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Pesquisa : D12.644.276.374.200.110.250 [Categoria DeCS]
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[PMID]:29480835
[Au] Autor:Li L; Tong M; Zhao YT; He Y; Zhou HY; Zhang GF; Zhang YJ
[Ad] Endereço:Department of Orthopedics, Traditional Chinese Medical Hospital of Xinjiang Uygur Autonomous Region, Urumqi.
[Ti] Título:Membrane translocation of Bruton kinase in multiple myeloma cells is associated with osteoclastogenic phenotype in bone metastatic lesions.
[So] Source:Medicine (Baltimore);97(2):e9482, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using bone biopsy samples, we examined whether osteolytic cytokine profile is changed in situ in bone samples of metastatic multiple myeloma, and whether this creates an environment of lysis within the bone to which it has spread. This also produces the clinical features of increased circulating plasma calcium, and deleterious effects on the kidney.Using multiple myeloma biopsy and cell extracts from bone metastatic lesions, Bruton kinase, a tyrosine kinase, was demonstrated to be translocated to the membrane. Several transcription factors were upregulated included activin A, inflammatory transcription activator like such as nuclear factor kappa B, and specific bone lytic factor such as receptor activator of nuclear factor kappa-B ligand that is known to drive osteoclastogenesis as opposed to a osteogenic environment. The transcript for Bruton kinase was also elevated in its expression.Cytokines that support osteolytic activity such as a proliferation-inducing ligand, RANTES (regulated on activation, normal T cell expressed and secreted), interleukin-8, and activin A were upregulated. Tartrate resistant acid phosphatase (TRAP)-positive osteoclastic enzymatic activity was significantly elevated in the bone microenvironment in metastatic multiple myeloma. Several tyrosine kinase inhibitors, including inhibitors for Bruton kinase such as ibrutinib have been developed. The results of the present study provide evidence that multiple myeloma possess signal transduction mechanisms to support a bone lytic environment.The results provide a preliminary molecular basis to design specific inhibitors for management of bone metastasis of multiple myeloma.
[Mh] Termos MeSH primário: Neoplasias Ósseas/enzimologia
Neoplasias Ósseas/secundário
Membrana Celular/enzimologia
Mieloma Múltiplo/enzimologia
Osteogênese/fisiologia
Proteínas Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Idoso
Quimiocina CCL5/metabolismo
Seres Humanos
Masculino
Meia-Idade
NF-kappa B/metabolismo
RNA Mensageiro/metabolismo
Fosfatase Ácida Resistente a Tartarato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (activin A); 104625-48-1 (Activins); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009482


  2 / 4168 MEDLINE  
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[PMID]:29216863
[Au] Autor:Gao D; Cazares LH; Fish EN
[Ad] Endereço:Toronto General Hospital Research Institute, University Health Network, Toronto, Canada.
[Ti] Título:CCL5-CCR5 interactions modulate metabolic events during tumor onset to promote tumorigenesis.
[So] Source:BMC Cancer;17(1):834, 2017 12 08.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In earlier studies we have shown that CCL5 activation of CCR5 induces the proliferation and survival of breast cancer cells in a mechanistic target of rapamycin (mTOR)-dependent manner and that this is in part due to CCR5-mediated increases in glycolytic metabolism. METHODS: Using the MDA-MB-231 triple negative human breast cancer cell line and mouse mammary tumor virus - polyomavirus middle T-antigen (MMTV-PyMT) mouse primary breast cancer cells, we conducted in vivo tumor transplant experiments to examine the effects of CCL5-CCR5 interactions in the context of regulating tumor metabolism. Additionally, we employed Matrix-Assisted Laser Desorption/Ionization Fourier Transform Ion Cyclotron Resonance Mass Spectrometry imaging (MALDI-FTICR-MSI) to evaluate tumor utilization of cellular metabolites. RESULTS: We provide evidence that, in the absence of CCR5, the early events associated with rapid tumor growth in the MMTV-PyMT mouse model of spontaneous breast cancer development, are diminished, as demonstrated by a delay in tumor onset. In tumor transplant studies into immunocompromised mice we identify a direct correlation between reduced tumor proliferation and decreased metabolic activity, specifically associated with tumor expression of CCR5. The reduction in tumorigenesis is accompanied by decreases in glucose uptake, glucose transporter-1 (GLUT-1) cell surface expression, intracellular ATP and lactate levels, as well as reduced CCL5 production. Using MALDI-FTICR-MS, we show that the rapid early tumor growth of CCR5 triple negative breast cancer cells in vivo is attributable to increased levels of glycolytic intermediates required for anabolic processes, in contrast to the slower growth rate of their corresponding CCR5 cells, that exhibit reduced glycolytic metabolism. CONCLUSIONS: These findings suggest that CCL5-CCR5 interactions in the tumor microenvironment modulate metabolic events during tumor onset to promote tumorigenesis.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Carcinogênese/metabolismo
Quimiocina CCL5/metabolismo
Receptores CCR5/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Feminino
Glicólise
Seres Humanos
Camundongos
Camundongos Endogâmicos NOD
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL5); 0 (Receptors, CCR5)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3817-0


  3 / 4168 MEDLINE  
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Baracat, Emílio Carlos Elias
Tresoldi, Antonia Teresinha
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[PMID]:29253610
[Au] Autor:Alvarez AE; Marson FAL; Bertuzzo CS; Bastos JCS; Baracat ECE; Brandão MB; Tresoldi AT; das Neves Romaneli MT; Almeida CCB; de Oliveira T; Schlodtmann PG; Corrêa E; de Miranda MLF; Dos Reis MC; De Pieri JV; Arns CW; Ribeiro JD
[Ad] Endereço:Department of Pediatrics, Faculty of Medical Sciences, University of Campinas, Rua Tessália Vieira de Camargo, 126, Cidade Universitária Zeferino Vaz, Campinas CEP 13083-887, São Paulo, Brazil. Electronic address: alfonso@cepap.med.br.
[Ti] Título:Association between single nucleotide polymorphisms in TLR4, TLR2, TLR9, VDR, NOS2 and CCL5 genes with acute viral bronchiolitis.
[So] Source:Gene;645:7-17, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute viral bronchiolitis is the leading cause of hospitalization among infants during the first year of life. Most infants hospitalized for bronchiolitis do not present risk factors and are otherwise healthy. Our objective was to determine the genetic features associated with the risk and a severe course of bronchiolitis. METHODS: We prospectively evaluated 181 infants with severe bronchiolitis admitted at three hospitals over a 2-year period, who required oxygen therapy. The control group consisted of 536 healthy adults. Patients were evaluated for the presence of comorbidities (premature birth, chronic respiratory disease, and congenital heart disease), underwent nasopharyngeal aspirate testing for virus detection by multiplex-PCR, and SNPs identification in immune response genes. Patient outcomes were assessed. RESULTS: We observed association between SNP rs2107538*CCL5 and bronchiolitis caused by respiratory syncytial virus(RSV) and RSV-subtype-A, and between rs1060826*NOS2 and bronchiolitis caused by rhinovirus. SNPs rs4986790*TLR4, rs1898830*TLR2, and rs2228570*VDR were associated with progression to death. SNP rs7656411*TLR2 was associated with length of oxygen use; SNPs rs352162*TLR9, rs187084*TLR9, and rs2280788*CCL5 were associated with requirement for intensive care unit admission; while SNPs rs1927911*TLR4, rs352162*TLR9, and rs2107538*CCL5 were associated with the need for mechanical ventilation. CONCLUSIONS: Our findings provide some evidence that SNPs in CCL5 and NOS2 are associated with presence of bronchiolitis and SNPs in TLR4, TLR2, TLR9, VDR and CCL5 are associated with severity of bronchiolitis.
[Mh] Termos MeSH primário: Bronquiolite Viral/genética
Quimiocina CCL5/genética
Óxido Nítrico Sintase Tipo II/genética
Polimorfismo de Nucleotídeo Único
Receptores de Calcitriol/genética
Receptores Toll-Like/genética
[Mh] Termos MeSH secundário: Bronquiolite Viral/virologia
Progressão da Doença
Feminino
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Lactente
Recém-Nascido
Masculino
Nasofaringe/virologia
Estudos Retrospectivos
Receptor 2 Toll-Like/genética
Receptor 4 Toll-Like/genética
Receptor Toll-Like 9/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Receptors, Calcitriol); 0 (TLR2 protein, human); 0 (TLR4 protein, human); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Toll-Like Receptor 9); 0 (Toll-Like Receptors); 0 (VDR protein, human); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


  4 / 4168 MEDLINE  
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[PMID]:29253007
[Au] Autor:Mitra S; Schiller D; Anderson C; Gamboni F; D'Alessandro A; Kelher M; Silliman CC; Banerjee A; Jones KL
[Ad] Endereço:Department of Surgery/Trauma Research Center, University of Colorado Denver, School of Medicine, Aurora, Colorado, United States of America.
[Ti] Título:Hypertonic saline attenuates the cytokine-induced pro-inflammatory signature in primary human lung epithelia.
[So] Source:PLoS One;12(12):e0189536, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trauma/hemorrhagic shock is a complex physiological phenomenon that leads to dysregulation of many molecular pathways. For over a decade, hypertonic saline (HTS) has been used as an alternative resuscitation fluid in the setting of trauma/hemorrhagic shock. In addition to restoring circulating volume within the vascular space, studies have shown a positive immunomodulatory effect of HTS. Targeted studies have shown that HTS affects the transcription of several pro-inflammatory cytokines by inhibiting the NF-κB-IκB pathway in model cell lines and rats. However, few studies have been undertaken to assess the unbiased effects of HTS on the whole transcriptome. This study was designed to interrogate the global transcriptional responses induced by HTS and provides insight into the underlying molecular mechanisms and pathways affected by HTS. In this study, RNA sequencing was employed to explore early changes in transcriptional response, identify key mediators, signaling pathways, and transcriptional modules that are affected by HTS in the presence of a strong inflammatory stimulus. Our results suggest that primary human small airway lung epithelial cells (SAECS) exposed to HTS in the presence and absence of a strong pro-inflammatory stimulus exhibit very distinct effects on cellular response, where HTS is highly effective in attenuating cytokine-induced pro-inflammatory responses via mechanisms that involve transcriptional regulation of inflammation which is cell type and stimulus specific. HTS is a highly effective anti-inflammatory agent that inhibits the chemotaxis of leucocytes towards a pro-inflammatory gradient and may attenuate the progression of both the innate and adaptive immune response.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Células Epiteliais/metabolismo
Pulmão/patologia
Solução Salina Hipertônica/química
Choque Hemorrágico/imunologia
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Núcleo Celular/metabolismo
Quimiocina CCL5/metabolismo
Quimiotaxia
Progressão da Doença
Seres Humanos
Inflamação
Fator Regulador 1 de Interferon/metabolismo
Leucócitos/metabolismo
Pulmão/metabolismo
Microcirculação
NF-kappa B/metabolismo
Neutrófilos/metabolismo
Ratos
Fator de Transcrição STAT1/metabolismo
Choque Hemorrágico/tratamento farmacológico
Transdução de Sinais
Baço/metabolismo
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Cytokines); 0 (IRF1 protein, human); 0 (Interferon Regulatory Factor-1); 0 (NF-kappa B); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (Saline Solution, Hypertonic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189536


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[PMID]:29277763
[Au] Autor:Kambayashi Y; Fujimura T; Furudate S; Lyu C; Hidaka T; Kakizaki A; Sato Y; Tanita K; Aiba S
[Ad] Endereço:Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:The Expression of Matrix Metalloproteinases in Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL)-expressing Cancer of Apocrine Origin.
[So] Source:Anticancer Res;38(1):113-120, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Primary cutaneous apocrine carcinoma (PCAC) is a rare and highly aggressive tumor entity. Since there is no conventional therapy for advanced PCAC, exploratory treatments are sometimes used. As we previously reported, receptor activator of nuclear factor kappa-B (RANK) ligand (RANKL)/RANK signaling on M2 macrophages promotes the production of chemokines and proinflammatory cytokines to maintain the immunosuppressive tumor environment of extramammary Paget's disease (EMPD). Since EMPD is a skin adenocarcinoma of apocrine gland origin that expresses high levels of RANKL and matrix metalloproteinase (MMP) 7, and EMPD is associated with the presence of RANK M2 macrophages, we hypothesized that tumor-associated macrophages (TAMs) in adenocarcinomas such as PCAC might also express RANKL and MMP7. MATERIALS AND METHODS: We employed immunohistochemical staining of RANKL and MMP7 in the lesional skin from five patients with PCAC, and microarray analysis of MMPs using human monocyte-derived macrophages. RESULTS: According to DNA microarray analysis, the expression of MMP1 and MMP25 was augmented. The DNA microarray results were verified by using real-time polymerase chain reaction (RT-PCR). Immunohistochemical staining of MMP1 and MMP25 as well as chemokine (C-C motif) ligand (CCL) 5 in the lesional skin from five patients with PCAC showed a substantial number of MMP1-bearing cells and MMP25-bearing cells, as well as CCL5-producing cells, that were distributed in the lesional skin. CONCLUSION: Our study suggests that the RANKL/RANK pathway contributes to the development and maintenance of the immunosuppressive tumor microenvironment and denosumab may be a promising adjuvant therapy targeting TAMs in cancer of apocrine origin.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Macrófagos/metabolismo
Metaloproteinases da Matriz/metabolismo
Ligante RANK/metabolismo
Neoplasias Cutâneas/metabolismo
[Mh] Termos MeSH secundário: Glândulas Apócrinas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Seres Humanos
Metaloproteinases da Matriz/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (RANK Ligand); 0 (TNFSF11 protein, human); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28982723
[Au] Autor:Fernandez-García CE; Tarin C; Roldan-Montero R; Martinez-Lopez D; Torres-Fonseca M; Lindhot JS; Vega de Ceniga M; Egido J; Lopez-Andres N; Blanco-Colio LM; Martín-Ventura JL
[Ad] Endereço:Vascular Research Lab, FIIS-Fundación Jiménez Díaz-Autonoma University, Madrid, Spain.
[Ti] Título:Increased galectin-3 levels are associated with abdominal aortic aneurysm progression and inhibition of galectin-3 decreases elastase-induced AAA development.
[So] Source:Clin Sci (Lond);131(22):2707-2719, 2017 Nov 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) evolution is unpredictable and no specific treatment exists for AAA, except surgery to prevent aortic rupture. Galectin-3 has been previously associated with CVD, but its potential role in AAA has not been addressed. Galectin-3 levels were increased in the plasma of AAA patients ( =225) compared with the control group ( =100). In addition, galectin-3 concentrations were associated with the need for surgical repair, independently of potential confounding factors. Galectin-3 mRNA and protein expression were increased in human AAA samples compared with healthy aortas. Experimental AAA in mice was induced via aortic elastase perfusion. Mice were treated intravenously with the galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every other day) or saline. Similar to humans, galectin-3 serum and aortic mRNA levels were also increased in elastase-induced AAA mice compared with control mice. Mice treated with MCP showed decreased aortic dilation, as well as elastin degradation, vascular smooth muscle cell (VSMC) loss, and macrophage content at day 14 postelastase perfusion compared with control mice. The underlying mechanism(s) of the protective effect of MCP was associated with a decrease in galectin-3 and cytokine (mainly CCL5) mRNA and protein expression. Interestingly, galectin-3 induced CCL5 expression by a mechanism involving STAT3 activation in VSMC. Accordingly, MCP treatment decreased STAT3 phosphorylation in elastase-induced AAA. In conclusion, increased galectin-3 levels are associated with AAA progression, while galectin-3 inhibition decreased experimental AAA development. Our data suggest the potential role of galectin-3 as a therapeutic target in AAA.
[Mh] Termos MeSH primário: Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/prevenção & controle
Galectina 3/antagonistas & inibidores
Galectina 3/sangue
Elastase Pancreática
Pectinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/enzimologia
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/sangue
Aneurisma da Aorta Abdominal/enzimologia
Aneurisma da Aorta Abdominal/patologia
Estudos de Casos e Controles
Células Cultivadas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Dilatação Patológica
Modelos Animais de Doenças
Progressão da Doença
Galectina 3/genética
Galectina 3/metabolismo
Seres Humanos
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Fosforilação
RNA Mensageiro/sangue
RNA Mensageiro/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 0 (Galectin 3); 0 (Lgals3 protein, mouse); 0 (Pectins); 0 (RNA, Messenger); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (citrus pectin); 0 (galectin-3, human); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171142


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[PMID]:28968684
[Au] Autor:McCoy SS; Reed TJ; Berthier CC; Tsou PS; Liu J; Gudjonsson JE; Khanna D; Kahlenberg JM
[Ad] Endereço:Department of Internal Medicine, Division of Rheumatology, University of Wisconsin, Madison, WI.
[Ti] Título:Scleroderma keratinocytes promote fibroblast activation independent of transforming growth factor beta.
[So] Source:Rheumatology (Oxford);56(11):1970-1981, 2017 Nov 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: SSc is a devastating disease that results in fibrosis of the skin and other organs. Fibroblasts are a key driver of the fibrotic process through deposition of extracellular matrix. The mechanisms by which fibroblasts are induced to become pro-fibrotic remain unclear. Thus, we examined the ability of SSc keratinocytes to promote fibroblast activation and the source of this effect. Methods: Keratinocytes were isolated from skin biopsies of 9 lcSSc, 10 dcSSc and 13 control patients. Conditioned media was saved from the cultures. Normal fresh primary fibroblasts were exposed to healthy control and SSc keratinocyte conditioned media in the presence or absence of neutralizing antibodies for TGF-ß. Gene expression was assessed by microarrays and real-time PCR. Immunocytochemistry was performed for α-smooth muscle actin (α-SMA), collagen type 1 (COL1A1) and CCL5 expression. Results: SSc keratinocyte conditioned media promoted fibroblast activation, characterized by increased α-SMA and COL1A1 mRNA and protein expression. This effect was independent of TGF-ß. Microarray analysis identified upregulation of nuclear factor κB (NF-κB) and downregulation of peroxisome proliferator-activated receptor γ (PPAR-γ) pathways in both SSc subtypes. Scleroderma keratinocytes exhibited increased expression of NF-κB-regulated cytokines and chemokines and lesional skin staining confirmed upregulation of CCL5 in basal keratinocytes. Conclusion: Scleroderma keratinocytes promote the activation of fibroblasts in a TGF-ß-independent manner and demonstrate an imbalance in NF-κB1 and PPAR-γ expression leading to increased cytokine and CCL5 production. Further study of keratinocyte mediators of fibrosis, including CCL5, may provide novel targets for skin fibrosis therapy.
[Mh] Termos MeSH primário: Diferenciação Celular
Fibroblastos/citologia
Queratinócitos/citologia
Escleroderma Sistêmico/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Idoso
Células Cultivadas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Meios de Cultivo Condicionados
Regulação para Baixo
Feminino
Fibroblastos/metabolismo
Fibrose
Perfilação da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Queratinócitos/metabolismo
Masculino
Meia-Idade
NF-kappa B/metabolismo
PPAR gama/metabolismo
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Esclerodermia Difusa
Esclerodermia Localizada
Escleroderma Sistêmico/genética
Escleroderma Sistêmico/patologia
Pele/patologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Collagen Type I); 0 (Culture Media, Conditioned); 0 (NF-kappa B); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kex280


  8 / 4168 MEDLINE  
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[PMID]:28954264
[Au] Autor:Pan Q; Feng Y; Peng Y; Zhou H; Deng Z; Li L; Han H; Lin J; Shi L; Wang S; An N; Yang C; Liu HF
[Ti] Título:Basophil Recruitment to Skin Lesions of Patients with Systemic Lupus Erythematosus Mediated by CCR1 and CCR2.
[So] Source:Cell Physiol Biochem;43(2):832-839, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Basophils have been reported to infiltrate skin lesions in various skin diseases, but not in systemic lupus erythematosus (SLE). This study investigated basophil infiltration in SLE and its mechanism. METHODS: Twenty newly diagnosed SLE patients and twenty healthy controls were enrolled. Nine SLE patients underwent skin biopsies. Flow cytometric analysis the phenotype of peripheral basophils and their migration rate toward RANTES and MCP-1 were analyzed with the transwell culture system, also the expression of these two chemokines in skin tissue were analyzed with immunohistochemistry. RESULTS: Increased activation and decreased numbers of peripheral basophils were observed in SLE patients compared with controls. Basophil migration into skin lesions of SLE patients were observed, but not in normal skin tissue. This migration was related to the upregulation of chemokine receptors CCR1 and CCR2 on basophils. In vitro studies showed that migration rate toward RANTES and MCP-1 increased significantly in basophils from SLE patients compared with those from controls. Consistently, high levels of RANTES and MCP-1 expression were observed in skin lesions from SLE patients but not in normal skin tissue. CONCLUSION: Basophil recruitment to skin lesions of SLE patients mediated by CCR1 and CCR2, which may contribute to tissue damage in SLE.
[Mh] Termos MeSH primário: Basófilos/patologia
Lúpus Eritematoso Sistêmico/patologia
Receptores CCR1/imunologia
Receptores CCR2/imunologia
Pele/patologia
[Mh] Termos MeSH secundário: Adulto
Basófilos/imunologia
Movimento Celular
Quimiocina CCL2/análise
Quimiocina CCL2/imunologia
Quimiocina CCL5/análise
Quimiocina CCL5/imunologia
Feminino
Seres Humanos
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Receptores CCR1/análise
Receptores CCR2/análise
Pele/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (CCR1 protein, human); 0 (CCR2 protein, human); 0 (Chemokine CCL2); 0 (Chemokine CCL5); 0 (Receptors, CCR1); 0 (Receptors, CCR2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1159/000481609


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[PMID]:28882870
[Au] Autor:Zhang H; Shi J; Hachet MA; Xue C; Bauer RC; Jiang H; Li W; Tohyama J; Millar J; Billheimer J; Phillips MC; Razani B; Rader DJ; Reilly MP
[Ad] Endereço:From the Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York (H.Z., J.S., M.A.H., C.X., R.C.B., M.P.R.); Irving Institute for Clinical and Translational Research, Columbia University, New York (H.J., M.P.R.); Cardiovascular Institute, Perelman School of Medic
[Ti] Título:CRISPR/Cas9-Mediated Gene Editing in Human iPSC-Derived Macrophage Reveals Lysosomal Acid Lipase Function in Human Macrophages-Brief Report.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2156-2160, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To gain mechanistic insights into the role of (lipase A), the gene encoding LAL (lysosomal acid lipase) protein, in human macrophages. APPROACH AND RESULTS: We used CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 (CRISPR-associated protein 9) technology to knock out in human induced pluripotent stem cells and then differentiate to macrophage (human-induced pluripotent stem cells-derived macrophage [IPSDM]) to explore the human macrophage loss-of-function phenotypes. was abundantly expressed in monocyte-derived macrophages and was markedly induced on IPSDM differentiation to comparable levels as in human monocyte-derived macrophage. IPSDM with knockout of ( ) had barely detectable LAL enzymatic activity. Control and IPSDM were loaded with [ H]-cholesteryl oleate-labeled AcLDL (acetylated low-density lipoprotein) followed by efflux to apolipoprotein A-I. Efflux of liberated [ H]-cholesterol to apolipoprotein A-I was abolished in IPSDM, indicating deficiency in LAL-mediated lysosomal cholesteryl ester hydrolysis. In cells loaded with [ H]-cholesterol-labeled AcLDL, [ H]-cholesterol efflux was, however, not different between control and IPSDM. (ATP-binding cassette, subfamily A, member 1) expression was upregulated by AcLDL loading but to a similar extent between control and IPSDM. In nonlipid loaded state, IPSDM had high levels of cholesteryl ester mass compared with minute amounts in control IPSDM. Yet, with AcLDL loading, overall cholesteryl ester mass was increased to similar levels in both control and IPSDM. did not impact lysosomal apolipoprotein-B degradation or expression of , , and CONCLUSIONS: IPSDM reveals macrophage-specific hallmarks of deficiency. CRISPR/Cas9 and IPSDM provide important tools to study human macrophage biology and more broadly for future studies of disease-associated genetic variation in human macrophages.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas
Edição de Genes/métodos
Células-Tronco Pluripotentes Induzidas/enzimologia
Lisossomos/enzimologia
Macrófagos/enzimologia
Esterol Esterase/metabolismo
[Mh] Termos MeSH secundário: Transportador 1 de Cassete de Ligação de ATP/genética
Transportador 1 de Cassete de Ligação de ATP/metabolismo
Apolipoproteína A-I/metabolismo
Apolipoproteína B-100/metabolismo
Diferenciação Celular
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Ésteres do Colesterol/metabolismo
Regulação Enzimológica da Expressão Gênica
Técnicas de Silenciamento de Genes
Genótipo
Células HEK293
Células Hep G2
Seres Humanos
Hidrólise
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Lipoproteínas LDL/metabolismo
Fenótipo
Proteólise
Esterol Esterase/genética
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA1 protein, human); 0 (APOA1 protein, human); 0 (APOB protein, human); 0 (ATP Binding Cassette Transporter 1); 0 (Apolipoprotein A-I); 0 (Apolipoprotein B-100); 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Cholesterol Esters); 0 (IL1B protein, human); 0 (IL6 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Lipoproteins, LDL); 0 (acetyl-LDL); 3DPK9KFN2M (cholesteryl oleate); EC 3.1.1.13 (LIPA protein, human); EC 3.1.1.13 (Sterol Esterase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.310023


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[PMID]:28877226
[Au] Autor:Levitz R; Gao Y; Dozmorov I; Song R; Wakeland EK; Kahn JS
[Ad] Endereço:Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
[Ti] Título:Distinct patterns of innate immune activation by clinical isolates of respiratory syncytial virus.
[So] Source:PLoS One;12(9):e0184318, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus (RSV) is a major respiratory pathogen of infants and young children. Multiple strains of both subgroup A and B viruses circulate during each seasonal epidemic. Genetic heterogeneity among RSV genomes, in large part due to the error prone RNA-dependent, RNA polymerase, could mediate variations in pathogenicity. We evaluated clinical strains of RSV for their ability to induce the innate immune response. Subgroup B viruses were used to infect human pulmonary epithelial cells (A549) and primary monocyte-derived human macrophages (MDM) from a variety of donors. Secretions of IL-6 and CCL5 (RANTES) from infected cells were measured following infection. Host and viral transcriptome expression were assessed using RNA-SEQ technology and the genomic sequences of several clinical isolates were determined. There were dramatic differences in the induction of IL-6 and CCL5 in both A549 cells and MDM infected with a variety of clinical isolates of RSV. Transcriptome analyses revealed that the pattern of innate immune activation in MDM was virus-specific and host-specific. Specifically, viruses that induced high levels of secreted IL-6 and CCL5 tended to induce cellular innate immune pathways whereas viruses that induced relatively low level of IL-6 or CCL5 did not induce or suppressed innate immune gene expression. Activation of the host innate immune response mapped to variations in the RSV G gene and the M2-1 gene. Viral transcriptome data indicated that there was a gradient of transcription across the RSV genome though in some strains, RSV G was the expressed in the highest amounts at late times post-infection. Clinical strains of RSV differ in cytokine/chemokine induction and in induction and suppression of host genes expression suggesting that these viruses may have inherent differences in virulence potential. Identification of the genetic elements responsible for these differences may lead to novel approaches to antiviral agents and vaccines.
[Mh] Termos MeSH primário: Imunidade Inata
Pulmão/metabolismo
Infecções por Vírus Respiratório Sincicial/imunologia
Vírus Sincicial Respiratório Humano/genética
[Mh] Termos MeSH secundário: Anticorpos Neutralizantes/imunologia
Anticorpos Antivirais/imunologia
Quimiocina CCL5/imunologia
Células Epiteliais/imunologia
Perfilação da Expressão Gênica
Genoma Viral
Seres Humanos
Interleucina-6/imunologia
Pulmão/virologia
Macrófagos/imunologia
Testes de Neutralização
Fenótipo
Análise de Sequência de RNA
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (IL6 protein, human); 0 (Interleukin-6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184318



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