Base de dados : MEDLINE
Pesquisa : E01.370.225.500.335 [Categoria DeCS]
Referências encontradas : 430 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 43 ir para página                         

  1 / 430 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:29267503
[Au] Autor:Wang ZK; Yang L; Wu LL; Mao H; Zhou YH; Zhang PF; Dai GH
[Ad] Endereço:The Second Department of Medical Oncology, Chinese People's Liberation Army General Hospital, Beijing, China.
[Ti] Título:Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy.
[So] Source:Braz J Med Biol Res;51(2):e6793, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and ß-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear ß-catenin through restraining ß-catenin from cytoplasm into nuclei or it could also promote ß-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cisplatino/farmacologia
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
RNA Longo não Codificante/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Proteínas Reguladoras de Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/fisiologia
Western Blotting
Ensaios de Migração Celular
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/fisiologia
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/fisiologia
Células HCT116
Células HT29
Seres Humanos
RNA Longo não Codificante/análise
RNA Longo não Codificante/efeitos dos fármacos
RNA Longo não Codificante/genética
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
Sais de Tetrazólio
Tiazóis
beta Catenina/efeitos dos fármacos
beta Catenina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (RNA, Long Noncoding); 0 (Tetrazolium Salts); 0 (Thiazoles); 0 (beta Catenin); 0 (long non-coding RNA 00261, human); EUY85H477I (thiazolyl blue); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:29267498
[Au] Autor:Ni XJ; Xu ZQ; Jin H; Zheng SL; Cai Y; Wang JJ
[Ad] Endereço:Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage.
[So] Source:Braz J Med Biol Res;51(2):e6611, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 µM) in the absence or presence of 5 µg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1ß, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 µM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Ginsenosídeos/farmacologia
Túbulos Renais/citologia
Lipopolissacarídeos
Nefrite/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Linhagem Celular
Ensaios de Migração Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Túbulos Renais/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/análise
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Proteínas Proto-Oncogênicas c-akt/análise
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Espécies Reativas de Oxigênio/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Ginsenosides); 0 (Lipopolysaccharides); 0 (Protective Agents); 0 (Reactive Oxygen Species); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  3 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28700652
[Au] Autor:Souza Vilela Podestá T; Venzel Rosembach T; Aparecida Dos Santos A; Lobato Martins M
[Ad] Endereço:Departamento de Física, Universidade Federal de Viçosa, Viçosa, Minas Gerais, Brazil.
[Ti] Título:Anomalous diffusion and q-Weibull velocity distributions in epithelial cell migration.
[So] Source:PLoS One;12(7):e0180777, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In multicellular organisms, cell motility is central in all morphogenetic processes, tissue maintenance, wound healing and immune surveillance. Hence, the control of cell motion is a major demand in the creation of artificial tissues and organs. Here, cell migration assays on plastic 2D surfaces involving normal (MDCK) and tumoral (B16F10) epithelial cell lines were performed varying the initial density of plated cells. Through time-lapse microscopy quantities such as speed distributions, velocity autocorrelations and spatial correlations, as well as the scaling of mean-squared displacements were determined. We find that these cells exhibit anomalous diffusion with q-Weibull speed distributions that evolves non-monotonically to a Maxwellian distribution as the initial density of plated cells increases. Although short-ranged spatial velocity correlations mark the formation of small cell clusters, the emergence of collective motion was not observed. Finally, simulational results from a correlated random walk and the Vicsek model of collective dynamics evidence that fluctuations in cell velocity orientations are sufficient to produce q-Weibull speed distributions seen in our migration assays.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Células Epiteliais/citologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Ensaios de Migração Celular
Cães
Células Epiteliais/fisiologia
Células Madin Darby de Rim Canino
Camundongos
Modelos Teóricos
Distribuições Estatísticas
Imagem com Lapso de Tempo
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180777


  4 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28608366
[Au] Autor:Shi H; Fang W; Liu M; Fu D
[Ad] Endereço:Department of Pancreatic Surgery, Pancreatic Disease Institute, Huashan Hospital, Fudan University, Shanghai, People's Republic of China.
[Ti] Título:Complement component 1, q subcomponent binding protein (C1QBP) in lipid rafts mediates hepatic metastasis of pancreatic cancer by regulating IGF-1/IGF-1R signaling.
[So] Source:Int J Cancer;141(7):1389-1401, 2017 Oct 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer shows a remarkable predilection for hepatic metastasis. Complement component 1, q subcomponent binding protein (C1QBP) can mediate growth factor-induced cancer cell chemotaxis and distant metastasis by activation of receptor tyrosine kinases. Coincidentally, insulin-like growth factor-1 (IGF-1) derived from the liver and cancer cells itself has been recognized as a critical inducer of hepatic metastasis. However, the mechanism underlying IGF-1-dependent hepatic metastasis of pancreatic cancer, in which C1QBP may be involved, remains unknown. In the study, we demonstrated a significant association between C1QBP expression and hepatic metastasis in patients with pancreatic cancer. IGF-1 induced the translocation of C1QBP from cytoplasm to lipid rafts and further drove the formation of CD44 variant 6 (CD44v6)/C1QBP complex in pancreatic cancer cells. C1QBP interacting with CD44v6 in lipid rafts promoted phosphorylation of IGF-1R and thus activated downstream PI3K and MAPK signaling pathways which mediated metastatic potential of pancreatic cancer cells including proliferation, apoptosis, invasion, adhesion and energy metabolism. Furthermore, C1QBP knockdown suppressed hepatic metastasis of pancreatic cancer cells in nude mice. We therefore conclude that C1QBP in lipid rafts serves a key regulator of IGF-1/IGF-1R-induced hepatic metastasis from pancreatic cancer. Our findings about C1QBP in lipid rafts provide a novel strategy to block IGF-1/IGF-1R signaling in pancreatic cancer and a reliable premise for more efficient combined modality therapies.
[Mh] Termos MeSH primário: Adenocarcinoma/secundário
Proteínas de Transporte/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Neoplasias Hepáticas/secundário
Proteínas Mitocondriais/metabolismo
Proteínas de Neoplasias/metabolismo
Neoplasias Pancreáticas/patologia
Receptor IGF Tipo 1/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Animais
Proteínas de Transporte/genética
Linhagem Celular Tumoral
Ensaios de Migração Celular
Movimento Celular
Proliferação Celular
Quimiotaxia
Citoplasma/metabolismo
Técnicas de Silenciamento de Genes
Seres Humanos
Receptores de Hialuronatos/metabolismo
Microdomínios da Membrana/metabolismo
Camundongos
Camundongos Nus
Proteínas Mitocondriais/genética
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Neoplasias Pancreáticas/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (C1QBP protein, human); 0 (CD44v6 antigen); 0 (Carrier Proteins); 0 (Hyaluronan Receptors); 0 (Mitochondrial Proteins); 0 (Neoplasm Proteins); 67763-96-6 (Insulin-Like Growth Factor I); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, IGF Type 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[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:170614
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30831


  5 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28500074
[Au] Autor:Lefèvre S; Schwarz M; Meier FMP; Zimmermann-Geller B; Tarner IH; Rickert M; Steinmeyer J; Sauerbier M; Rehart S; Müller-Ladner U; Neumann E
[Ad] Endereço:Department of Internal Medicine and Rheumatology, Justus-Liebig-University of Giessen, Kerckhoff Clinic, 61231 Bad Nauheim, Germany.
[Ti] Título:Disease-Specific Effects of Matrix and Growth Factors on Adhesion and Migration of Rheumatoid Synovial Fibroblasts.
[So] Source:J Immunol;198(12):4588-4595, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In rheumatoid arthritis (RA), cartilage and bone matrix are degraded, and extracellular matrix (ECM) proteins, acting as cellular activators, are liberated. Similar to ECM proteins, matrix-bound chemokines, cytokines, and growth factors (GFs) influence functional properties of key cells in RA, especially synovial fibroblasts. The role of these molecules on attachment, migration, and proinflammatory and prodestructive activation of RASFs was analyzed. Adhesion/migration of RASFs were examined under GF-enriched (GF ) or -reduced (GF ) conditions with or without addition of matrix-associated GFs, TGF-ß, and platelet-derived GF to GF or culture supernatants. Fibroblast adhesion and alterations in proinflammatory/prodestructive properties (e.g., IL-6/matrix metalloproteinase 3-release) in response to matrix-associated molecules were compared. Effects of GF , GF , and other ECM components on human RASF-mediated cartilage invasion were examined in the SCID mouse model. RASF adhesion under GF conditions was significantly lower compared with GF conditions (6.8- versus 8.3-fold). This effect was specific for RA because control cells showed opposite effects (e.g., osteoarthritis synovial fibroblasts [SF]; GF versus GF : 10.7- versus 8-fold). Addition of TGF-ß to GF increased RASF attachment (12.7-fold) compared with other matrices and components. RASF adhesion to GF matrix resulted in the strongest IL-6 and matrix metalloproteinase-3 release, and was even more pronounced compared with supplementation of single GFs. In vivo, GF matrix decreased RASF-mediated cartilage invasion compared with GF matrix. ECM components and especially GFs when bound within ECM actively enhance RASF attraction and cartilage adhesion. This observation was specific for RASFs as a reverse behavior was observed for controls.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Adesão Celular
Movimento Celular
Fibroblastos/fisiologia
Peptídeos e Proteínas de Sinalização Intercelular/fisiologia
Membrana Sinovial/citologia
[Mh] Termos MeSH secundário: Animais
Ensaios de Migração Celular
Movimento Celular/efeitos dos fármacos
Matriz Extracelular
Fibroblastos/efeitos dos fármacos
Fibroblastos/imunologia
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Interleucina-6/metabolismo
Metaloproteinase 3 da Matriz/biossíntese
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos SCID
Fator de Crescimento Derivado de Plaquetas/farmacologia
Membrana Sinovial/efeitos dos fármacos
Membrana Sinovial/imunologia
Fator de Crescimento Transformador beta1/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-6); 0 (Platelet-Derived Growth Factor); 0 (Transforming Growth Factor beta1); 0 (platelet-derived growth factor A); EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600989


  6 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28407787
[Au] Autor:Zheng NQ; Zheng ZH; Xu HX; Huang MX; Peng XM
[Ad] Endereço:Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
[Ti] Título:Glucose-regulated protein 78 demonstrates antiviral effects but is more suitable for hepatocellular carcinoma prevention in hepatitis B.
[So] Source:Virol J;14(1):77, 2017 Apr 13.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hepatitis B virus (HBV) is the leading cause of liver cirrhosis and hepatocellular carcinoma in Asia and Africa. Existing antivirals cannot cure HBV or eliminate risk of hepatocellular carcinoma. Glucose-regulated protein 78 (GRP78) can inhibit HBV replication, but promote virion secretion and hepatocellular cancer cell invasion. For these reasons, the overall effect of GRP78 on HBV production and whether to utilize the HBV replication-inhibitory effect of GRP78 up-regulation or the hepatocellular cancer cell invasion-inhibitory effect of its down-regulation were further investigated in order to improve the efficacy of current antiviral therapy. METHODS: GRP78 regulations in HepG2.2.15 cells were conducted by transfections of expressing vector and small interfering RNA, respectively. The changes in HBV replication, hepatitis B e antigen (HBeAg) synthesis and hepatoma cell motility were monitored. RESULTS: GRP78 overall decreased HBV production due to its HBV replication-inhibitory effect time-dependently overwhelming virion secretion-promoting effect in HepG2.2.15 cells. Unlike the parental cells (HepG2), HepG2.2.15 cells demonstrated decreased expressions of the major genes in the interferon-ß1-dependent pathway. Moreover, the expressions of these genes were not affected by GRP78 regulations. However, GRP78 was found to inhibit HBeAg secretion and to increase the retro-transportation of capsid assembly-interfering HBeAg precursor from the endoplasmic reticulum into the cytosol where new viral nucleocapsids formed. Furthermore, GRP78 overexpression promoted wound healing process (the motility) of HepG2.2.15 cells. In contrast, GRP78 knockdown enhanced HBV replication and HBeAg secretion, but they were abolished by entecavir and furin inhibitor, respectively. CONCLUSIONS: GRP78 mainly demonstrates anti-HBV effects, reducing HBV production and HBeAg secretion. With due regard to the hepatocellular cancer invasion risk of the overexpression and the rectifiability of the unpleasant effects of the knockdown, GRP78 down-regulation may be more suitable to serve as an additive strategy to cover the hepatocellular cancer prevention shortage of current antiviral therapy in the future.
[Mh] Termos MeSH primário: Movimento Celular
Proteínas de Choque Térmico/metabolismo
Vírus da Hepatite B/crescimento & desenvolvimento
Hepatócitos/fisiologia
Hepatócitos/virologia
[Mh] Termos MeSH secundário: Ensaios de Migração Celular
Expressão Gênica
Técnicas de Silenciamento de Genes
Proteínas de Choque Térmico/genética
Células Hep G2
Antígenos E da Hepatite B/análise
Vírus da Hepatite B/imunologia
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/prevenção & controle
Neoplasias Hepáticas/virologia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (Hepatitis B e Antigens); 0 (molecular chaperone GRP78)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1186/s12985-017-0747-z


  7 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28367571
[Au] Autor:Yang K; Wu J; Xu G; Xie D; Peretz-Soroka H; Santos S; Alexander M; Zhu L; Zhang M; Liu Y; Lin F
[Ad] Endereço:Institute of Applied Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, P. R. China.
[Ti] Título:A dual-docking microfluidic cell migration assay (D -Chip) for testing neutrophil chemotaxis and the memory effect.
[So] Source:Integr Biol (Camb);9(4):303-312, 2017 Apr 18.
[Is] ISSN:1757-9708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chemotaxis is a classic mechanism for guiding cell migration and an important topic in both fundamental cell biology and health sciences. Neutrophils are a widely used model to study eukaryotic cell migration and neutrophil chemotaxis itself can lead to protective or harmful immune actions to the body. While much has been learnt from past research about how neutrophils effectively navigate through a chemoattractant gradient, many interesting questions remain unclear. For example, while it is tempting to model neutrophil chemotaxis using the well-established biased random walk theory, the experimental proof was challenged by the cell's highly persistent migrating nature. A special experimental design is required to test the key predictions from the random walk model. Another question that has interested the cell migration community for decades concerns the existence of chemotactic memory and its underlying mechanism. Although chemotactic memory has been suggested in various studies, a clear quantitative experimental demonstration will improve our understanding of the migratory memory effect. Motivated by these questions, we developed a microfluidic cell migration assay (so-called dual-docking chip or D -Chip) that can test both the biased random walk model and the memory effect for neutrophil chemotaxis on a single chip enabled by multi-region gradient generation and dual-region cell alignment. Our results provide experimental support for the biased random walk model and chemotactic memory for neutrophil chemotaxis. Quantitative data analyses provide new insights into neutrophil chemotaxis and memory by making connections to entropic disorder, cell morphology and oscillating migratory response.
[Mh] Termos MeSH primário: Ensaios de Migração Celular
Quimiotaxia
Neutrófilos/citologia
[Mh] Termos MeSH secundário: Movimento Celular
Fatores Quimiotáticos
Simulação por Computador
Seres Humanos
Sistema Imunitário
Memória Imunológica
Técnicas Analíticas Microfluídicas
Neutrófilos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemotactic Factors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1039/c7ib00037e


  8 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28302111
[Au] Autor:Simpson MJ; Lo KY; Sun YS
[Ad] Endereço:School of Mathematical Sciences, Queensland University of Technology (QUT), Brisbane, Australia. matthew.simpson@qut.edu.au.
[Ti] Título:Quantifying the roles of random motility and directed motility using advection-diffusion theory for a 3T3 fibroblast cell migration assay stimulated with an electric field.
[So] Source:BMC Syst Biol;11(1):39, 2017 Mar 17.
[Is] ISSN:1752-0509
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Directed cell migration can be driven by a range of external stimuli, such as spatial gradients of: chemical signals (chemotaxis); adhesion sites (haptotaxis); or temperature (thermotaxis). Continuum models of cell migration typically include a diffusion term to capture the undirected component of cell motility and an advection term to capture the directed component of cell motility. However, there is no consensus in the literature about the form that the advection term takes. Some theoretical studies suggest that the advection term ought to include receptor saturation effects. However, others adopt a much simpler constant coefficient. One of the limitations of including receptor saturation effects is that it introduces several additional unknown parameters into the model. Therefore, a relevant research question is to investigate whether directed cell migration is best described by a simple constant tactic coefficient or a more complicated model incorporating saturation effects. RESULTS: We study directed cell migration using an experimental device in which the directed component of the cell motility is driven by a spatial gradient of electric potential, which is known as electrotaxis. The electric field (EF) is proportional to the spatial gradient of the electric potential. The spatial variation of electric potential across the experimental device varies in such a way that there are several subregions on the device in which the EF takes on different values that are approximately constant within those subregions. We use cell trajectory data to quantify the motion of 3T3 fibroblast cells at different locations on the device to examine how different values of the EF influences cell motility. The undirected (random) motility of the cells is quantified in terms of the cell diffusivity, D, and the directed motility is quantified in terms of a cell drift velocity, v. Estimates D and v are obtained under a range of four different EF conditions, which correspond to normal physiological conditions. Our results suggest that there is no anisotropy in D, and that D appears to be approximately independent of the EF and the electric potential. The drift velocity increases approximately linearly with the EF, suggesting that the simplest linear advection term, with no additional saturation parameters, provides a good explanation of these physiologically relevant data. CONCLUSIONS: We find that the simplest linear advection term in a continuum model of directed cell motility is sufficient to describe a range of different electrotaxis experiments for 3T3 fibroblast cells subject to normal physiological values of the electric field. This is useful information because alternative models that include saturation effects involve additional parameters that need to be estimated before a partial differential equation model can be applied to interpret or predict a cell migration experiment.
[Mh] Termos MeSH primário: Ensaios de Migração Celular
Movimento Celular
Eletricidade
Modelos Biológicos
[Mh] Termos MeSH secundário: Células 3T3
Animais
Difusão
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.1186/s12918-017-0413-5


  9 / 430 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28270519
[Au] Autor:Honjo K; Munakata S; Tashiro Y; Salama Y; Shimazu H; Eiamboonsert S; Dhahri D; Ichimura A; Dan T; Miyata T; Takeda K; Sakamoto K; Hattori K; Heissig B
[Ad] Endereço:Division of Stem Cell Dynamics, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
[Ti] Título:Plasminogen activator inhibitor-1 regulates macrophage-dependent postoperative adhesion by enhancing EGF-HER1 signaling in mice.
[So] Source:FASEB J;31(6):2625-2637, 2017 Jun.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adhesive small bowel obstruction remains a common problem for surgeons. After surgery, platelet aggregation contributes to coagulation cascade and fibrin clot formation. With clotting, fibrin degradation is simultaneously enhanced, driven by tissue plasminogen activator-mediated cleavage of plasminogen to form plasmin. The aim of this study was to investigate the cellular events and proteolytic responses that surround plasminogen activator inhibitor (PAI-1; ) inhibition of postoperative adhesion. Peritoneal adhesion was induced by gauze deposition in the abdominal cavity in C57BL/6 mice and those that were deficient in fibrinolytic factors, such as and In addition, C57BL/6 mice were treated with the novel PAI-1 inhibitor, TM5275. Some animals were treated with clodronate to deplete macrophages. Epidermal growth factor (EGF) experiments were performed to understand the role of macrophages and how EGF contributes to adhesion. In the early phase of adhesive small bowel obstruction, increased PAI-1 activity was observed in the peritoneal cavity. Genetic and pharmacologic PAI-1 inhibition prevented progression of adhesion and increased circulating plasmin. Whereas Serpine1 mice showed intra-abdominal bleeding, mice that were treated with TM5275 did not. Mechanistically, PAI-1, in combination with tissue plasminogen activator, served as a chemoattractant for macrophages that, in turn, secreted EGF and up-regulated the receptor, HER1, on peritoneal mesothelial cells, which led to PAI-1 secretion, further fueling the vicious cycle of impaired fibrinolysis at the adhesive site. Controlled inhibition of PAI-1 not only enhanced activation of the fibrinolytic system, but also prevented recruitment of EGF-secreting macrophages. Pharmacologic PAI-1 inhibition ameliorated adhesion formation in a macrophage-dependent manner.-Honjo, K., Munakata, S., Tashiro, Y., Salama, Y., Shimazu, H., Eiamboonsert, S., Dhahri, D., Ichimura, A., Dan, T., Miyata, T., Takeda, K., Sakamoto, K., Hattori, K., Heissig, B. Plasminogen activator inhibitor-1 regulates macrophage-dependent postoperative adhesion by enhancing EGF-HER1 signaling in mice.
[Mh] Termos MeSH primário: Macrófagos/fisiologia
Piperazinas/uso terapêutico
Receptor do Fator de Crescimento Epidérmico/metabolismo
Serpina E2/antagonistas & inibidores
Aderências Teciduais/patologia
para-Aminobenzoatos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b
Ensaios de Migração Celular
Movimento Celular/efeitos dos fármacos
Cetuximab/farmacologia
Fator de Crescimento Epidérmico
Regulação da Expressão Gênica/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Complicações Pós-Operatórias/prevenção & controle
Células RAW 264.7
Receptor do Fator de Crescimento Epidérmico/genética
Serpina E2/genética
Serpina E2/metabolismo
Transdução de Sinais
Aderências Teciduais/metabolismo
Ativador de Plasminogênio Tecidual/genética
Ativador de Plasminogênio Tecidual/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-chloro-2-(((2-(4-(diphenylmethyl)piperazin-1-yl)-2-oxoethoxy)acetyl)amino)benzoate); 0 (CD11b Antigen); 0 (Piperazines); 0 (Serpin E2); 0 (Serpine2 protein, mouse); 0 (para-Aminobenzoates); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.21.68 (Tissue Plasminogen Activator); PQX0D8J21J (Cetuximab)
[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:170309
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600871RR


  10 / 430 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28218910
[Au] Autor:Labernadie A; Kato T; Brugués A; Serra-Picamal X; Derzsi S; Arwert E; Weston A; González-Tarragó V; Elosegui-Artola A; Albertazzi L; Alcaraz J; Roca-Cusachs P; Sahai E; Trepat X
[Ad] Endereço:Institute for Bioengineering of Catalonia, Barcelona 08028, Spain.
[Ti] Título:A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion.
[So] Source:Nat Cell Biol;19(3):224-237, 2017 Mar.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancer-associated fibroblasts (CAFs) promote tumour invasion and metastasis. We show that CAFs exert a physical force on cancer cells that enables their collective invasion. Force transmission is mediated by a heterophilic adhesion involving N-cadherin at the CAF membrane and E-cadherin at the cancer cell membrane. This adhesion is mechanically active; when subjected to force it triggers ß-catenin recruitment and adhesion reinforcement dependent on α-catenin/vinculin interaction. Impairment of E-cadherin/N-cadherin adhesion abrogates the ability of CAFs to guide collective cell migration and blocks cancer cell invasion. N-cadherin also mediates repolarization of the CAFs away from the cancer cells. In parallel, nectins and afadin are recruited to the cancer cell/CAF interface and CAF repolarization is afadin dependent. Heterotypic junctions between CAFs and cancer cells are observed in patient-derived material. Together, our findings show that a mechanically active heterophilic adhesion between CAFs and cancer cells enables cooperative tumour invasion.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Fibroblastos Associados a Câncer/metabolismo
Fibroblastos Associados a Câncer/patologia
Neoplasias/patologia
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Fenômenos Biomecânicos
Fibroblastos Associados a Câncer/ultraestrutura
Adesão Celular
Moléculas de Adesão Celular/metabolismo
Linhagem Celular Tumoral
Ensaios de Migração Celular
Movimento Celular
Polaridade Celular
Técnicas de Cocultura
Feminino
Seres Humanos
Imagem Tridimensional
Neoplasias Pulmonares/patologia
Mecanotransdução Celular
Proteínas dos Microfilamentos
Nectinas
Invasividade Neoplásica
Neoplasias/metabolismo
Neoplasias de Células Escamosas/patologia
Pinças Ópticas
Esferoides Celulares/patologia
Neoplasias Vulvares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cell Adhesion Molecules); 0 (Microfilament Proteins); 0 (Nectins); 0 (afadin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3478



página 1 de 43 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde