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  1 / 13701 MEDLINE  
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[PMID]:29364896
[Au] Autor:Nakagawa P; Romero CA; Jiang X; D'Ambrosio M; Bordcoch G; Peterson EL; Harding P; Yang XP; Carretero OA
[Ad] Endereço:Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan, United States of America.
[Ti] Título:Ac-SDKP decreases mortality and cardiac rupture after acute myocardial infarction.
[So] Source:PLoS One;13(1):e0190300, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The natural peptide N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) decreases inflammation in chronic diseases such as hypertension and heart failure. However, Ac-SDKP effects on acute inflammatory responses during myocardial infarction (MI) are unknown. During the first 72 hours post-MI, neutrophils, M1 macrophages (pro-inflammatory), and M2 macrophages (pro-resolution) and release of myeloperoxidase (MPO) and matrix metalloproteinases (MMP) are involved in cardiac rupture. We hypothesized that in the acute stage of MI, Ac-SDKP decreases the incidence of cardiac rupture and mortality by preventing immune cell infiltration as well as by decreasing MPO and MMP expression. MI was induced by ligating the left descending coronary artery in C57BL/6 mice. Vehicle or Ac-SDKP (1.6 mg/kg/d) was infused via osmotic minipump. Cardiac immune cell infiltration was assessed by flow cytometry, cardiac MPO and MMP levels were measured at 24-48 hrs post-MI. Cardiac rupture and mortality incidence were determined at 7 days post-MI. In infarcted mice, Ac-SDKP significantly decreased cardiac rupture incidence from 51.0% (26 of 51 animals) to 27.3% (12 of 44) and mortality from 56.9% (29 of 51) to 31.8% (14 of 44). Ac-SDKP reduced M1 macrophages in cardiac tissue after MI, without affecting M2 macrophages and neutrophils. Ac-SDKP decreased MMP-9 activation in infarcted hearts with no changes on MPO expression. Ac-SDKP prevents cardiac rupture and decreases mortality post-acute MI. These protective effects of Ac-SDKP are associated with decreased pro-inflammatory M1 macrophage infiltration and MMP-9 activation.
[Mh] Termos MeSH primário: Ruptura Cardíaca/prevenção & controle
Infarto do Miocárdio/prevenção & controle
Oligopeptídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Quimiotaxia de Leucócito
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Macrófagos/patologia
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Infarto do Miocárdio/mortalidade
Infarto do Miocárdio/patologia
Peroxidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Oligopeptides); EC 1.11.1.7 (Peroxidase); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190300


  2 / 13701 MEDLINE  
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[PMID]:28469031
[Au] Autor:Dorward DA; Lucas CD; Doherty MK; Chapman GB; Scholefield EJ; Conway Morris A; Felton JM; Kipari T; Humphries DC; Robb CT; Simpson AJ; Whitfield PD; Haslett C; Dhaliwal K; Rossi AG
[Ad] Endereço:The MRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
[Ti] Título:Novel role for endogenous mitochondrial formylated peptide-driven formyl peptide receptor 1 signalling in acute respiratory distress syndrome.
[So] Source:Thorax;72(10):928-936, 2017 10.
[Is] ISSN:1468-3296
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute respiratory distress syndrome (ARDS) is an often fatal neutrophil-dominant lung disease. Although influenced by multiple proinflammatory mediators, identification of suitable therapeutic candidates remains elusive. We aimed to delineate the presence of mitochondrial formylated peptides in ARDS and characterise the functional importance of formyl peptide receptor 1 (FPR1) signalling in sterile lung inflammation. METHODS: Mitochondrial formylated peptides were identified in bronchoalveolar lavage fluid (BALF) and serum of patients with ARDS by liquid chromatography-tandem mass spectrometry. In vitro, human neutrophils were stimulated with mitochondrial formylated peptides and their effects assessed by flow cytometry and chemotaxis assay. Mouse lung injury was induced by mitochondrial formylated peptides or hydrochloric acid. Bone marrow chimeras determined the contribution of myeloid and parenchymal FPR1 to sterile lung inflammation. RESULTS: Mitochondrial formylated peptides were elevated in BALF and serum from patients with ARDS. These peptides drove neutrophil activation and chemotaxis through FPR1-dependent mechanisms in vitro and in vivo. In mouse lung injury, inflammation was attenuated in Fpr1-/- mice, effects recapitulated by a pharmacological FPR1 antagonist even when administered after the onset of injury. FPR1 expression was present in alveolar epithelium and chimeric mice demonstrated that both myeloid and parenchymal FPR1 contributed to lung inflammation. CONCLUSIONS: We provide the first definitive evidence of mitochondrial formylated peptides in human disease and demonstrate them to be elevated in ARDS and important in a mouse model of lung injury. This work reveals mitochondrial formylated peptide FPR1 signalling as a key driver of sterile acute lung injury and a potential therapeutic target in ARDS.
[Mh] Termos MeSH primário: Receptores de Formil Peptídeo/imunologia
Síndrome do Desconforto Respiratório do Adulto/imunologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/química
Quimiotaxia de Leucócito/imunologia
Cromatografia Líquida de Alta Pressão
Modelos Animais de Doenças
Citometria de Fluxo
Seres Humanos
Camundongos
Mitocôndrias/imunologia
Ativação de Neutrófilo/imunologia
Neutrófilos/imunologia
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FPR1 protein, human); 0 (Receptors, Formyl Peptide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1136/thoraxjnl-2017-210030


  3 / 13701 MEDLINE  
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[PMID]:29287105
[Au] Autor:Labens R; Daniel C; Hall S; Xia XR; Schwarz T
[Ad] Endereço:School of Animal and Veterinary Sciences, Faculty of Science, Charles Sturt University, Wagga Wagga, New South Wales, Australia.
[Ti] Título:Effect of intra-articular administration of superparamagnetic iron oxide nanoparticles (SPIONs) for MRI assessment of the cartilage barrier in a large animal model.
[So] Source:PLoS One;12(12):e0190216, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Early diagnosis of cartilage disease at a time when changes are limited to depletion of extracellular matrix components represents an important diagnostic target to reduce patient morbidity. This report is to present proof of concept for nanoparticle dependent cartilage barrier imaging in a large animal model including the use of clinical magnetic resonance imaging (MRI). Conditioned (following matrix depletion) and unconditioned porcine metacarpophalangeal cartilage was evaluated on the basis of fluorophore conjugated 30 nm and 80 nm spherical gold nanoparticle permeation and multiphoton laser scanning and bright field microscopy after autometallographic particle enhancement. Consequently, conditioned and unconditioned joints underwent MRI pre- and post-injection with 12 nm superparamagnetic iron oxide nanoparticles (SPIONs) to evaluate particle permeation in the context of matrix depletion and use of a clinical 1.5 Tesla MRI scanner. To gauge the potential pro-inflammatory effect of intra-articular nanoparticle delivery co-cultures of equine synovium and cartilage tissue were exposed to an escalating dose of SPIONs and IL-6, IL-10, IFN-γ and PGE2 were assessed in culture media. The chemotactic potential of growth media samples was subsequently assessed in transwell migration assays on isolated equine neutrophils. Results demonstrate an increase in MRI signal following conditioning of porcine joints which suggests that nanoparticle dependent compositional cartilage imaging is feasible. Tissue culture and neutrophil migration assays highlight a dose dependent inflammatory response following SPION exposure which at the imaging dose investigated was not different from controls. The preliminary safety and imaging data support the continued investigation of nanoparticle dependent compositional cartilage imaging. To our knowledge, this is the first report in using SPIONs as intra-articular MRI contrast agent for studying cartilage barrier function, which could potentially lead to a new diagnostic technique for early detection of cartilage disease.
[Mh] Termos MeSH primário: Cartilagem Articular/diagnóstico por imagem
Articulações
Imagem por Ressonância Magnética/métodos
Nanopartículas de Magnetita/administração & dosagem
Modelos Animais
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Cartilagem Articular/metabolismo
Quimiotaxia de Leucócito
Técnicas de Cocultura
Vias de Administração de Medicamentos
Feminino
Corantes Fluorescentes
Cavalos
Masculino
Microscopia Confocal
Neutrófilos/citologia
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fluorescent Dyes); 0 (Magnetite Nanoparticles)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190216


  4 / 13701 MEDLINE  
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[PMID]:28741728
[Au] Autor:Ki S; Thyagarajan HM; Hu Z; Lancaster JN; Ehrlich LIR
[Ad] Endereço:Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX, USA.
[Ti] Título:EBI2 contributes to the induction of thymic central tolerance in mice by promoting rapid motility of medullary thymocytes.
[So] Source:Eur J Immunol;47(11):1906-1917, 2017 11.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Maturing thymocytes enter the thymic medulla, where they encounter numerous self-antigens presented by antigen presenting cells (APCs). Those thymocytes that are strongly self-reactive undergo either negative selection or diversion into the regulatory T-cell lineage. Although the majority of the proteome is expressed in the medulla, many self-antigens are expressed by only a minor fraction of medullary APCs; thus, thymocytes must efficiently enter the medulla and scan APCs to ensure central tolerance. Chemokine receptors promote lymphocyte migration, organization within tissues, and interactions with APCs in lymphoid organs. The chemokine receptor EBI2 governs localization of T cells, B cells, and dendritic cells (DCs) during immune responses in secondary lymphoid organs. However, the role of EBI2 in thymocyte development has not been elucidated. Here, we demonstrate that EBI2 is expressed by murine CD4 single positive (CD4SP) thymocytes and thymic DCs. EBI2 deficiency alters the TCR repertoire, but does not grossly impact thymocyte cellularity or subset distribution. EBI2 deficiency also impairs negative selection of OT-II TCR transgenic thymocytes responding to an endogenous self-antigen. Two-photon imaging revealed that EBI2 deficiency results in reduced migration and impaired medullary accumulation of CD4SP thymocytes. These data identify a role for EBI2 in promoting efficient thymic central tolerance.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Tolerância Central/imunologia
Receptores Acoplados a Proteínas-G/imunologia
Timócitos/imunologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiotaxia de Leucócito/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gpr183 protein, mouse); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747020


  5 / 13701 MEDLINE  
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[PMID]:29236764
[Au] Autor:Kim BY; Son Y; Lee J; Choi J; Kim CD; Bae SS; Eo SK; Kim K
[Ad] Endereço:Department of Pharmacology, Pusan National University-School of Medicine, Yangsan, Gyeongnam, Republic of Korea.
[Ti] Título:Dexamethasone inhibits activation of monocytes/macrophages in a milieu rich in 27-oxygenated cholesterol.
[So] Source:PLoS One;12(12):e0189643, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Molecular mechanisms underlying the decreased number of macrophages and T cells in the arteries of cholesterol-fed-rabbits following dexamethasone administration are unknown. We investigated the possibility that dexamethasone could affect activation of monocytic cells induced by oxygenated derivatives of cholesterol (oxysterols) using THP-1 monocyte/macrophage cells. 27-Hydroxycholesterol (27OHChol), an oxysterol elevated with hypercholesterolemia, enhanced production of CCL2, known as MCP1, chemokine from monocytes/macrophages and migration of the monocytic cells, but the CCL2 production and the cell migration were reduced by treatment with dexamethasone. Dexamethasone inhibited superproduction of CCL2 induced by 27OHChol plus LPS and attenuated transcription of matrix metalloproteinase 9 as well as secretion of its active gene product induced by 27OHChol. The drug downregulated cellular and surface levels of CD14 and blocked release of soluble CD14 without altering transcription of the gene. Dexamethasone also inhibited expression and phosphorylation of the NF-κB p65 subunit enhanced by 27OHChol. Collectively, these results indicate that dexamethasone inhibits activation of monocytes/macrophages in response to 27OHChol, thereby leading to decreased migration of inflammatory cells in milieu rich in oxygenated derivatives of cholesterol.
[Mh] Termos MeSH primário: Dexametasona/farmacologia
Hidroxicolesteróis/metabolismo
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular
Quimiocina CCL2/biossíntese
Quimiocina CCL2/metabolismo
Quimiotaxia de Leucócito
Regulação para Baixo
Seres Humanos
Macrófagos/imunologia
Macrófagos/metabolismo
Monócitos/imunologia
Monócitos/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição RelA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Hydroxycholesterols); 0 (Transcription Factor RelA); 6T2NA6P5SQ (27-hydroxycholesterol); 7S5I7G3JQL (Dexamethasone)
[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:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189643


  6 / 13701 MEDLINE  
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[PMID]:29220376
[Au] Autor:Hornum L; Hansen AJ; Tornehave D; Fjording MS; Colmenero P; Wätjen IF; Søe Nielsen NH; Bliddal H; Bartels EM
[Ad] Endereço:Novo Nordisk A/S, Måløv, Denmark.
[Ti] Título:C5a and C5aR are elevated in joints of rheumatoid and psoriatic arthritis patients, and C5aR blockade attenuates leukocyte migration to synovial fluid.
[So] Source:PLoS One;12(12):e0189017, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complement activation correlates to rheumatoid arthritis disease activity, and increased amounts of the complement split product C5a is observed in synovial fluids from rheumatoid arthritis patients. Blockade of C5a or its receptor (C5aR) is efficacious in several arthritis models. The aim of this study was to investigate the role of C5a and C5aR in human rheumatoid arthritis and psoriatic arthritis-both with respect to expression and function. Synovial fluid, blood and synovial samples were obtained from rheumatoid arthritis, psoriatic arthritis and osteoarthritis patients as a less inflammatory arthritis type, and blood from healthy subjects. Cells infiltrating synovial tissue were analysed by immunohistochemistry and flow cytometry. SF and blood were analysed for biomarkers by flow cytometry or ELISA. The effect of a blocking anti-human C5aR mAb on leukocyte migration was determined using a Boyden chamber. Appropriate statistical tests were applied for comparisons. C5aR+ cells were detected in most rheumatoid arthritis, in all psoriatic arthritis, but not in non-inflammatory control synovia. C5aR+ cells were primarily neutrophils and macrophages. C5aR+ macrophages were mainly found in lymphoid aggregates in close contact with T cells. C5a levels were increased in both rheumatoid arthritis and psoriatic arthritis synovial fluid compared to osteoarthritis, and in blood from rheumatoid arthritis compared to healthy subjects. Neutrophil and monocyte migration to rheumatoid arthritis synovial fluid was significantly inhibited by anti-C5aR. The data support that the C5a-C5aR axis may be driving the infiltration of inflammatory cells into the synovial fluid and synovium in both rheumatoid and psoriatic arthritis, and suggest that C5a or C5aR may be a promising treatment target in both diseases.
[Mh] Termos MeSH primário: Artrite Psoriásica/metabolismo
Artrite Reumatoide/metabolismo
Quimiotaxia de Leucócito
Complemento C5a/metabolismo
Leucócitos/patologia
Receptor da Anafilatoxina C5a/metabolismo
Líquido Sinovial/metabolismo
[Mh] Termos MeSH secundário: Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Seres Humanos
Imuno-Histoquímica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Anaphylatoxin C5a); 80295-54-1 (Complement C5a)
[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:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189017


  7 / 13701 MEDLINE  
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[PMID]:28982143
[Au] Autor:Ellison MA; Gearheart CM; Porter CC; Ambruso DR
[Ad] Endereço:Department of Pediatrics, University of Colorado Denver, The Anschutz Medical Campus, Aurora, Colorado, United States of America.
[Ti] Título:IFN-γ alters the expression of diverse immunity related genes in a cell culture model designed to represent maturing neutrophils.
[So] Source:PLoS One;12(10):e0185956, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokine interferon-γ (IFN-γ) is approved as a drug to treat chronic granulomatous disease (CGD) and osteopetrosis and is also used in hyperimmunoglobulin E syndromes. Patients with CGD have defects in proteins of the NOX2 NADPH oxidase system. This leads to reduced production of microbicidal ROS by PMNs and recurrent life threatening infections. The goal of this study was to better understand how IFN-γ might support phagocyte function in these diseases, and to obtain information that might expand potential uses for IFN-γ. Neutrophils mature in the bone marrow and then enter the blood where they quickly undergo apoptotic cell death with a half-life of only 5-10 hours. Therefore we reasoned that IFN-γ might exert its effects on neutrophils via prolonged exposure to cells undergoing maturation in the marrow rather than by its brief exposure to short-lived circulating cells. To explore this possibility we made use of PLB-985 cells, a myeloblast-like myeloid cell line that can be differentiated into a mature, neutrophil-like state by treatment with various agents including DMSO. In initial studies we investigated transcription and protein expression in PLB-985 cells undergoing maturation in the presence or absence of IFN-γ. We observed IFN-γ induced differences in expression of genes known to be involved in classical aspects of neutrophil function (transmigration, chemotaxis, phagocytosis, killing and pattern recognition) as well as genes involved in apoptosis and other mechanisms that regulating neutrophil number. We also observed differences for genes involved in the major histocompatibility complex I (MHCI) and MHCII systems whose involvement in neutrophil function is controversial and not well defined. Finally, we observed significant changes in expression of genes encoding guanylate binding proteins (Gbps) that are known to have roles in immunity but which have not as yet been linked to neutrophil function. We propose that changes in the expression within these classes of genes could help explain the immune supportive effects of IFN-γ. Next we explored if the effect of IFN-γ on expression of these genes is dependent on whether the cells are undergoing maturation; to do this we compared the effects of IFN-γ on cells cultured with and without DMSO. For a subset of genes the expression level changes caused by IFN-γ were much greater in maturing cells than non-maturing cells. These findings indicate that developmental changes associated with cell maturation can modulate the effects of IFN-γ but that this is gene specific. Since the effects of IFN-γ depend on whether cells are maturing, the gene expression changes observed in this study must be due to more than just prolonged application of IFN-γ and are instead the result of interplay between cell maturation and changes caused by the chemokine. This supports our hypothesis that the effects of IFN-γ on developing neutrophils in the bone marrow may be very different from its effects on mature cells in the blood. Collectively the findings in this study enhance our understanding of the effects of IFN-γ on maturing myeloid cells and indicate possible mechanisms by which this cytokine could support immune function.
[Mh] Termos MeSH primário: Imunidade Inata/genética
Interferon gama/fisiologia
Neutrófilos/citologia
[Mh] Termos MeSH secundário: Apoptose
Western Blotting
Linhagem Celular
Quimiotaxia de Leucócito
Regulação da Expressão Gênica
Seres Humanos
Muramidase/metabolismo
NADPH Oxidases/metabolismo
Neutrófilos/enzimologia
Neutrófilos/imunologia
Análise de Sequência com Séries de Oligonucleotídeos
Peroxidase/metabolismo
Fagocitose
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
82115-62-6 (Interferon-gamma); EC 1.11.1.7 (Peroxidase); EC 1.6.3.- (NADPH Oxidases); EC 3.2.1.17 (Muramidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185956


  8 / 13701 MEDLINE  
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[PMID]:28912363
[Au] Autor:Lareyre F; Clément M; Raffort J; Pohlod S; Patel M; Esposito B; Master L; Finigan A; Vandestienne M; Stergiopulos N; Taleb S; Trachet B; Mallat Z
[Ad] Endereço:From the Division of Cardiovascular Medicine, University of Cambridge, UK (F.L., M.C., J.R., M.P., L.M., A.F., Z.M.); Université Côte d'Azur, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Institute for Research on Cancer and Aging in Nice, F
[Ti] Título:TGFß (Transforming Growth Factor-ß) Blockade Induces a Human-Like Disease in a Nondissecting Mouse Model of Abdominal Aortic Aneurysm.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2171-2181, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Current experimental models of abdominal aortic aneurysm (AAA) do not accurately reproduce the major features of human AAA. We hypothesized that blockade of TGFß (transforming growth factor-ß) activity-a guardian of vascular integrity and immune homeostasis-would impair vascular healing in models of nondissecting AAA and would lead to sustained aneurysmal growth until rupture. APPROACH AND RESULTS: Here, we test this hypothesis in the elastase-induced AAA model in mice. We analyze AAA development and progression using ultrasound in vivo, synchrotron-based ultrahigh resolution imaging ex vivo, and a combination of biological, histological, and flow cytometry-based cellular and molecular approaches in vitro. Systemic blockade of TGFß using a monoclonal antibody induces a transition from a self-contained aortic dilatation to a model of sustained aneurysmal growth, associated with the formation of an intraluminal thrombus. AAA growth is associated with wall disruption but no medial dissection and culminates in fatal transmural aortic wall rupture. TGFß blockade enhances leukocyte infiltration both in the aortic wall and the intraluminal thrombus and aggravates extracellular matrix degradation. Early blockade of IL-1ß or monocyte-dependent responses substantially limits AAA severity. However, blockade of IL-1ß after disease initiation has no effect on AAA progression to rupture. CONCLUSIONS: Endogenous TGFß activity is required for the healing of AAA. TGFß blockade may be harnessed to generate new models of AAA with better relevance to the human disease. We expect that the new models will improve our understanding of the pathophysiology of AAA and will be useful in the identification of new therapeutic targets.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/toxicidade
Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/induzido quimicamente
Ruptura Aórtica/induzido quimicamente
Elastase Pancreática
Fator de Crescimento Transformador beta/antagonistas & inibidores
Remodelação Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/imunologia
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/imunologia
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Ruptura Aórtica/imunologia
Ruptura Aórtica/metabolismo
Ruptura Aórtica/patologia
Apolipoproteínas E/genética
Apolipoproteínas E/metabolismo
Quimiotaxia de Leucócito/efeitos dos fármacos
Dilatação Patológica
Modelos Animais de Doenças
Progressão da Doença
Matriz Extracelular/efeitos dos fármacos
Matriz Extracelular/metabolismo
Matriz Extracelular/patologia
Interleucina-1beta/metabolismo
Cinética
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Síncrotrons
Trombose/induzido quimicamente
Trombose/metabolismo
Trombose/patologia
Fator de Crescimento Transformador beta/imunologia
Fator de Crescimento Transformador beta/metabolismo
Ultrassonografia
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Apolipoproteins E); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (Transforming Growth Factor beta); EC 3.4.21.36 (Pancreatic Elastase)
[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:170916
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309999


  9 / 13701 MEDLINE  
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[PMID]:28846922
[Au] Autor:Wu CY; Tsai YY; Chen SY; Lin YP; Shin JW; Wu CC; Yang BC
[Ad] Endereço:Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 70428, Taiwan. Electronic address: jawork520@yahoo.com.tw.
[Ti] Título:Interaction of Zap70 and CXCR4 receptor at lamellipodia that determines the directionality during Jurkat T cells chemotaxis.
[So] Source:Mol Immunol;90:245-254, 2017 Oct.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Directional migration of T-lymphocytes is a key process during immune activation and is tightly regulated both temporally and spatially. The initial cell membrane protrusion at a particular site is critical for determining the direction of cell migration. In this study, we found that ZAP-70 protein appeared not only at the margin of the spreading areas of polarized Jurkat T cells but also formed clusters near the center of the cell body on a fibronectin plate. Specifically, some pZAP-70 was located at the lamellipodia/filopodia and was closely associated with the most extended membrane contact. To visualize the dynamic distribution of ZAP-70 on migrating Jurkat T cells, we generated a fluorescent ZAP-70-EGFP fusion protein (hZAP70G). Expression of the hZAP70G in P116 cells, a ZAP-70 defective Jurkat derivative, restored its chemotactic migration toward SDF-1, adhesion to fibronectin matrix, and integrin activation. In addition, the distribution of hZAP70G protein is associated with changes in cell shape, specifically the membrane protrusion step, forming filopodia/lamellipodia and a retracting uropod. Furthermore, SDF-1 stimulated the formation of ZAP-70 and CXCR4 complex. CXCR4 was observed mainly at the leading edge of migrating cell. The localization of ZAP-70 at the very front edge of protruding lamellipodia was close to CXCR4 and a part of them were overlapped. Collectively, our data describe the critical early step of directional cell movement toward SDF-1 that ZAP-70 is recruited to the CXCR4 at the leading edge of membrane and consequently modulates lamellipodia/filopodia formation and integrin activation.
[Mh] Termos MeSH primário: Quimiocina CXCL12/metabolismo
Quimiotaxia de Leucócito/fisiologia
Pseudópodes/metabolismo
Receptores CXCR4/metabolismo
Proteína-Tirosina Quinase ZAP-70/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular/genética
Linhagem Celular Tumoral
Quimiotaxia de Leucócito/genética
Fibronectinas/metabolismo
Proteínas de Fluorescência Verde/genética
Seres Humanos
Integrinas/metabolismo
Células Jurkat
Ativação Linfocitária/imunologia
Células MCF-7
Transdução de Sinais/imunologia
Linfócitos T/imunologia
Linfócitos T/fisiologia
Proteína-Tirosina Quinase ZAP-70/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Fibronectins); 0 (Integrins); 0 (Receptors, CXCR4); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase); EC 2.7.10.2 (ZAP70 protein, human)
[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:170829
[St] Status:MEDLINE


  10 / 13701 MEDLINE  
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[PMID]:28843961
[Au] Autor:Liu B; Chen P; Xi D; Zhu H; Gao Y
[Ad] Endereço:Departments of Assisted Reproduction, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200092, China.
[Ti] Título:ATF4 regulates CCL2 expression to promote endometrial cancer growth by controlling macrophage infiltration.
[So] Source:Exp Cell Res;360(2):105-112, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activating transcription factor 4 (ATF4), an endoplasmic reticulum stress-inducible transcription factor, plays important roles in cancer progression and resistance to therapy. However, no report is available about its roles in endometrial cancer (EC). In this study, we found that ATF4 is commonly expressed in EC cell lines. Loss-of-function studies in two EC cell lines showed that ATF4 knockdown suppresses tumor growth of EC in vivo without influencing cell proliferation in vitro. And xenograft tumors derived from ATF4-knockdown cells had reduced M2 macrophage infiltration. In clinical specimens, ATF4-high expressing tumors indeed contained more macrophage infiltration compared to those with lower ATF4 expression. Moreover, we identified that ATF4-mediated chemokine CCL2 expression ultimately results in macrophage infiltration and tumor growth of EC. Taken together, our findings suggest that ATF4 contributes to tumor growth of EC by promoting CCL2 and subsequent recruitment of macrophage, and that ATF4/CCL2 axis might be a potential therapeutic target for EC.
[Mh] Termos MeSH primário: Fator 4 Ativador da Transcrição/fisiologia
Carcinoma Endometrioide/genética
Proliferação Celular/genética
Quimiocina CCL2/genética
Quimiotaxia de Leucócito/genética
Neoplasias do Endométrio/genética
Macrófagos/fisiologia
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/antagonistas & inibidores
Fator 4 Ativador da Transcrição/genética
Animais
Carcinoma Endometrioide/patologia
Células Cultivadas
Neoplasias do Endométrio/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Células HEK293
Seres Humanos
Camundongos
Camundongos Nus
Evasão Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATF4 protein, human); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 145891-90-3 (Activating Transcription Factor 4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170828
[St] Status:MEDLINE



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