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Pesquisa : D12.644.276.374.200.120.075 [Categoria DeCS]
Referências encontradas : 278 [refinar]
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[PMID]:28759013
[Au] Autor:Krawczyk KM; Nilsson H; Allaoui R; Lindgren D; Arvidsson M; Leandersson K; Johansson ME
[Ad] Endereço:Department of Translational Medicine, Center for Molecular Pathology, Lund University, Malmö, Sweden.
[Ti] Título:Papillary renal cell carcinoma-derived chemerin, IL-8, and CXCL16 promote monocyte recruitment and differentiation into foam-cell macrophages.
[So] Source:Lab Invest;97(11):1296-1305, 2017 Nov.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Papillary renal cell carcinoma (pRCC) is the second most common type of renal cell carcinoma. The only curative treatment available for pRCC is radical surgery. If the disease becomes widespread, neither chemo- nor radiotherapy will have therapeutic effect, hence further research on pRCC is of utmost importance. Histologically, pRCC is characterized by a papillary growth pattern with focal aggregation of macrophages of the foam cell phenotype. In other forms of cancer, a clear role for tumor-associated macrophages during cancer growth and progression has been shown. Although the presence of foamy macrophages is a histological hallmark of pRCC tumors, little is known regarding their role in pRCC biology. In order to study the interaction between pRCC tumor and myeloid cells, we established primary cultures from pRCC tissue. We show that human pRCC cells secrete the chemokines IL-8, CXCL16, and chemerin, and that these factors attract primary human monocytes in vitro. RNAseq data from The Cancer Genome Atlas confirmed a high expression of these factors in pRCC tissue. Conditioned medium from pRCC cultures induced a shift in human monocytes toward the M2 macrophage phenotype. In extended cultures, these macrophages became enlarged and loaded with lipids, adopting the foam cell morphology found in pRCC tissue. These results show for the first time that pRCC primary tumor cells secrete factors that attract and differentiate monocytes into anti-inflammatory tumor-associated macrophages with foam cell histology.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/metabolismo
Quimiocinas CXC/metabolismo
Quimiocinas/metabolismo
Células Espumosas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Interleucina-8/metabolismo
Neoplasias Renais/metabolismo
Monócitos/metabolismo
Receptores Depuradores/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma de Células Renais/imunologia
Carcinoma de Células Renais/patologia
Carcinoma de Células Renais/cirurgia
Transdiferenciação Celular
Células Cultivadas
Quimiocina CXCL16
Quimiocinas/secreção
Quimiocinas CXC/secreção
Quimiotaxia de Leucócito
Técnicas de Cocultura
Meios de Cultivo Condicionados
Células Espumosas/imunologia
Células Espumosas/patologia
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Interleucina-8/secreção
Neoplasias Renais/imunologia
Neoplasias Renais/patologia
Neoplasias Renais/secreção
Masculino
Meia-Idade
Monócitos/imunologia
Monócitos/patologia
Gradação de Tumores
Proteínas de Neoplasias/metabolismo
Proteínas de Neoplasias/secreção
Nefrectomia
Carga Tumoral
Células Tumorais Cultivadas
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines); 0 (Chemokines, CXC); 0 (Culture Media, Conditioned); 0 (IL8 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-8); 0 (Neoplasm Proteins); 0 (Receptors, Scavenger); 0 (chemerin protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2017.78


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[PMID]:28600292
[Au] Autor:Reyat JS; Chimen M; Noy PJ; Szyroka J; Rainger GE; Tomlinson MG
[Ad] Endereço:School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom; and.
[Ti] Título:ADAM10-Interacting Tetraspanins Tspan5 and Tspan17 Regulate VE-Cadherin Expression and Promote T Lymphocyte Transmigration.
[So] Source:J Immunol;199(2):666-676, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recruitment of blood leukocytes across the endothelium to sites of tissue infection is central to inflammation, but also promotes chronic inflammatory diseases. A disintegrin and metalloproteinase 10 (ADAM10) is a ubiquitous transmembrane molecular scissor that is implicated in leukocyte transmigration by proteolytically cleaving its endothelial substrates. These include VE-cadherin, a homotypic adhesion molecule that regulates endothelial barrier function, and transmembrane chemokines CX3CL1 and CXCL16, which have receptors on leukocytes. However, a definitive role for endothelial ADAM10 in transmigration of freshly isolated primary leukocytes under flow has not been demonstrated, and the relative importance of distinct ADAM10 substrates is unknown. Emerging evidence suggests that ADAM10 can be regarded as six different molecular scissors with different substrate specificities, depending on which of six TspanC8 tetraspanins it is associated with, but TspanC8s remain unstudied in leukocyte transmigration. In the current study, ADAM10 knockdown on primary HUVECs was found to impair transmigration of freshly isolated human peripheral blood T lymphocytes, but not neutrophils or B lymphocytes, in an in vitro flow assay. This impairment was due to delayed transmigration rather than a complete block, and was overcome in the presence of neutrophils. Transmigration of purified lymphocytes was dependent on ADAM10 regulation of VE-cadherin, but not CX3CL1 and CXCL16. Tspan5 and Tspan17, the two most closely related TspanC8s by sequence, were the only TspanC8s that regulated VE-cadherin expression and were required for lymphocyte transmigration. Therefore endothelial Tspan5- and Tspan17-ADAM10 complexes may regulate inflammation by maintaining normal VE-cadherin expression and promoting T lymphocyte transmigration.
[Mh] Termos MeSH primário: Proteína ADAM10/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Antígenos CD/genética
Caderinas/genética
Proteínas de Membrana/metabolismo
Linfócitos T/fisiologia
Tetraspaninas/metabolismo
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Proteína ADAM10/deficiência
Proteína ADAM10/genética
Proteína ADAM10/imunologia
Secretases da Proteína Precursora do Amiloide/deficiência
Secretases da Proteína Precursora do Amiloide/genética
Secretases da Proteína Precursora do Amiloide/imunologia
Antígenos CD/metabolismo
Linfócitos B/imunologia
Linfócitos B/fisiologia
Caderinas/metabolismo
Células Cultivadas
Quimiocina CX3CL1/genética
Quimiocina CX3CL1/imunologia
Quimiocina CXCL16
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Células Endoteliais/imunologia
Células Endoteliais/fisiologia
Seres Humanos
Inflamação/imunologia
Proteínas de Membrana/deficiência
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Neutrófilos/imunologia
Neutrófilos/fisiologia
Receptores Depuradores/genética
Receptores Depuradores/imunologia
Linfócitos T/imunologia
Tetraspaninas/genética
Tetraspaninas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CX3CL1 protein, human); 0 (CXCL16 protein, human); 0 (Cadherins); 0 (Chemokine CX3CL1); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Membrane Proteins); 0 (Receptors, Scavenger); 0 (TSPAN17 protein, human); 0 (TSPAN5 protein, human); 0 (Tetraspanins); 0 (cadherin 5); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600713


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[PMID]:28478039
[Au] Autor:Ye Y; Chen Q; Li J; Jin L; Zheng J; Li X; Lin Z; Gong F
[Ad] Endereço:School of Pharmacy, Wenzhou Medical University, Chashan College Park, Wenzhou, Zhejiang, China.
[Ti] Título:CXCL16 deficiency attenuates diabetic nephropathy through decreasing oxidative stress and inflammation.
[So] Source:Biochem Biophys Res Commun;491(3):848-854, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soluble C-X-C chemokine ligand 16 (CXCL16) is related to the inflammatory response in liver injury and involved in the pathogenesis of renal dysfunction in diabetes patients. However, the exact role of elevated CXCL16 in diabetic nephropathy (DN) remains unclear. In this study, we investigated the role of CXCL16 in streptozcin (STZ)-induced diabetic nephropathy (DN) in mice. The results showed that fasting blood glucose (FBG) and 24 h urinary protein, triglyceride, and cholesterol levels increased in diabetic mice, and these changes were partially ameliorated in CXCL16 KO mice. Meanwhile, the results also showed that ROS generation was suppressed and the expression levels of inflammatory factors and infiltration factors were inhibited both in vivo and in vitro using DN models. In addition, the total AKT protein and p-AKT levels were decreased in CXCL16-depleted HK-2 cells that were treated with LPS. These findings suggest that the CXCL16 gene product promotes inflammatory factors and cell infiltration factors, and inhibits the expression of antioxidant factors to accelerate the development of DN, and CXCL16 deficiency attenuates DN may be involved in the AKT signaling pathway.
[Mh] Termos MeSH primário: Glicemia/imunologia
Quimiocina CXCL6/imunologia
Nefropatias Diabéticas/imunologia
Inflamação/imunologia
Estresse Oxidativo/imunologia
Espécies Reativas de Oxigênio/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL16
Nefropatias Diabéticas/induzido quimicamente
Nefropatias Diabéticas/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Chemokine CXCL16); 0 (Chemokine CXCL6); 0 (Cxcl16 protein, mouse); 0 (Reactive Oxygen Species); 5W494URQ81 (Streptozocin)
[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:170508
[St] Status:MEDLINE


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[PMID]:28286356
[Au] Autor:Xu S; Cheng J; Cai MY; Liang LL; Cen JM; Yang XL; Chen C; Liu X; Xiong XD
[Ad] Endereço:Institute of Aging Research, Guangdong Medical University, Dongguan, China; Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, Dongguan, China; Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Zhanjiang, China.
[Ti] Título:The Impact of tagSNPs in CXCL16 Gene on the Risk of Myocardial Infarction in a Chinese Han Population.
[So] Source:Dis Markers;2017:9463272, 2017.
[Is] ISSN:1875-8630
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:has been demonstrated to be involved in the development of atherosclerosis and myocardial infarction (MI). Nonetheless, the role of the polymorphisms on MI pathogenesis is far to be elucidated. We herein genotyped four tagSNPs in gene (rs2304973, rs1050998, rs3744700, and rs8123) in 275 MI patients and 670 control subjects, aimed at probing into the impact of polymorphisms on individual susceptibility to MI. Multivariate logistic regression analysis showed that C allele (OR = 1.31, 95% CI = 1.03-1.66, and = 0.029) and CC genotype (OR = 1.84, 95% CI = 1.11-3.06, and = 0.018) of rs1050998 were associated with increased MI risk; and C allele (OR = 0.77, 95% CI = 0.60-0.98, and = 0.036) of rs8123 exhibited decreased MI risk, while the other two tagSNPs had no significant effect. Consistently, the haplotype rs2304973T-rs1050998C-rs3744700G-rs8123A containing the C allele of rs1050998 and A allele of rs8123 exhibited elevated MI risk (OR = 1.41, 95% CI = 1.02-1.96, and = 0.037). Further stratified analysis unveiled a more apparent association with MI risk among younger subjects (≤60 years old). Taken together, our results provided the first evidence that polymorphisms significantly impacted MI risk in Chinese subjects.
[Mh] Termos MeSH primário: Quimiocinas CXC/genética
Infarto do Miocárdio/genética
Polimorfismo de Nucleotídeo Único
Receptores Depuradores/genética
[Mh] Termos MeSH secundário: Idoso
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
Quimiocina CXCL16
Feminino
Predisposição Genética para Doença
Haplótipos
Seres Humanos
Masculino
Meia-Idade
Análise Multivariada
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Receptors, Scavenger)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1155/2017/9463272


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[PMID]:28246376
[Au] Autor:Wang L; Qi H; Baker PN; Zhen Q; Zeng Q; Shi R; Tong C; Ge Q
[Ad] Endereço:Department of Reproduction Health and Infertility, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China (mainland).
[Ti] Título:Altered Circulating Inflammatory Cytokines Are Associated with Anovulatory Polycystic Ovary Syndrome (PCOS) Women Resistant to Clomiphene Citrate Treatment.
[So] Source:Med Sci Monit;23:1083-1089, 2017 Mar 01.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Polycystic ovary syndrome (PCOS) is a common gynecological disease characterized by chronic oligoanovulation, clinical/biochemical hyperandrogenism, polycystic ovaries, and insulin resistance. Accumulating evidence has shown that PCOS-related ovarian dysfunction is the main cause of anovulatory infertility. Clomiphene citrate (CC) is the first-line therapy for PCOS patients; however, approximately 15-40% PCOS patients are resistant to CC treatment. It has been demonstrated that PCOS is a chronic pro-inflammatory state, as some pro-inflammatory cytokines were elevated in the peripheral circulation of PCOS patients, but whether altered inflammatory cytokines expression in PCOS patients is associated with blunted response to CC remains unknown. MATERIAL AND METHODS We recruited 44 CC-resistant PCOS patients, along with 55 age and body mass index (BMI)-matched CC-sensitive PCOS patients. Ovulation was induced by administrating 50-100 mg/day CC on days 5 to 9 of each menstrual cycle. The cytokine profiles were detected by cytokine antibody microarrays and further validated by ELISAs. RESULTS CC-resistant patients had higher levels of high-sensitivity C-reactive protein (hsCRP) than the CC-sensitive individuals. A growth factor, angiopoietin-2, was significantly reduced [1.64 (0.93-1.95) vs. 1.08 (0.85-1.34), p<0.05], while a chemokine CXCL-16 was significantly increased (9.10±2.35 vs. 10.41±2.82, p<0.05) in CC-resistant patients compared to the CC-sensitive subjects. CXCL-16 was positively correlated with hsCRP (r=0.33, p<0.01). Logistic regression analysis showed that angiopoietin-2 and CXCL-16 are associated with CC resistance. CONCLUSIONS Circulating cytokines are disturbed in CC-resistant PCOS patients. Altered angiopoietin-2 and CXCL-16 levels might compromise the responsiveness of the ovary to CC through up-regulating angiogenesis and inflammation.
[Mh] Termos MeSH primário: Clomifeno/uso terapêutico
Citocinas/sangue
Síndrome do Ovário Policístico/sangue
Síndrome do Ovário Policístico/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Angiopoietina-2/sangue
Proteína C-Reativa/metabolismo
Quimiocina CXCL16
Quimiocinas CXC/sangue
Resistência a Medicamentos
Feminino
Seres Humanos
Ovário/efeitos dos fármacos
Ovário/metabolismo
Receptores Depuradores/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiopoietin-2); 0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Cytokines); 0 (Receptors, Scavenger); 1HRS458QU2 (Clomiphene); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE


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[PMID]:27869573
[Au] Autor:Gruber HE; Marrero E; Ingram JA; Hoelscher GL; Hanley EN
[Ad] Endereço:a Department of Orthopaedic Surgery , Carolinas Medical Center , Charlotte , North Carolina.
[Ti] Título:The chemokine, CXCL16, and its receptor, CXCR6, are constitutively expressed in human annulus fibrosus and expression of CXCL16 is up-regulated by exposure to IL-1ß in vitro.
[So] Source:Biotech Histochem;92(1):7-14, 2017.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chemokines are an important group of soluble molecules with specialized functions in inflammation. The roles of many specialized chemokines and their receptors remain poorly understood in the human intervertebral disc. We investigated CXCL16 and its receptor, CXCR6, to determine their immunolocalization in disc tissue and their presence following exposure of cultured human annulus fibrosus cells to proinflammatory cytokines. CXCL16 is a marker for inflammation; it also can induce hypoxia-inducible factor 1α (HIF-1α), which is a phenotypic marker of heathy nucleus pulposus tissue. We found CXCL16 and CXCR6 immunostaining in many cells of the annulus portion of the disc. Molecular studies showed that annulus fibrosus cells exposed to IL-1ß, but not TNF-α, exhibited significant up-regulation of CXCL16 expression vs. control cells. There was no significant difference in the percentage of annulus cells that exhibited immunolocalization of CXCL16 in grade I/II, grade III or grade IV/V specimens. The presence of CXCL16 and its receptor, CXCR6, in the annulus in vivo suggests the need for future research concerning the role of this chemokine in proinflammatory functions, HIF-1α expression and disc vascularization.
[Mh] Termos MeSH primário: Anel Fibroso/metabolismo
Quimiocinas CXC/metabolismo
Interleucina-1beta/farmacologia
Receptores de Quimiocinas/metabolismo
Receptores Depuradores/metabolismo
Receptores Virais/metabolismo
[Mh] Termos MeSH secundário: Anel Fibroso/citologia
Técnicas de Cultura de Células
Células Cultivadas
Quimiocina CXCL16
Quimiocinas CXC/genética
Seres Humanos
Transporte Proteico
Receptores CXCR6
Receptores de Quimiocinas/genética
Receptores Depuradores/genética
Receptores Virais/genética
Fator de Necrose Tumoral alfa/farmacologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (CXCR6 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Interleukin-1beta); 0 (Receptors, CXCR6); 0 (Receptors, Chemokine); 0 (Receptors, Scavenger); 0 (Receptors, Virus); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE
[do] DOI:10.1080/10520295.2016.1237672


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[PMID]:27877078
[Au] Autor:Hu ZB; Chen Y; Gong YX; Gao M; Zhang Y; Wang GH; Tang RN; Liu H; Liu BC; Ma KL
[Ad] Endereço:Institute of Nephrology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, 210009, China.
[Ti] Título:Activation of the CXCL16/CXCR6 Pathway by Inflammation Contributes to Atherosclerosis in Patients with End-stage Renal Disease.
[So] Source:Int J Med Sci;13(11):858-867, 2016.
[Is] ISSN:1449-1907
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Chronic inflammation plays a critical role in the progression of atherosclerosis (AS). This study aimed to determine the effects of the CXC chemokine ligand 16 (CXCL16)/CXC chemokine receptor 6 (CXCR6) pathway on cholesterol accumulation in the radial arteries of end-stage renal disease (ESRD) patients with concomitant microinflammation and to further investigate the potential effects of the purinergic receptor P2X ligand-gated ion channel 7 (P2X7R). Forty-three ESRD patients were divided into the control group (n=17) and the inflamed group (n=26) based on plasma C-reactive protein (CRP) levels. Biochemical indexes and lipid profiles of the patients were determined. Surgically removed tissues from the radial arteries of patients receiving arteriovenostomy were used for preliminary evaluation of AS. Haematoxylin-eosin (HE) and Filipin staining were performed to assess foam cell formation. CXCL16/CXCR6 pathway-related protein expression, P2X7R protein expression and the expression of monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-α (TNF-α), and CD68 were detected by immunohistochemical and immunofluorescence staining. Inflammation increased both MCP-1 and TNF-α expression and macrophage infiltration in radial arteries. Additionally, foam cell formation significantly increased in the radial arteries of the inflamed group compared to that of the controls. Further analysis showed that protein expression of CXCL16, CXCR6, disintegrin and metalloproteinase-10 (ADAM10) in the radial arteries of the inflamed group was significantly increased. Furthermore, CXCL16 expression was positively correlated with P2X7R expression in the radial arteries of ESRD patients. Inflammation contributed to foam cell formation in the radial arteries of ESRD patients via activation of the CXCL16/CXCR6 pathway, which may be regulated by P2X7R.
[Mh] Termos MeSH primário: Aterosclerose/etiologia
Quimiocinas CXC/metabolismo
Inflamação/complicações
Falência Renal Crônica/complicações
Receptores de Quimiocinas/metabolismo
Receptores Depuradores/metabolismo
Receptores Virais/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM10/metabolismo
Adulto
Idoso
Secretases da Proteína Precursora do Amiloide/metabolismo
Aterosclerose/metabolismo
Quimiocina CCL2/metabolismo
Quimiocina CXCL16
Quimiocinas CXC/genética
Feminino
Seres Humanos
Inflamação/metabolismo
Falência Renal Crônica/metabolismo
Masculino
Proteínas de Membrana/metabolismo
Meia-Idade
Receptores CXCR6
Receptores de Quimiocinas/genética
Receptores Purinérgicos P2X7/metabolismo
Receptores Depuradores/genética
Receptores Virais/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (CXCL16 protein, human); 0 (CXCR6 protein, human); 0 (Chemokine CCL2); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Membrane Proteins); 0 (P2RX7 protein, human); 0 (Receptors, CXCR6); 0 (Receptors, Chemokine); 0 (Receptors, Purinergic P2X7); 0 (Receptors, Scavenger); 0 (Receptors, Virus); 0 (Tumor Necrosis Factor-alpha); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE


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[PMID]:27784296
[Au] Autor:Hattermann K; Bartsch K; Gebhardt HH; Mehdorn HM; Synowitz M; Schmitt AD; Mentlein R; Held-Feindt J
[Ad] Endereço:Department of Anatomy, University of Kiel, Otto-Hahn-Place 8, 24118, Kiel, Germany.
[Ti] Título:"Inverse signaling" of the transmembrane chemokine CXCL16 contributes to proliferative and anti-apoptotic effects in cultured human meningioma cells.
[So] Source:Cell Commun Signal;14(1):26, 2016 10 27.
[Is] ISSN:1478-811X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chemokines and their receptors play a decisive role in tumor progression and metastasis. We recently found a new signaling mechanism in malignant glioma cells mediated by transmembrane chemokines that we termed "inverse signaling". According to this hypothesis, soluble (s)-CXCL16 binds to the surface-expressed transmembrane (tm) -CXCL16, and induces signaling and different biological effects in the stimulated cells, so that the transmembrane ligand itself acts as a receptor for its soluble counterpart. Now, we hypothesized that "inverse signaling" via tm-CXCL16 might also take place in meningiomas, a completely different, benign tumor entity. METHODS: We used quantitative reverse-transcription polymerase chain reaction, immunocytochemistry and western blot to detect CXCL16 and CXCR6 in human meningioma cells isolated from 28 human meningiomas. Subsequently, we stimulated cultured human tm-CXCL16-positive, CXCR6-negative meningioma cells with recombinant s-CXCL16 and analyzed binding, signaling and biological effects using RNAi silencing to verify specificity. RESULTS: In fact, cultured human meningioma cells considerably express CXCL16, but substantially lack CXCR6, the only known CXCL16 receptor. These receptor-negative cells could bind s-CXCL16, and responded to s-CXCL16 application with activation of the intracellular kinases ERK1/2 und Akt. As a consequence, we observed increased proliferation and rescue of apoptosis of cultured meningioma cells. Since binding and signaling were abolished by siRNA silencing, we concluded that tm-CXCL16 specifically acts as a receptor for s-CXCL16 also in human meningioma cells. CONCLUSION: These findings underline our recent report on the mechanism of inverse signaling as a broad biological process also observable in more benign tumor cells and contributing to tumor progression.
[Mh] Termos MeSH primário: Apoptose
Proliferação Celular
Quimiocinas CXC/metabolismo
Neoplasias Meníngeas/metabolismo
Meningioma/metabolismo
Receptores Depuradores/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Células Cultivadas
Quimiocina CXCL16
Quimiocinas CXC/genética
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Ligação Proteica
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores Depuradores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Receptors, Scavenger); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE


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[PMID]:27720639
[Au] Autor:Yoon MS; Pham CT; Phan MT; Shin DJ; Jang YY; Park MH; Kim SK; Kim S; Cho D
[Ad] Endereço:Department of Radiation Oncology, Chonnam National University Hwasun Hospital, Chonnam National University Medical School, Gwangju, South Korea. Electronic address: meesunyoon@jnu.ac.kr.
[Ti] Título:Irradiation of breast cancer cells enhances CXCL16 ligand expression and induces the migration of natural killer cells expressing the CXCR6 receptor.
[So] Source:Cytotherapy;18(12):1532-1542, 2016 Dec.
[Is] ISSN:1477-2566
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AIMS: Few studies have examined the migration pattern of natural killer (NK) cells, especially after radiation treatment for cancer. We investigated whether irradiation can modulate the expression of chemokines in cancer cells and the migration of NK cells to irradiated tumor cells. METHODS: The expression of chemokine receptors (CXCR3, CXCR4 and CXCR6) on interleukin-2 (IL-2)/IL-15-activated NK cells was assessed using flow cytometry. Related chemokine ligands (CXCL11, CXCL12 and CXCL16) in human breast cancer cell lines (MCF7, SKBR3 and MDA-MB231) irradiated at various doses were assessed using reverse transcription-polymerase chain reaction (RT-PCR), fluorescence-activated cell sorting (FACS) and enzyme-linked immunosorbent assay (ELISA). The cell-free culture supernatant was collected 96 h after irradiation of breast cancer cell lines for migration and blocking assays. RESULTS: The activated NK cells expressed CXCR6. Expression of the CXCR6 ligand CXCL16 increased in a time- and dose-dependent manner in all analyzed cancer cell lines. CXCL16 expression was statistically significantly enhanced in all breast cancer cell lines on day 3 after 20 Gy irradiation. Activated NK cells migration correlated with CXCL16 concentration (R = 0.91; P <0.0001). Significantly enhanced migration of NK cells to irradiated cancer cells was observed for a dose of 20 Gy in MCF7 (P = 0.043) and SKBR3 (P = 0.043) cells, but not in MDA-MB231 (P = 0.225) cells. A blocking assay using a CXCR6 antibody showed a significant decrease in the migration of activated NK cells in all cancer cell lines. CONCLUSIONS: Our data indicate that irradiation induces CXCL16 chemokine expression in cancer cells and enhances the migration of activated NK cells expressing CXCR6 to irradiated breast cancer cells. These results suggest that radiation would improve the anti-tumor effect of NK cells through enhanced migration of NK cells to tumor site for the treatment of patients with breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/radioterapia
Movimento Celular/efeitos da radiação
Quimiocinas CXC/biossíntese
Células Matadoras Naturais/imunologia
Receptores de Quimiocinas/biossíntese
Receptores Depuradores/biossíntese
Receptores Virais/biossíntese
[Mh] Termos MeSH secundário: Anticorpos Bloqueadores/farmacologia
Linhagem Celular Tumoral
Quimiocina CXCL12/biossíntese
Quimiocina CXCL16
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Seres Humanos
Interleucina-15/metabolismo
Interleucina-2/metabolismo
Células Matadoras Naturais/metabolismo
Células MCF-7
Receptores CXCR3/biossíntese
Receptores CXCR4/biossíntese
Receptores CXCR6
Receptores de Quimiocinas/imunologia
Receptores Virais/imunologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (CXCL12 protein, human); 0 (CXCL16 protein, human); 0 (CXCR3 protein, human); 0 (CXCR4 protein, human); 0 (CXCR6 protein, human); 0 (Chemokine CXCL12); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Receptors, CXCR3); 0 (Receptors, CXCR4); 0 (Receptors, CXCR6); 0 (Receptors, Chemokine); 0 (Receptors, Scavenger); 0 (Receptors, Virus)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


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[PMID]:27665581
[Au] Autor:Elewa U; Sanchez-Niño MD; Mahillo-Fernández I; Martin-Cleary C; Belen Sanz A; Perez-Gomez MV; Fernandez-Fernandez B; Ortiz A
[Ad] Endereço:IIS-Fundación Jiménez Díaz, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain.
[Ti] Título:Circulating CXCL16 in Diabetic Kidney Disease.
[So] Source:Kidney Blood Press Res;41(5):663-671, 2016.
[Is] ISSN:1423-0143
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Chronic kidney disease and, specifically, diabetic kidney disease, is among the fastest increasing causes of death worldwide. A better understanding of the factors contributing to the high mortality may help design novel monitoring and therapeutic approaches. CXCL16 is both a cholesterol receptor and a chemokine with a potential role in vascular injury and inflammation. We aimed at identifying predictors of circulating CXCL16 levels in diabetic patients with chronic kidney disease. METHODS: We have now studied plasma CXCL16 in 134 European patients with diabetic kidney disease with estimated glomerular filtration rate (eGFR) categories G1-G4 and albuminuria categories A1-A3, in order to identify factors influencing plasma CXCL16 in this population. RESULTS: Plasma CXCL16 levels were 4.0±0.9 ng/ml. Plasma CXCL16 increased with increasing eGFR category from G1 to G4 (that is, with decreasing eGFR values) and with increasing albuminuria category. Plasma CXCL16 was higher in patients with prior cardiovascular disease (4.33±1.03 vs 3.88±0.86 ng/ml; p=0.013). In multivariate analysis, eGFR and serum albumin had an independent and significant negative correlation with plasma CXCL16. CONCLUSION: In diabetic kidney disease patients, GFR and serum albumin independently predicted plasma CXCL16 levels.
[Mh] Termos MeSH primário: Quimiocinas CXC/sangue
Nefropatias Diabéticas/sangue
Receptores Depuradores/sangue
[Mh] Termos MeSH secundário: Idoso
Albuminúria
Doenças Cardiovasculares
Quimiocina CXCL16
Grupo com Ancestrais do Continente Europeu
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Masculino
Valor Preditivo dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Receptors, Scavenger)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160926
[St] Status:MEDLINE



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