustained normal vascular reactivity and contractile responses, whereas deficiency favored a synthetic phenotype, the occurrence of macrophage-like SMCs in the lesions, and impaired cholesterol efflux. Regression analyses in humans (n=259 796) identified the C-allele at within the locus to be associated with increased risk for coronary heart disease. In line, C/C risk genotype carriers showed reduced CXCR4 expression in carotid artery plaques (n=188), which was furthermore associated with symptomatic disease. CONCLUSIONS: Our data clearly establish that vascular CXCR4 limits atherosclerosis by maintaining arterial integrity, preserving endothelial barrier function, and a normal contractile SMC phenotype. Enhancing these beneficial functions of arterial CXCR4 by selective modulators might open novel therapeutic options in atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Aterosclerose/prevenção & controle
Células Endoteliais/metabolismo
Receptores CXCR4/biossíntese
[Mh] Termos MeSH secundário: Animais
Aterosclerose/genética
Permeabilidade Capilar/fisiologia
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores CXCR4/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, human); 0 (CXCR4 protein, mouse); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.117.027646


  4 / 7004 MEDLINE  
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[PMID]:27775742
[Au] Autor:Kingsmore KM; Logsdon DK; Floyd DH; Peirce SM; Purow BW; Munson JM
[Ad] Endereço:Department of Biomedical Engineering, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
[Ti] Título:Interstitial flow differentially increases patient-derived glioblastoma stem cell invasion via CXCR4, CXCL12, and CD44-mediated mechanisms.
[So] Source:Integr Biol (Camb);8(12):1246-1260, 2016 12 05.
[Is] ISSN:1757-9708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) prognosis remains dismal due in part to the invasiveness of GBM cells. Interstitial fluid flow (IFF) has been shown to increase invasion of glioma cells in vitro through the CXCR4 receptor interacting with autologous, pericellular gradients of CXCL12 (autologous chemotaxis) or through the CD44 receptor interactions with the extracellular matrix (hyaluronan-mediated mechanotransduction). These mechanisms have not been examined together and thus we hypothesized that both mechanisms contribute to invasion in populations of cancer cells. Therefore, we examined IFF-stimulated CXCR4-, CXCL12-, and CD44-dependent invasion in patient-derived glioblastoma stem cells (GSCs). Using our 3D in vitro assay and correlative in vivo studies we demonstrated GSC lines show increased invasion with flow. This flow-stimulated invasion was reduced by blockade of CXCR4, CXCL12, and/or CD44, revealing that GSC invasion may be mediated simultaneously by both mechanisms. Characterization of CXCR4 , CXCL12 , and CD44 populations in four GSC lines revealed different percentages of protein positive subpopulations for each line. We developed an agent-based model to identify the contributions of each subpopulation to flow-stimulated invasion and validated the model through comparisons with experimental blocking studies. Clinically relevant radiation therapy increased flow-stimulated invasion in one GSC line. Our agent-based model predicted that IFF-stimulated invasion is driven primarily by CXCR4 CXCL12 populations, and, indeed our irradiated cells had an increase in this subpopulation. Together, these data indicate that different mechanisms govern the flow response across GSCs, but that within a single patient, there are subpopulations of GSCs that respond to flow via either CD44- or CXCR4-CXCL12 mechanisms.
[Mh] Termos MeSH primário: Quimiocina CXCL12/imunologia
Glioblastoma/imunologia
Glioblastoma/patologia
Receptores de Hialuronatos/imunologia
Mecanotransdução Celular/imunologia
Células-Tronco Neoplásicas/imunologia
Receptores CXCR4/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Líquido Extracelular/imunologia
Seres Humanos
Invasividade Neoplásica
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD44 protein, human); 0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Hyaluronan Receptors); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  5 / 7004 MEDLINE  
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[PMID]:29183039
[Au] Autor:Sun T; Li X; Song H; Gao F; Zhou G; Li X; Chen Z; Chen L
[Ad] Endereço:Department of Orthopaedics, Jining No. 1 People's Hospital, Jining, China.
[Ti] Título:MiR-146a Aggravates LPS-Induced Inflammatory Injury by Targeting CXCR4 in the Articular Chondrocytes.
[So] Source:Cell Physiol Biochem;44(4):1282-1294, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Osteoarthritis (OA) as a degenerative disease is a major problem in ageing populations. To better understand the molecular mechanisms in the pathogenesis of OA, this study explored the role of microRNA (miR)-146a in the articular chondrocytes. METHODS: The articular chondrocyte line ATDC5 was used to simulate inflammatory injury by LPS administration in vitro. Cell viability, apoptosis, mRNA expressions and productions of inflammatory factors were assessed, respectively. Mir-146a and Cxcr4 mRNA expressions were measured by qRT-PCR. Targeting effect of miR-146a on Cxcr4 3'UTR was assessed by luciferase activity analysis. Protein expression levels of CXCR4 and main factors in PI3K/AKT, Wnt/ß-catenin signal pathways were measured by western blotting. RESULTS: LPS exposure suppressed cell viability, prompted apoptosis of ATDC5 cells, and stimulated expression and release of inflammatory factors. MiR-146a was upregulated in LPS-induced cells. Overexpression of miR-146a further aggravated LPS-induced inflammatory injury, while it was reduced after miR-146a was knocked down. CXCR4 expression was negatively regulated by miR-146a. CXCR4 was a direct target of miR-146a and thus involved in regulatory effect of miR-146a on the injured chondrocytes, which was also related with phosphorylation levels of PI3K/AKT and expressions of Wnt/ß-catenin signal factors. CONCLUSION: miR-146a promoted inflammatory response of articular chondrocytes via targeting CXCR4 and suppressing CXCR4 expression. Overexpression of CXCR4 could attenuate the inflammatory injury. Our findings provided novel evidence which might be useful for further studies exploring therapeutic approaches for OA via targeting miR-146a.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Lipopolissacarídeos/toxicidade
MicroRNAs/metabolismo
Receptores CXCR4/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Antagomirs/metabolismo
Sequência de Bases
Cartilagem Articular/citologia
Cartilagem Articular/efeitos dos fármacos
Cartilagem Articular/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Camundongos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Receptores CXCR4/antagonistas & inibidores
Receptores CXCR4/genética
Alinhamento de Sequência
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima/efeitos dos fármacos
Proteínas Wnt/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (CXCR4 protein, mouse); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Lipopolysaccharides); 0 (MicroRNAs); 0 (Mirn146 microRNA, mouse); 0 (RNA, Small Interfering); 0 (Receptors, CXCR4); 0 (Tumor Necrosis Factor-alpha); 0 (Wnt Proteins); 0 (beta Catenin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1159/000485488


  6 / 7004 MEDLINE  
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[PMID]:29232699
[Au] Autor:Ramonell KM; Zhang W; Hadley A; Chen CW; Fay KT; Lyons JD; Klingensmith NJ; McConnell KW; Coopersmith CM; Ford ML
[Ad] Endereço:Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, United States of America.
[Ti] Título:CXCR4 blockade decreases CD4+ T cell exhaustion and improves survival in a murine model of polymicrobial sepsis.
[So] Source:PLoS One;12(12):e0188882, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is a dysregulated systemic response to infection involving many inflammatory pathways and the induction of counter-regulatory anti-inflammatory processes that results in a state of immune incompetence and can lead to multi-organ failure. CXCR4 is a chemokine receptor that, following ligation by CXCL12, directs cells to bone marrow niches and also plays an important role in T cell cosignaling and formation of the immunological synapse. Here, we investigated the expression and function of CXCR4 in a murine model of polymicrobial sepsis. Results indicate that CXCR4 is selectively upregulated on naïve CD4+ and CD8+ T cells and CD4+ central memory T cells following the induction of sepsis, and that CXCR4 antagonism resulted in a significant decrease in sepsis-induced mortality. We probed the mechanistic basis for these findings and found that CXCR4 antagonism significantly increased the number of peripheral CD4+ and CD8+ T cells following sepsis. Moreover, mice treated with the CXCR4 antagonist contained fewer PD-1+ LAG-3+ 2B4+ cells, suggesting that blockade of CXCR4 mitigates CD4+ T cell exhaustion during sepsis. Taken together, these results characterize CXCR4 as an important pathway that modulates immune dysfunction and mortality following sepsis, which may hold promise as a target for future therapeutic intervention in septic patients.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Modelos Animais de Doenças
Receptores CXCR4/antagonistas & inibidores
Sepse/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/imunologia
Feminino
Citometria de Fluxo
Memória Imunológica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Sepse/microbiologia
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188882


  7 / 7004 MEDLINE  
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[PMID]:29262350
[Au] Autor:Suan D; Kräutler NJ; Maag JLV; Butt D; Bourne K; Hermes JR; Avery DT; Young C; Statham A; Elliott M; Dinger ME; Basten A; Tangye SG; Brink R
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia; Westmead Clinical School, University of Sydney, Sydney, NSW 2145, Australia.
[Ti] Título:CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.
[So] Source:Immunity;47(6):1142-1153.e4, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6 GC B cells were highly enriched within the GC light zone (LZ), were the most quiescent of all GC B cells, exhibited a cell-surface phenotype and gene expression signature indicative of an MBC transition, and possessed the augmented response characteristics of MBCs. MBC precursors within the GC LZ predominantly possessed a low affinity for antigen but also included cells from within the high-affinity pool. These data indicate a fundamental dichotomy between the processes that drive MBC and PC differentiation during GC responses.
[Mh] Termos MeSH primário: Centro Germinativo/imunologia
Imunidade Humoral
Plasmócitos/imunologia
Células Precursoras de Linfócitos B/imunologia
Receptores CCR6/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/genética
Antígeno B7-2/imunologia
Diferenciação Celular
Linhagem da Célula/imunologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Centro Germinativo/citologia
Seres Humanos
Memória Imunológica
Imunofenotipagem
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Plasmócitos/citologia
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Células Precursoras de Linfócitos B/citologia
Receptores CCR6/genética
Receptores CXCR4/genética
Receptores CXCR4/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CCR6 protein, mouse); 0 (CXCR4 protein, mouse); 0 (Cd86 protein, mouse); 0 (Prdm1 protein, mouse); 0 (Receptors, CCR6); 0 (Receptors, CXCR4); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  8 / 7004 MEDLINE  
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[PMID]:27775528
[Au] Autor:Hou J; Luo T; Ng KL; Leung AY; Liang R; Sun D
[Ti] Título:Characterization of Drug Effect on Leukemia Cells Through Single Cell Assay With Optical Tweezers and Dielectrophoresis.
[So] Source:IEEE Trans Nanobioscience;15(8):820-827, 2016 12.
[Is] ISSN:1558-2639
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:One of the greatest challenges in acute myeloid leukemia (AML) treatment is preventing relapse. Leukemia cells can hide in bone marrow niche or vascular niche. Hence, many chemical drugs cannot kill these cells. To characterize migration and adhesion properties of leukemia cells in specific niches, CXCR4/SDF- 1α signal pathway has been widely used for investigation. AMD3100 is treated as one of the most common chemical drugs that can inhibit this signal. In the current study, we particularly investigate the effect of AMD3100 on the adhesion property of leukemia cells on stromal cells by using engineering tools, namely, optical tweezers (OT) and dielectrophoresis (DEP), to probe single cell property. AMD3100 not only inhibits the CXCR4/SDF- 1α signal pathway but also reduces gene expression of CXCR4 and VLA-4 on leukemia cells. The drug also softens leukemia cells. This work provides a new way to investigate cell behavior under drug treatment. The use of combined engineering tools will benefit drug discovery and assessment for leukemia treatment.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Eletroforese/métodos
Compostos Heterocíclicos/farmacologia
Leucemia Mieloide Aguda/metabolismo
Pinças Ópticas
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Quimiocina CXCL12/análise
Quimiocina CXCL12/genética
Quimiocina CXCL12/metabolismo
Técnicas de Cocultura
Seres Humanos
Receptores CXCR4/análise
Receptores CXCR4/genética
Receptores CXCR4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Estromais/citologia
Células Estromais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Heterocyclic Compounds); 0 (Receptors, CXCR4); 155148-31-5 (JM 3100)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1109/TNB.2016.2616160


  9 / 7004 MEDLINE  
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[PMID]:27770832
[Au] Autor:Bjorke B; Shoja-Taheri F; Kim M; Robinson GE; Fontelonga T; Kim KT; Song MR; Mastick GS
[Ad] Endereço:Department of Biology, University of Nevada, Reno, NV, 89557, USA.
[Ti] Título:Contralateral migration of oculomotor neurons is regulated by Slit/Robo signaling.
[So] Source:Neural Dev;11(1):18, 2016 10 22.
[Is] ISSN:1749-8104
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oculomotor neurons develop initially like typical motor neurons, projecting axons out of the ventral midbrain to their ipsilateral targets, the extraocular muscles. However, in all vertebrates, after the oculomotor nerve (nIII) has reached the extraocular muscle primordia, the cell bodies that innervate the superior rectus migrate to join the contralateral nucleus. This motor neuron migration represents a unique strategy to form a contralateral motor projection. Whether migration is guided by diffusible cues remains unknown. METHODS: We examined the role of Slit chemorepellent signals in contralateral oculomotor migration by analyzing mutant mouse embryos. RESULTS: We found that the ventral midbrain expresses high levels of both Slit1 and 2, and that oculomotor neurons express the repellent Slit receptors Robo1 and Robo2. Therefore, Slit signals are in a position to influence the migration of oculomotor neurons. In Slit 1/2 or Robo1/2 double mutant embryos, motor neuron cell bodies migrated into the ventral midbrain on E10.5, three days prior to normal migration. These early migrating neurons had leading projections into and across the floor plate. In contrast to the double mutants, embryos which were mutant for single Slit or Robo genes did not have premature migration or outgrowth on E10.5, demonstrating a cooperative requirement of Slit1 and 2, as well as Robo1 and 2. To test how Slit/Robo midline repulsion is modulated, we found that the normal migration did not require the receptors Robo3 and CXCR4, or the chemoattractant, Netrin 1. The signal to initiate contralateral migration is likely autonomous to the midbrain because oculomotor neurons migrate in embryos that lack either nerve outgrowth or extraocular muscles, or in cultured midbrains that lacked peripheral tissue. CONCLUSION: Overall, our results demonstrate that a migratory subset of motor neurons respond to floor plate-derived Slit repulsion to properly control the timing of contralateral migration.
[Mh] Termos MeSH primário: Orientação de Axônios
Movimento Celular
Peptídeos e Proteínas de Sinalização Intercelular/fisiologia
Neurônios Motores/fisiologia
Proteínas do Tecido Nervoso/fisiologia
Nervo Oculomotor/crescimento & desenvolvimento
Receptores Imunológicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Membrana/fisiologia
Mesencéfalo/fisiologia
Camundongos
Fatores de Crescimento Neural/fisiologia
Netrina-1
Receptores CXCR4/fisiologia
Transdução de Sinais
Proteínas Supressoras de Tumor/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Nerve Growth Factors); 0 (Nerve Tissue Proteins); 0 (Ntn1 protein, mouse); 0 (Receptors, CXCR4); 0 (Receptors, Immunologic); 0 (Robo2 protein, mouse); 0 (Robo3 protein, mouse); 0 (Slit homolog 2 protein); 0 (Slit1 protein, mouse); 0 (Tumor Suppressor Proteins); 0 (roundabout protein); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29017963
[Au] Autor:Meng W; Xue S; Chen Y
[Ad] Endereço:Division of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Institute of Genetics, Zhejiang University, Hangzhou, Zhejiang, China.
[Ti] Título:The role of CXCL12 in tumor microenvironment.
[So] Source:Gene;641:105-110, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The chemokine ligand C-X-C motif chemokine ligand 12 (CXCL12) is a kind of small molecules of cytokines that widely expressed in diversified tissues. Recent evidence suggests that CXCL12 plays an important role in the communication of tumor cells with their surrounding microenvironment. The interaction of CXCL12 and its receptors subsequently excite the downstream signaling pathways to affect tumor angiogenesis, tumor cell proliferation and chemoresistance, and thus represents a potential target for cancer therapy. Outpouring molecules targeting CXCL12/CXCR4 axis in tumor microenvironment combined with traditional chemotherapy have drawn more and more attentions, which will be a promising method in anti-cancer therapies. Our review focuses on these roles of CXCL12 and summarizes strategies for treating cancer by disrupting this interaction with special emphasis on the CXCR4/CXCL12 axis.
[Mh] Termos MeSH primário: Comunicação Celular/fisiologia
Quimiocina CXCL12/metabolismo
Neoplasias/patologia
Neovascularização Patológica/patologia
Receptores CXCR4/metabolismo
Microambiente Tumoral/fisiologia
[Mh] Termos MeSH secundário: Antineoplásicos/uso terapêutico
Adesão Celular/fisiologia
Seres Humanos
Metástase Neoplásica/patologia
Neoplasias/tratamento farmacológico
Neoplasias/genética
Microambiente Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE



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