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Pesquisa : D12.776.543.750.705.408.850 [Categoria DeCS]
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[PMID]:22993215
[Au] Autor:Kiessling F
[Ad] Endereço:Department of Experimental Molecular Imaging University Clinics, RWTH Aachen University Pauwelsstrasse 20, 52074 Aachen, Germany. fkiessling@ukaachen.de
[Ti] Título:Science to practice: genetic engineering meets cell tracking--a promising approach for cell-based therapies?
[So] Source:Radiology;265(1):1-3, 2012 Oct.
[Is] ISSN:1527-1315
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell-based therapies are gaining increasing importance and have been evaluated in many settings, including cancer, Parkinson disease, myocardial repair, stroke, and diabetes. In this context, it is of major importance that the cells are implanted into an optimal tissue environment and, correspondingly, that they reach the diseased region. Intravenous cell injection often is the route of choice, particularly if the cells are expected to circulate in the blood for longer periods of time and are able to actively migrate to the diseased tissue. Unfortunately, often only a small percentage of intravenously injected cells reach the target area. Higher accumulation can be achieved if the cells are injected into an artery that feeds the diseased area. However, in this case, fast blood velocities and substantial sheer stress make it difficult for the cells to adhere. In the study by Gorelik and colleagues (1), genetic engineering was used to overcome this limitation. Glial precursor cells were transiently transfected with very late antigen-4 (VLA-4) binding to vascular cell adhesion molecule-1 (VCAM-1), which is upregulated in inflamed endothelial cells. After labeling these cells with superparamagnetic iron oxide (SPIO) containing rhodamine, significantly increased binding to inflamed brain endothelial cells was shown and their homogeneous distribution over the inflamed brain tissue was convincingly demonstrated with magnetic resonance (MR) imaging and histologic examination. The authors concluded that transient transfection of SPIO-labeled cells with VLA-4 in combination with their arterial injection and the use of MR imaging monitoring may be an elegant way to increase the efficacy of cell-based treatments of inflammatory brain diseases.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Rastreamento de Células/métodos
Integrina alfa4beta1/metabolismo
Imagem por Ressonância Magnética/métodos
Neuroglia/metabolismo
Receptores de Antígeno muito Tardio/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (Receptors, Very Late Antigen)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:120920
[Lr] Data última revisão:
120920
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120921
[St] Status:MEDLINE


  2 / 580 MEDLINE  
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[PMID]:22923719
[Au] Autor:Gorelik M; Orukari I; Wang J; Galpoththawela S; Kim H; Levy M; Gilad AA; Bar-Shir A; Kerr DA; Levchenko A; Bulte JW; Walczak P
[Ad] Endereço:Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Cellular Imaging Section and Vascular Biology Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, 733 N Broadway, Broadway Research Building, Room 649, Baltimore, MD 21205, USA.
[Ti] Título:Use of MR cell tracking to evaluate targeting of glial precursor cells to inflammatory tissue by exploiting the very late antigen-4 docking receptor.
[So] Source:Radiology;265(1):175-85, 2012 Oct.
[Is] ISSN:1527-1315
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To determine if glial precursor cells can be targeted to inflamed brain through overexpression of very late antigen-4 (VLA-4) and whether this docking process can be monitored with magnetic resonance (MR) cell tracking after intraarterial injection. MATERIALS AND METHODS: All experimental procedures were performed between August 2010 and February 2012 and were approved by the institutional animal care and use committee. Human glial precursor cells (hGPs) were transfected with VLA-4 and labeled with superparamagnetic iron oxide that contained rhodamine. A microfluidic adhesion assay was used for assessing VLA-4 receptor-mediated cell docking in vitro. A rat model of global lipopolysaccharide (LPS)-mediated brain inflammation was used to induce global vascular cell adhesion molecule-1 (VCAM-1) expression. hGPs were infused into the carotid artery in four animal cohorts (consisting of three rats each): rats that received VLA-4-naive hGPs but did not receive LPS, rats that received VLA-4-expressing hGPs but not LPS, rats that received VLA-4-naive hGPs and LPS, and rats that received VLA-4-expressing hGPs and LPS. MR imaging was performed at 9.4 T before and 1, 10, 20, and 30 minutes after injection. Brain tissue was processed for histologic examination. Quantification of low-signal-intensity pixels was performed with pixel-by-pixel analysis for MR images obtained before and after cell injection. RESULTS: With use of the microfluidic adhesion assay, cell binding to activated brain endothelium significantly increased compared with VLA-4-naive control cells (71.5 cells per field of view±11.7 vs 36.4 cells per field of view±3.3, respectively; P<.05). Real-time quantitative in vivo MR cell tracking revealed that VLA-4-expressing cells docked exclusively within the vascular bed of the ipsilateral carotid artery and that VLA-4-expressing cells exhibited significantly enhanced homing as compared with VLA-4-naive cells (1448 significant pixels±366.5 vs 113.3 significant pixels±19.88, respectively; P<.05). Furthermore, MR cell tracking was crucial for correct cell delivery and proper ligation of specific arteries. CONCLUSION: Targeted intraarterial delivery and homing of VLA-4-expressing hGPs to inflamed endothelium is feasible and can be monitored in real time by using MR imaging in a quantitative, dynamic manner.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Rastreamento de Células/métodos
Integrina alfa4beta1/metabolismo
Imagem por Ressonância Magnética/métodos
Neuroglia/metabolismo
Receptores de Antígeno muito Tardio/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Encéfalo/citologia
Artérias Carótidas
Adesão Celular
Meios de Contraste/farmacologia
Dextranos/farmacologia
Expressão Gênica
Seres Humanos
Processamento de Imagem Assistida por Computador
Integrina alfa4beta1/genética
Lipopolissacarídeos
Nanopartículas de Magnetita
Microfluídica
Microscopia de Fluorescência
Ratos
Receptores de Antígeno muito Tardio/genética
Rodaminas/farmacologia
Transfecção
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Contrast Media); 0 (Dextrans); 0 (Integrin alpha4beta1); 0 (Lipopolysaccharides); 0 (Magnetite Nanoparticles); 0 (Receptors, Very Late Antigen); 0 (Rhodamines); 0 (Vascular Cell Adhesion Molecule-1); G6N3J05W84 (ferumoxides)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120828
[St] Status:MEDLINE


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[PMID]:22889880
[Au] Autor:Cheng H; Mollica MY; Lee SH; Wang L; Velázquez-Martínez CA; Wu S
[Ad] Endereço:Edison Biotechnology Institute, Ohio University, Athens, OH 45701, USA.
[Ti] Título:Effects of nitric oxide-releasing nonsteroidal anti-inflammatory drugs (NONO-NSAIDs) on melanoma cell adhesion.
[So] Source:Toxicol Appl Pharmacol;264(2):161-6, 2012 Oct 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A new class of nitric oxide (NO•)-releasing nonsteroidal anti-inflammatory drugs (NONO-NSAIDs) were developed in recent years and have shown promising potential as NSAID substitutes due to their gentle nature on cardiovascular and gastrointestinal systems. Since nitric oxide plays a role in regulation of cell adhesion, we assessed the potential use of NONO-NSAIDs as anti-metastasis drugs. In this regard, we compared the effects of NONO-aspirin and a novel NONO-naproxen to those exerted by their respective parent NSAIDs on avidities of human melanoma M624 cells. Both NONO-NSAIDs, but not the corresponding parent NSAIDs, reduced M624 adhesion on vascular cellular adhesion molecule-1 (VCAM-1) by 20-30% and fibronectin by 25-44% under fluid flow conditions and static conditions, respectively. Only NONO-naproxen reduced (~56%) the activity of ß1 integrin, which binds to α4 integrin to form very late antigen-4 (VLA-4), the ligand of VCAM-1. These results indicate that the diazeniumdiolate (NO•)-donor moiety is critical for reducing the adhesion between VLA-4 and its ligands, while the NSAID moiety can impact the regulation mechanism of melanoma cell adhesion.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Adesão Celular/efeitos dos fármacos
Melanoma/patologia
Doadores de Óxido Nítrico/farmacologia
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Aspirina/farmacologia
Compostos Azo/farmacologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Fibronectinas/metabolismo
Citometria de Fluxo
Seres Humanos
Integrinas/biossíntese
Naproxeno/farmacologia
Metástase Neoplásica/prevenção & controle
Receptores de Antígeno muito Tardio/efeitos dos fármacos
Molécula 1 de Adesão de Célula Vascular/metabolismo
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Azo Compounds); 0 (Fibronectins); 0 (Integrins); 0 (Nitric Oxide Donors); 0 (Receptors, Very Late Antigen); 0 (Vascular Cell Adhesion Molecule-1); 0 (diazeniumdiolate); 31C4KY9ESH (Nitric Oxide); 57Y76R9ATQ (Naproxen); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:161207
[Lr] Data última revisão:
161207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120815
[St] Status:MEDLINE


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[PMID]:18242984
[Au] Autor:Chang LL; Yang GX; McCauley E; Mumford RA; Schmidt JA; Hagmann WK
[Ad] Endereço:Department of Medicinal Chemical Research, Merck Research Laboratories, Rahway, NJ, USA. linda_chang@merck.com
[Ti] Título:Constraining the amide bond in N-sulfonylated dipeptide VLA-4 antagonists.
[So] Source:Bioorg Med Chem Lett;18(5):1688-91, 2008 Mar 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The integrin VLA-4 is implicated in several inflammatory disease states. In search of non-peptidic antagonists of VLA-4, rotational constraints were imposed on the amide bond of prototypical N-sulfonylated dipeptide VLA-4 antagonists. By judicious structural modification of the side chains, trisubstituted imidazoles with moderate binding potencies were obtained, for example, 19, VLA-4 IC(50)=237 nM.
[Mh] Termos MeSH primário: Dipeptídeos/química
Dipeptídeos/farmacologia
Integrina alfa4beta1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Estrutura Molecular
Receptores de Antígeno muito Tardio/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptides); 0 (Integrin alpha4beta1); 0 (Receptors, Very Late Antigen)
[Em] Mês de entrada:0805
[Cu] Atualização por classe:080310
[Lr] Data última revisão:
080310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080205
[St] Status:MEDLINE
[do] DOI:10.1016/j.bmcl.2008.01.045


  5 / 580 MEDLINE  
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[PMID]:17331499
[Au] Autor:Pec MK; Artwohl M; Fernández JJ; Souto ML; Alvarez de la Rosa D; Giraldez T; Valenzuela-Fernández A; Díaz-González F
[Ad] Endereço:Servicio de Reumatología, Hospital Universitario de Canarias, C/Ofra s/n, La Cuesta, 38320 La Laguna, Santa Cruz de Tenerife, Spain.
[Ti] Título:Chemical modulation of VLA integrin affinity in human breast cancer cells.
[So] Source:Exp Cell Res;313(6):1121-34, 2007 Apr 01.
[Is] ISSN:0014-4827
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The fact that disruption of integrin-extracellular matrix contacts leads to cell death, has converted cell adhesion into a potential target for the control of invasive cancer. In this work, we studied the functional consequences of the interference with the activity of the very late activation antigen (VLA) family of integrins in human breast cancer cell lines of distinct malignancy. The alpha2beta1-mediated adhesion reduced the entry of highly malignant, hormone-independent breast cancer cells into apoptosis. Adhesion of breast cancer cells through the VLA integrins alpha2beta1 and alpha5beta1 was significantly reduced by an apoptosis-inducing natural triterpenoid, dehydrothyrsiferol (DT), when studied on low amounts of extracellular matrix. This effect was dose-dependent, not related to cell toxicity and not shared with apoptosis-inducing standard chemotherapeutics, such as doxorubicin and taxol. The compound did not affect either the cell surface expression level of VLA integrins or cell distribution of vinculin and actin during cell spreading. In addition, neither phosphorylation of the focal adhesion kinase pp125FAK on Tyr397 nor the protein kinase B (Akt/PKB) on Ser473 was significantly altered by DT. The integrin activation level, assessed by binding of soluble collagen to the alpha2beta1 integrin, was reduced upon cell treatment with DT. Importantly, the TS2/16, an anti-beta1 activating monoclonal antibody was able to rescue DT-treated cells from apoptosis. Since the activation state of integrins is increasingly recognized as an essential factor in metastasis formation, findings presented herein reveal that the chemical regulation of integrin affinity may be a potential therapeutic strategy in cancer therapy.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Matriz Extracelular/metabolismo
Integrina alfa2beta1/metabolismo
Integrina alfa5beta1/metabolismo
Receptores de Antígeno muito Tardio/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Apoptose
Adesão Celular
Linhagem Celular Tumoral
Matriz Extracelular/fisiologia
Quinase 1 de Adesão Focal/metabolismo
Seres Humanos
Integrina alfa2beta1/fisiologia
Integrina alfa5beta1/fisiologia
Integrinas/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Piranos/farmacologia
Vinculina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Integrin alpha2beta1); 0 (Integrin alpha5beta1); 0 (Integrins); 0 (Pyrans); 0 (Receptors, Very Late Antigen); 0 (dehydrothyrsiferol); 125361-02-6 (Vinculin); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:0705
[Cu] Atualização por classe:121115
[Lr] Data última revisão:
121115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070303
[St] Status:MEDLINE


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[PMID]:16472093
[Au] Autor:Palumbo RN; Wang C
[Ad] Endereço:Department of Biomedical Engineering, University of Minnesota, 7-116 BSBE, 312 Church Street S. E., Minneapolis, MN, USA.
[Ti] Título:Bacterial invasin: structure, function, and implication for targeted oral gene delivery.
[So] Source:Curr Drug Deliv;3(1):47-53, 2006 Jan.
[Is] ISSN:1567-2018
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:The mucosal surface of the gastrointestinal (GI) tract is the first line of defense against foreign pathogens and toxins ingested orally. The content of the GI tract is constantly being sampled by the immune system through specialized epithelial cells known as M-cells, which are present in the Peyer's patches of the gut, providing a thin covering over lymphoid tissue. In this way, once a harmful entity is found an immune response can be activated to eliminate the threat. Many bacterial pathogens, such as Yersinia, Listeria, Salmonella, and Shigella, have evolved ways of exploiting M-cells to gain entrance to the body. The Yersinia species is of particular interest since its extracellular protein invasin provides one of the most direct and efficient manners of host cell invasion. Invasin binds to a subset of beta1 integrin receptors located on the apical membrane of intestinal M-cells, thereby facilitating the bacteria's entry into the cells and the lymphatic system underneath. This mechanism is highly specific and effective, making the invasin protein a very attractive modality for use in the oral delivery of molecules that include therapeutic genes and gene-based vaccines. This article provides a brief overview of the molecular structure and properties of the Yersinia invasin as related to the protein's ability to facilitate binding and entry into M-cells. Also discussed are several innovative approaches that demonstrate the use of invasin as an effective targeting agent for biological and synthetic gene carrier systems, and the future prospect of developing invasin-based oral gene delivery formulations.
[Mh] Termos MeSH primário: Adesinas Bacterianas
Sistemas de Liberação de Medicamentos
Técnicas de Transferência de Genes
Terapia Genética/métodos
[Mh] Termos MeSH secundário: Adesinas Bacterianas/química
Adesinas Bacterianas/metabolismo
Administração Oral
Animais
Células Epiteliais/metabolismo
Células Epiteliais/microbiologia
Mucosa Intestinal/citologia
Mucosa Intestinal/metabolismo
Mucosa Intestinal/microbiologia
Receptores de Antígeno muito Tardio/metabolismo
Yersinia/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adhesins, Bacterial); 0 (Receptors, Very Late Antigen); 114073-91-5 (invasin, Yersinia)
[Em] Mês de entrada:0603
[Cu] Atualização por classe:121115
[Lr] Data última revisão:
121115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060214
[St] Status:MEDLINE


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[PMID]:16120091
[Au] Autor:Diamant Z; Kuperus J; Baan R; Nietzmann K; Millet S; Mendes P; Miller B; Amin D; Rohatagi S; Sterk PJ; Hoogsteden HC; Prins JB
[Ad] Endereço:Erasmus University Medical Centre, Lung Function Lab, Rotterdam, The Netherlands. z.diamant@gems.demon.nl
[Ti] Título:Effect of a very late antigen-4 receptor antagonist on allergen-induced airway responses and inflammation in asthma.
[So] Source:Clin Exp Allergy;35(8):1080-7, 2005 Aug.
[Is] ISSN:0954-7894
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Very late antigen-4 (VLA(4)) plays a key role in the recruitment of eosinophils in allergic responses in animal studies. OBJECTIVE: We investigated whether pretreatment with multiple doses of a VLA(4) receptor antagonist, HMR 1031, protects against allergen-induced airway responses and airway inflammation in humans. METHODS: Fourteen asthmatics (7F/7M), 18-49 years, PC(20) forced expiratory volume in 1 s (FEV(1)) methacholine (M) (<8 mg/mL; FEV(1) 82.3-116.1% predicted) with dual responses to inhaled allergen participated in a double-blind, placebo-controlled, cross-over study. Each treatment period consisted of 9 days, separated by >or=2 weeks. Exhaled nitric oxide (eNO), PC(20)FEV(1)(M) and hypertonic saline-induced sputum was obtained on Days 1, 7 and 9. Subjects inhaled HMR 1031 (20 mg b.i.d.) or placebo (P) on Days 1--8. On Day 8, an allergen bronchoprovocation test was performed, the airway response was measured by FEV(1), and expressed as %fall from baseline. Data from 12 evaluable subjects are presented here. RESULTS: Both treatments were well tolerated. There was no significant difference between HMR 1031 and P in the early asthamatic response: mean AUC (0-3 h)+/-SEM (%fall h): 26.01+/-4.26 and 17.41+/-4.26, respectively (P=0.18), nor in the late response: mean AUC (3-9 h)+/-SEM (%fall h): 97.09+/-8.63 and 97.61+/-8.63, respectively, P=0.97. This corresponded to the absence of significant allergen-induced changes in PC(20)FEV(1)(M), eNO, sputum eosinophils and soluble inflammation markers between both treatment periods. CONCLUSIONS: Treatment with multiple inhaled doses of the VLA(4) antagonist, HMR 1031, did not result in detectable protection against allergen-induced airway responses or airway inflammation in asthma.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Asma/imunologia
Imidazóis/imunologia
Integrina alfa4beta1/imunologia
Propionatos/imunologia
Receptores de Antígeno muito Tardio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Administração por Inalação
Adolescente
Adulto
Brônquios/imunologia
Testes de Provocação Brônquica/métodos
Broncospirometria/métodos
Estudos Cross-Over
Método Duplo-Cego
Feminino
Volume Expiratório Forçado/imunologia
Seres Humanos
Imidazóis/administração & dosagem
Masculino
Cloreto de Metacolina/imunologia
Meia-Idade
Óxido Nítrico/imunologia
Propionatos/administração & dosagem
Receptores de Antígeno muito Tardio/imunologia
Escarro/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 ((3S)-3-(((2S)-2-(4,4-dimethyl-3-(4-((((2-methylphenyl)amino)carbonyl)amino)benzyl)-2,5-dioxoimidazolidin-1-yl)-4-methylpentanoyl)amino)-3-phenylpropanoic acid); 0 (Allergens); 0 (Imidazoles); 0 (Integrin alpha4beta1); 0 (Propionates); 0 (Receptors, Very Late Antigen); 0W5ETF9M2K (Methacholine Chloride); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:0601
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050827
[St] Status:MEDLINE


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[PMID]:22294119
[Au] Autor:Mehlin C
[Ad] Endereço:University of Washington, Seattle, Washington, USA.
[Ti] Título:Measurement of VLA-4/CS-1 and VLA-4/VCAM adhesion inhibition.
[So] Source:Curr Protoc Pharmacol;Chapter 12:Unit 12.7, 2004 May 01.
[Is] ISSN:1934-8290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell adhesion, a critical early step in the inflammatory process, has increasingly become the target of drug discovery efforts. Described in this unit are techniques for measuring inhibitors of VLA-4-mediated adhesion to either VCAM or the connecting segment (CS-1) of fibronectin.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Integrina alfa4beta1/antagonistas & inibidores
Receptores de Antígeno muito Tardio/fisiologia
Molécula 1 de Adesão de Célula Vascular/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Transformada
Linhagem Celular Tumoral
Cloretos/farmacologia
Coleta de Dados
Fibronectinas/metabolismo
Seres Humanos
Compostos de Manganês/farmacologia
Manejo de Espécimes/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Fibronectins); 0 (Integrin alpha4beta1); 0 (Manganese Compounds); 0 (Receptors, Very Late Antigen); 0 (Vascular Cell Adhesion Molecule-1); QQE170PANO (manganese chloride)
[Em] Mês de entrada:1203
[Cu] Atualização por classe:161021
[Lr] Data última revisão:
161021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120202
[St] Status:MEDLINE
[do] DOI:10.1002/0471141755.ph1207s24


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[PMID]:15553848
[Au] Autor:Fu B; Wu Z; Dong C; Qin J
[Ad] Endereço:Key lab of Biomechanics & Tissue Engineering College of Bioengineering under Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, China.
[Ti] Título:[Integrin beta1 mediates hepatocellular carcinoma cells adhesion & chemotaxis to type IV collagen].
[So] Source:Sheng Wu Yi Xue Gong Cheng Xue Za Zhi;21(5):741-5, 2004 Oct.
[Is] ISSN:1001-5515
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:A micropipette technique was adopted to investigate the effect of blockade of integrin betal on adhesion of hepatocellular carcinoma (HCC) cells onto type IV collagen (Col IV) coated surfaces and pseudopod protrusion of HCC cells in response to Col IV stimulation. Adhesion strength was expressed as an adhesion force, which was defined as the product of the cross sectional area and critical negative pressure needed to detach single cell away from the substrate. Chemotactic pseudopod protrusion of an HCC cell was evaluated using a dual-pipette set-up, in which two pipettes filled with Col IV solution were positional in close contact with the same cell and pseudopod protrusion into each pipette was viewed dynamically and recorded with a tape recorder. The lengths of pseudopods were measured and plotted against time to obtain a pseudopod growth curve. The integrin beta1 subunit on the surfaces of HCC cells was analyzed by flow cytometry. The results showed that the adhesion forces for HCC cells adhering on 5 microg/ml Col IV coated surfaces were 932 +/- 134 (x 10(-10) N, n = 60). Upon treatment of HCC cells with Anti-CD29 in a protein concentration of 5 microg/ml and 10 microg/ml, the value decreased significantly to 449 +/- 119 (x 10(-10) N, n = 60) and 220 +/- 78 (x 10(-10) N, n = 55), respectively. In dual pipette chemotaxis experiment, when the two pipettes were filled with Col IV in an identical concentration of 600 microg/ml, pseudopods extended from the HCC cell into each of the pipettes nearly symmetrically, i.e., with nearly identical maximum pseudopod length and similar pseudopod growth curves. Upon addition of Anti-CD29 to one of the pipettes in a protein concentration of 20 microg/ml, pseudopod protrusion was blocked nearly completely while protrusion into the opposite pipette became more evidently, with larger maximum length. Expression of integrin beta1 was up to 95.78% to cells chosen in the experiment. These results suggested that integrin beta1 subunit was important constituent receptor subunit for mediating HCC cell adhesion and chemotactic pseudopod protrusion to Col IV.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Quimiotaxia/imunologia
Colágeno Tipo IV/metabolismo
Integrina beta1/biossíntese
Neoplasias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/farmacologia
Carcinoma Hepatocelular/patologia
Adesão Celular
Seres Humanos
Integrina beta1/imunologia
Neoplasias Hepáticas/patologia
Invasividade Neoplásica
Receptores de Antígeno muito Tardio/biossíntese
Receptores de Antígeno muito Tardio/imunologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Collagen Type IV); 0 (Integrin beta1); 0 (Receptors, Very Late Antigen)
[Em] Mês de entrada:0511
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:041124
[St] Status:MEDLINE


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[PMID]:15098200
[Au] Autor:Crofts F; Rohatagi S; Pino M; DeLise B; Zhang J; Nguyen M; Guittin P; Barbellion S; Brunel P; Hofmann T; Schmidt J; Wong M; Lockey P; Lerman S; Clark R
[Ad] Endereço:Department of Drug Safety Evaluation, Aventis Inc., Bridgewater, New Jersey 08807, USA. Frances.Crofts@aventis.com
[Ti] Título:Critical period for a teratogenic VLA-4 antagonist: Developmental effects and comparison of embryo drug concentrations of teratogenic and non-teratogenic VLA-4 antagonists.
[So] Source:Birth Defects Res B Dev Reprod Toxicol;71(2):69-79, 2004 Apr.
[Is] ISSN:1542-9733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Integrins such as VLA-4 (Very late antigen 4, integrin alpha4beta1) play key roles in cell-cell interactions that are critical for development. Homozygous null knockouts of the VLA-4 alpha4-subunit or VCAM-1 (VLA-4 cell surface ligand) in mice result in failure of the allantois and chorion to fuse leading to interrupted placentation and cardiac development and embryo lethality. Embryo-fetal studies of three VLA-4 antagonists, IVL745, IVL984, and HMR1031 [Crofts et al., Birth Defects Res B 71:55-68 (this issue), 2004] with exposure on gestation days (GD) 6-17 (rat), 6-18 (rabbit) or 6-15 (mouse) showed that only IVL984 treatment resulted in embryo lethality and cardiac defects. Objectives of the current study were to determine the critical period for inducing IVL984-related embryo-fetal effects, and to test the hypothesis that these effects were due to higher embryo drug concentrations. METHODS: IVL984 was administered at 40 mg/kg/day to pregnant rats on GD 4 and 5, GD 6 and 7, GD 8 and 9, GD 10 and 11, or GD 12 and 13. Animals were euthanized on GD 21 and uteri and fetuses were examined. A treatment period of GD 10-12 was selected for subsequent toxicokinetic (TK) studies in which IVL984, HMR1031, or IVL745 was administered to pregnant rats and rabbits. On GD 12, maternal plasma, extra-embryonic tissue (placenta and amniotic fluid), and embryonic tissue were collected and analyzed for drug concentrations. RESULTS: In the IVL984 critical period study in pregnant rats, treatment on GD 10 and 11 resulted in increased post-implantation loss, skeletal variations, and spiral septal defects similar to those observed in standard embryo-fetal development studies with treatment throughout organogenesis. There were no embryo-fetal effects after treatment on GD 4 and 5, GD 6 and 7, or GD 8 and 9. There was a single aorta malformation after treatment on GD 12 and 13. In the TK studies, IVL745, HMR1031, and IVL984 were all detectable in embryonic tissue and there was no evidence for accumulation. Rat and rabbit embryo exposures (AUC or dose-adjusted AUC) on GD 12 could not explain the observed teratology (IVL984
[Mh] Termos MeSH primário: Anormalidades Induzidas por Medicamentos
Embrião de Mamíferos/efeitos dos fármacos
Desenvolvimento Embrionário/efeitos dos fármacos
Imidazóis/toxicidade
Integrina alfa4beta1/antagonistas & inibidores
Fenilalanina/análogos & derivados
Fenilalanina/toxicidade
Compostos de Fenilureia/toxicidade
Propionatos/toxicidade
Teratogênios
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aorta/embriologia
Área Sob a Curva
Derivados de Benzeno
Adesão Celular
Linhagem Celular
Córion/efeitos dos fármacos
Relação Dose-Resposta a Droga
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos
Feminino
Coração/efeitos dos fármacos
Seres Humanos
Concentração Inibidora 50
Integrina alfa4beta1/metabolismo
Exposição Materna
Troca Materno-Fetal
Modelos Químicos
Gravidez
Prenhez
Ligação Proteica
Coelhos
Ratos
Ratos Sprague-Dawley
Receptores de Antígeno muito Tardio/metabolismo
Especificidade da Espécie
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((3S)-3-(((2S)-2-(4,4-dimethyl-3-(4-((((2-methylphenyl)amino)carbonyl)amino)benzyl)-2,5-dioxoimidazolidin-1-yl)-4-methylpentanoyl)amino)-3-phenylpropanoic acid); 0 (3-(N-(3,4-dimethoxybenzyl)-2-(2-(3-methoxy-4-(3-o-tolylureido)phenyl)acetylamino)acetamido)propanoic acid); 0 (Benzene Derivatives); 0 (IVL 984); 0 (Imidazoles); 0 (Integrin alpha4beta1); 0 (Phenylurea Compounds); 0 (Propionates); 0 (Receptors, Very Late Antigen); 0 (Teratogens); 47E5O17Y3R (Phenylalanine)
[Em] Mês de entrada:0412
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040421
[St] Status:MEDLINE



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