Base de dados : MEDLINE
Pesquisa : G03.143.962 [Categoria DeCS]
Referências encontradas : 333 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 34 ir para página                         

  1 / 333 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28920924
[Au] Autor:Kim J; Park DY; Bae H; Park DY; Kim D; Lee CK; Song S; Chung TY; Lim DH; Kubota Y; Hong YK; He Y; Augustin HG; Oliver G; Koh GY
[Ad] Endereço:Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
[Ti] Título:Impaired angiopoietin/Tie2 signaling compromises Schlemm's canal integrity and induces glaucoma.
[So] Source:J Clin Invest;127(10):3877-3896, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary open-angle glaucoma (POAG) is often caused by elevated intraocular pressure (IOP), which arises due to increased resistance to aqueous humor outflow (AHO). Aqueous humor flows through Schlemm's canal (SC), a lymphatic-like vessel encircling the cornea, and via intercellular spaces of ciliary muscle cells. However, the mechanisms underlying increased AHO resistance are poorly understood. Here, we demonstrate that signaling between angiopoietin (Angpt) and the Angpt receptor Tie2, which is critical for SC formation, is also indispensable for maintaining SC integrity during adulthood. Deletion of Angpt1/Angpt2 or Tie2 in adult mice severely impaired SC integrity and transcytosis, leading to elevated IOP, retinal neuron damage, and impairment of retinal ganglion cell function, all hallmarks of POAG in humans. We found that SC integrity is maintained by interconnected and coordinated functions of Angpt-Tie2 signaling, AHO, and Prox1 activity. These functions diminish in the SC during aging, leading to impaired integrity and transcytosis. Intriguingly, Tie2 reactivation using a Tie2 agonistic antibody rescued the POAG phenotype in Angpt1/Angpt2-deficient mice and rejuvenated the SC in aged mice. These results indicate that the Angpt-Tie2 system is essential for SC integrity. The impairment of this system underlies POAG-associated pathogenesis, supporting the possibility that Tie2 agonists could be a therapeutic option for glaucoma.
[Mh] Termos MeSH primário: Angiopoietina-1/metabolismo
Angiopoietina-2/metabolismo
Córnea/metabolismo
Glaucoma de Ângulo Aberto/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Angiopoietina-1/genética
Angiopoietina-2/genética
Animais
Córnea/irrigação sanguínea
Córnea/patologia
Feminino
Glaucoma de Ângulo Aberto/genética
Glaucoma de Ângulo Aberto/patologia
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Transcitose/genética
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPT1 protein, human); 0 (ANGPT2 protein, human); 0 (Angiopoietin-1); 0 (Angiopoietin-2); 0 (Angpt1 protein, mouse); 0 (Homeodomain Proteins); 0 (Tumor Suppressor Proteins); 0 (prospero-related homeobox 1 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


  2 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28919207
[Au] Autor:Yamashita N; Joshi R; Zhang S; Zhang ZY; Kuruvilla R
[Ad] Endereço:Department of Biology, Johns Hopkins University, 3400 N. Charles St, 227 Mudd Hall, Baltimore, MD 21218, USA.
[Ti] Título:Phospho-Regulation of Soma-to-Axon Transcytosis of Neurotrophin Receptors.
[So] Source:Dev Cell;42(6):626-639.e5, 2017 Sep 25.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Axonal targeting of signaling receptors is essential for neuronal responses to extracellular cues. Here, we report that retrograde signaling by target-derived nerve growth factor (NGF) is necessary for soma-to-axon transcytosis of TrkA receptors in sympathetic neurons, and we define the molecular underpinnings of this positive feedback regulation that enhances neuronal sensitivity to trophic factors. Activated TrkA receptors are retrogradely transported in signaling endosomes from distal axons to cell bodies, where they are inserted on soma surfaces and promote phosphorylation of resident naive receptors, resulting in their internalization. Endocytosed TrkA receptors are then dephosphorylated by PTP1B, an ER-resident protein tyrosine phosphatase, prior to axonal transport. PTP1B inactivation prevents TrkA exit from soma and causes receptor degradation, suggesting a "gatekeeper" mechanism that ensures targeting of inactive receptors to axons to engage with ligand. In mice, PTP1B deletion reduces axonal TrkA levels and attenuates neuron survival and target innervation under limiting NGF (NGF ) conditions.
[Mh] Termos MeSH primário: Axônios/metabolismo
Receptores de Fator de Crescimento Neural/metabolismo
Transcitose
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Corpo Celular/efeitos dos fármacos
Corpo Celular/metabolismo
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/metabolismo
Deleção de Genes
Células HEK293
Seres Humanos
Lisossomos/efeitos dos fármacos
Lisossomos/metabolismo
Camundongos
Fatores de Crescimento Neural/farmacologia
Fosforilação/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Proteína Tirosina Fosfatase não Receptora Tipo 1/metabolismo
Proteólise/efeitos dos fármacos
Ratos Sprague-Dawley
Transcitose/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nerve Growth Factors); 0 (Receptors, Nerve Growth Factor); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1); EC 3.1.3.48 (Ptpn1 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


  3 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28617450
[Au] Autor:Beloqui A; Brayden DJ; Artursson P; Préat V; des Rieux A
[Ad] Endereço:Department of Advanced Drug Delivery and Biomaterials, Louvain Drug Research Institute, Université catholique de Louvain, Brussels, Belgium.
[Ti] Título:A human intestinal M-cell-like model for investigating particle, antigen and microorganism translocation.
[So] Source:Nat Protoc;12(7):1387-1399, 2017 Jul.
[Is] ISSN:1750-2799
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The specialized microfold cells (M cells) in the follicle-associated epithelium (FAE) of intestinal Peyer's patches serve as antigen-sampling cells of the intestinal innate immune system. Unlike 'classical' enterocytes, they are able to translocate diverse particulates without digesting them. They act as pathways for microorganism invasion and mediate food tolerance by transcellular transport of intestinal microbiota and antigens. Their ability to transcytose intact particles can be used to develop oral drug delivery and oral immunization strategies. This protocol describes a reproducible and versatile human M-cell-like in vitro model. This model can be exploited to evaluate M-cell transport of microparticles and nanoparticles for protein, drug or vaccine delivery and to study bacterial adherence and translocation across M cells. The inverted in vitro M-cell model consists of three main steps. First, Caco-2 cells are seeded at the apical side of the inserts. Second, the inserts are inverted and B lymphocytes are seeded at the basolateral side of the inserts. Third, the conversion to M cells is assessed. Although various M-cell culture systems exist, this model provides several advantages over the rest: (i) it is based on coculture with well-established differentiated human cell lines; (ii) it is reproducible under the conditions described herein; (iii) it can be easily mastered; and (iv) it does not require the isolation of primary cells or the use of animals. The protocol requires skills in cell culture and microscopy analysis. The model is obtained after 3 weeks, and transport experiments across the differentiated model can be carried out over periods of up to 10 h.
[Mh] Termos MeSH primário: Antígenos/metabolismo
Técnicas Citológicas/métodos
Células Epiteliais/fisiologia
Material Particulado/metabolismo
Nódulos Linfáticos Agregados/citologia
Transcitose
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Particulate Matter)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1038/nprot.2017.041


  4 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28501799
[Au] Autor:Lisney AR; Szelinski F; Reiter K; Burmester GR; Rose T; Dörner T
[Ad] Endereço:Department of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Título:High maternal expression of SIGLEC1 on monocytes as a surrogate marker of a type I interferon signature is a risk factor for the development of autoimmune congenital heart block.
[So] Source:Ann Rheum Dis;76(8):1476-1480, 2017 Aug.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Autoimmune congenital heart block (CHB) is associated with placental transcytosis of maternal autoantibodies directed against Ro/SS-A and La/SS-B. However, only about 2% of children born to mothers with the respective antibodies are affected, indicating that further risk factors exist, which are not yet fully understood. In this study, we investigated whether a maternal type I interferon (IFN) signature represents a risk factor for the development of CHB. METHODS: Blood samples, clinical data and serological parameters from 9 women with CHB pregnancies, 14 pregnant women with antibodies against Ro/SS-A but without a CHB complication and another 30 healthy pregnant women as controls were studied. SIGLEC1 expression was measured by flow cytometry and was correlated to plasma IFN-α levels measured by ELISA, and IFN-γ-induced protein 10 (IP-10) levels measured by Bio-Plex technique. RESULTS: Mothers of affected children had a significantly higher expression of SIGLEC1 (p=0.0034) and IFN-α (p=0.014), but not of IP-10 (p=0.14, all MWU) compared to mothers of unaffected children. SIGLEC1 and IFN-α expression were reduced by hydroxychloroquine and oral glucocorticoids. CONCLUSIONS: High expression of SIGLEC1 in pregnant women with autoantibodies against Ro/SS-A indicates an enhanced risk for CHB development, and these women may benefit especially from IFN-α directed therapy, for example with hydroxychloroquine.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Quimiocina CXCL10/imunologia
Bloqueio Cardíaco/congênito
Interferon-alfa/imunologia
Troca Materno-Fetal/imunologia
Monócitos/imunologia
Complicações na Gravidez/imunologia
Lectina 1 Semelhante a Ig de Ligação ao Ácido Siálico/imunologia
[Mh] Termos MeSH secundário: Adulto
Anticorpos Antinucleares/imunologia
Antirreumáticos/uso terapêutico
Doenças Autoimunes/epidemiologia
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Glucocorticoides/uso terapêutico
Bloqueio Cardíaco/epidemiologia
Bloqueio Cardíaco/imunologia
Seres Humanos
Hidroxicloroquina/uso terapêutico
Recém-Nascido
Interferon Tipo I/imunologia
Lúpus Eritematoso Sistêmico/tratamento farmacológico
Lúpus Eritematoso Sistêmico/epidemiologia
Lúpus Eritematoso Sistêmico/imunologia
Gravidez
Complicações na Gravidez/tratamento farmacológico
Complicações na Gravidez/epidemiologia
Fatores de Risco
Síndrome de Sjogren/tratamento farmacológico
Síndrome de Sjogren/epidemiologia
Síndrome de Sjogren/imunologia
Transcitose
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Antirheumatic Agents); 0 (Chemokine CXCL10); 0 (Glucocorticoids); 0 (Interferon Type I); 0 (Interferon-alpha); 0 (SIGLEC1 protein, human); 0 (SS-A antibodies); 0 (SS-B antibodies); 0 (Sialic Acid Binding Ig-like Lectin 1); 4QWG6N8QKH (Hydroxychloroquine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170515
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-210927


  5 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28416077
[Au] Autor:Andreone BJ; Chow BW; Tata A; Lacoste B; Ben-Zvi A; Bullock K; Deik AA; Ginty DD; Clish CB; Gu C
[Ad] Endereço:Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
[Ti] Título:Blood-Brain Barrier Permeability Is Regulated by Lipid Transport-Dependent Suppression of Caveolae-Mediated Transcytosis.
[So] Source:Neuron;94(3):581-594.e5, 2017 May 03.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The blood-brain barrier (BBB) provides a constant homeostatic brain environment that is essential for proper neural function. An unusually low rate of vesicular transport (transcytosis) has been identified as one of the two unique properties of CNS endothelial cells, relative to peripheral endothelial cells, that maintain the restrictive quality of the BBB. However, it is not known how this low rate of transcytosis is achieved. Here we provide a mechanism whereby the regulation of CNS endothelial cell lipid composition specifically inhibits the caveolae-mediated transcytotic route readily used in the periphery. An unbiased lipidomic analysis reveals significant differences in endothelial cell lipid signatures from the CNS and periphery, which underlie a suppression of caveolae vesicle formation and trafficking in brain endothelial cells. Furthermore, lipids transported by Mfsd2a establish a unique lipid environment that inhibits caveolae vesicle formation in CNS endothelial cells to suppress transcytosis and ensure BBB integrity.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/metabolismo
Cavéolas/metabolismo
Metabolismo dos Lipídeos/genética
Proteínas de Membrana Transportadoras/genética
Transcitose/genética
[Mh] Termos MeSH secundário: Animais
Barreira Hematoencefálica/ultraestrutura
Western Blotting
Cavéolas/ultraestrutura
Células Endoteliais
Células HEK293
Seres Humanos
Imuno-Histoquímica
Proteínas de Membrana Transportadoras/metabolismo
Camundongos
Camundongos Knockout
Microscopia Confocal
Microscopia Eletrônica de Transmissão
Permeabilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (Mfsd2a protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE


  6 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28414297
[Au] Autor:Liu X; Lin P; Perrett I; Lin J; Liao YP; Chang CH; Jiang J; Wu N; Donahue T; Wainberg Z; Nel AE; Meng H
[Ti] Título:Tumor-penetrating peptide enhances transcytosis of silicasome-based chemotherapy for pancreatic cancer.
[So] Source:J Clin Invest;127(5):2007-2018, 2017 May 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic ductal adenocarcinoma (PDAC) is almost uniformly fatal; however, some improvement in overall survival has been achieved with the introduction of nanocarriers that deliver irinotecan or paclitaxel. Although it is generally assumed that nanocarriers rely principally on abnormal leaky vasculature for tumor access, a transcytosis transport pathway that is regulated by neuropilin-1 (NRP-1) has recently been reported. NRP-1-mediated transport can be triggered by the cyclic tumor-penetrating peptide iRGD. In a KRAS-induced orthotopic PDAC model, coadministration of iRGD enhanced the uptake of an irinotecan-loaded silicasome carrier that comprises lipid bilayer-coated mesoporous silica nanoparticles (MSNPs); this uptake resulted in enhanced survival and markedly reduced metastasis. Further, ultrastructural imaging of the treated tumors revealed that iRGD coadministration induced a vesicular transport pathway that carried Au-labeled silicacomes from the blood vessel lumen to a perinuclear site within cancer cells. iRGD-mediated enhancement of silicasome uptake was also observed in patient-derived xenografts, commensurate with the level of NRP-1 expression on tumor blood vessels. These results demonstrate that iRGD enhances the efficacy of irinotecan-loaded silicasome-based therapy and may be a suitable adjuvant in nanoparticle-based treatments for PDAC.
[Mh] Termos MeSH primário: Antineoplásicos
Camptotecina/análogos & derivados
Carcinoma Ductal Pancreático
Nanopartículas
Neoplasias Experimentais
Oligopeptídeos
Dióxido de Silício
Transcitose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacocinética
Antineoplásicos/farmacologia
Camptotecina/química
Camptotecina/farmacocinética
Camptotecina/farmacologia
Carcinoma Ductal Pancreático/tratamento farmacológico
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/patologia
Seres Humanos
Camundongos
Nanopartículas/química
Nanopartículas/uso terapêutico
Metástase Neoplásica
Neoplasias Experimentais/tratamento farmacológico
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/patologia
Oligopeptídeos/química
Oligopeptídeos/farmacocinética
Oligopeptídeos/farmacologia
Dióxido de Silício/química
Dióxido de Silício/farmacocinética
Dióxido de Silício/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (N-end cysteine peptide tumor-homing peptide); 0 (Oligopeptides); 7631-86-9 (Silicon Dioxide); 7673326042 (irinotecan); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  7 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28390677
[Au] Autor:Stewart T; Koval WT; Molina SA; Bock SM; Lillard JW; Ross RF; Desai TA; Koval M
[Ad] Endereço:Morehouse School of Medicine, Atlanta, GA, United States; Division of Pulmonary Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University School of Medicine, United States.
[Ti] Título:Calibrated flux measurements reveal a nanostructure-stimulated transcytotic pathway.
[So] Source:Exp Cell Res;355(2):153-161, 2017 Jun 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transport of therapeutic agents across epithelial barriers is an important element in drug delivery. Transepithelial flux is widely used as a measure of transit across an epithelium, however it is most typically employed as a relative as opposed to absolute measure of molecular movement. Here, we have used the calcium switch approach to measure the maximum rate of paracellular flux through unencumbered intercellular junctions as a method to calibrate the flux rates for a series of tracers ranging in 0.6-900kDa in size across barriers composed of human colon epithelial (Caco-2) cells. We then examined the effects of nanostructured films (NSFs) on transepithelial transport. Two different NSF patterns were used, Defined Nanostructure (DN) 2 imprinted on polypropylene (PP) and DN3 imprinted on polyether ether ketone (PEEK). NSFs made direct contact with cells and decreased their barrier function, as measured by transepithelial resistance (TER), however cell viability was not affected. When NSF-induced transepithelial transport of Fab fragment (55kDa) and IgG (160kDa) was measured, it was unexpectedly found to be significantly greater than the maximum paracellular rate as predicted using cells cultured in low calcium. These data suggested that NSFs stimulate an active transport pathway, most likely transcytosis, in addition to increasing paracellular flux. Transport of IgG via transcytosis was confirmed by immunofluorescence confocal microscopy, since NSFs induced a significant level of IgG endocytosis by Caco-2 cells. Thus, NSF-induced IgG flux was attributable to both transcytosis and the paracellular route. These data provide the first demonstration that transcytosis can be stimulated by NSFs and that this was concurrent with increased paracellular permeability. Moreover, NSFs with distinct architecture paired with specific substrates have the potential to provide an effective means to regulate transepithelial transport in order to optimize drug delivery.
[Mh] Termos MeSH primário: Células Epiteliais/efeitos dos fármacos
Epitélio/efeitos dos fármacos
Epitélio/metabolismo
Nanoestruturas/química
Transcitose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células CACO-2
Linhagem Celular Tumoral
Sistemas de Liberação de Medicamentos
Seres Humanos
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170410
[St] Status:MEDLINE


  8 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28334606
[Au] Autor:Chow BW; Gu C
[Ad] Endereço:Department of Neurobiology, Harvard Medical School, 220 Longwood Ave., Boston, MA 02115, USA.
[Ti] Título:Gradual Suppression of Transcytosis Governs Functional Blood-Retinal Barrier Formation.
[So] Source:Neuron;93(6):1325-1333.e3, 2017 Mar 22.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Blood-central nervous system (CNS) barriers partition neural tissues from the blood, providing a homeostatic environment for proper neural function. The endothelial cells that form blood-CNS barriers have specialized tight junctions and low rates of transcytosis to limit the flux of substances between blood and CNS. However, the relative contributions of these properties to CNS barrier permeability are unknown. Here, by studying functional blood-retinal barrier (BRB) formation in mice, we found that immature vessel leakage occurs entirely through transcytosis, as specialized tight junctions are functional as early as vessel entry into the CNS. A functional barrier forms only when transcytosis is gradually suppressed during development. Mutant mice with elevated or reduced levels of transcytosis have delayed or precocious sealing of the BRB, respectively. Therefore, the temporal regulation of transcytosis governs the development of a functional BRB, and suppression of transcytosis is a principal contributor for functional barrier formation.
[Mh] Termos MeSH primário: Barreira Hematorretiniana/crescimento & desenvolvimento
Transcitose/fisiologia
[Mh] Termos MeSH secundário: Animais
Barreira Hematorretiniana/ultraestrutura
Caveolina 1/genética
Caveolina 1/fisiologia
Células Endoteliais/fisiologia
Feminino
Masculino
Proteínas de Membrana Transportadoras/biossíntese
Proteínas de Membrana Transportadoras/genética
Proteínas de Membrana Transportadoras/fisiologia
Camundongos
Camundongos Knockout
Junções Íntimas/genética
Junções Íntimas/fisiologia
Transcitose/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolin 1); 0 (Membrane Transport Proteins); 0 (Mfsd2a protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE


  9 / 333 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28241053
[Au] Autor:Yasen A; Herrera R; Rosbe K; Lien K; Tugizov SM
[Ad] Endereço:Department of Medicine, University of California-San Francisco, San Francisco, California, United States of America.
[Ti] Título:Release of HIV-1 sequestered in the vesicles of oral and genital mucosal epithelial cells by epithelial-lymphocyte interaction.
[So] Source:PLoS Pathog;13(2):e1006247, 2017 Feb.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oropharyngeal mucosal epithelia of fetuses/neonates/infants and the genital epithelia of adults play a critical role in HIV-1 mother-to-child transmission and sexual transmission of virus, respectively. To study the mechanisms of HIV-1 transmission through mucosal epithelium, we established polarized tonsil, cervical and foreskin epithelial cells. Analysis of HIV-1 transmission through epithelial cells showed that approximately 0.05% of initially inoculated virions transmigrated via epithelium. More than 90% of internalized virions were sequestered in the endosomes of epithelial cells, including multivesicular bodies (MVBs) and vacuoles. Intraepithelial HIV-1 remained infectious for 9 days without viral release. Release of sequestered intraepithelial HIV-1 was induced by the calcium ionophore ionomycin and by cytochalasin D, which increase intracellular calcium and disrupt the cortical actin of epithelial cells, respectively. Cocultivation of epithelial cells containing HIV-1 with activated peripheral blood mononuclear cells and CD4+ T lymphocytes led to the disruption of epithelial cortical actin and spread of virus from epithelial cells to lymphocytes. Treatment of epithelial cells with proinflammatory cytokines tumor necrosis factor-alpha and interferon gamma also induced reorganization of cortical actin and release of virus. Inhibition of MVB formation by small interfering RNA (siRNA)-mediated silencing of its critical protein hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs) expression reduced viral sequestration in epithelial cells and its transmission from epithelial cells to lymphocytes by ~60-70%. Furthermore, inhibition of vacuole formation of epithelial cells by siRNA-inactivated rabankyrin-5 expression also significantly reduced HIV-1 sequestration in epithelial cells and spread of virus from epithelial cells to lymphocytes. Interaction of the intercellular adhesion molecule-1 of epithelial cells with the function-associated antigen-1 of lymphocytes was important for inducing the release of sequestered HIV-1 from epithelial cells and facilitating cell-to-cell spread of virus from epithelial cells to lymphocytes. This mechanism may serve as a pathway of HIV-1 mucosal transmission.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/virologia
Células Epiteliais/virologia
Infecções por HIV/transmissão
Membrana Mucosa/virologia
Transcitose/fisiologia
[Mh] Termos MeSH secundário: Western Blotting
Colo do Útero/virologia
Técnicas de Cocultura
Células Dendríticas/virologia
Feminino
Imunofluorescência
Prepúcio do Pênis/virologia
HIV-1
Seres Humanos
Leucócitos Mononucleares/virologia
Macrófagos/virologia
Masculino
Tonsila Palatina/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006247


  10 / 333 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28204818
[Au] Autor:Bian F; Cui J; Zheng T; Jin S
[Ad] Endereço:Department of Pharmacy, The Affiliated Hospital of Xiangyang Central Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441000, P.R. China.
[Ti] Título:Reactive oxygen species mediate angiotensin II-induced transcytosis of low-density lipoprotein across endothelial cells.
[So] Source:Int J Mol Med;39(3):629-635, 2017 Mar.
[Is] ISSN:1791-244X
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The retention of plasma low-density lipoprotein (LDL) particles to subendothelial spaces through transcytosis across the endothelium is the initial step of atherosclerosis (AS). Angiotensin II (Ang II), as the principal effector molecule of the renin-angiotensin system (RAS), is implicated in several important steps of AS development. However, whether or not Ang II can directly exert a pro­atherogenic effect by promoting LDL transcytosis across endothelial barriers, has not been defined. In the present study, we found that Ang II upregulated intracellular reactive oxygen species (ROS) levels in endothelial cells (ECs) by measuring fluorescence of 2',7'-dichlorofluorescein (DCF­DA). Based on our transcytosis model, we observed that Ang II significantly accelerated LDL transcytosis, whereas transcytosis inhibitor methyl-ß-cyclodextrin (MßCD) and ROS inhibitor dithiothreitol (DTT), markedly blocked the Ang II-stimulated increase in LDL transcytosis. Confocal imaging analysis revealed that both LDL uptake by cells and LDL retention in human umbilical venous walls were highly elevated after Ang II exposure, while MßCD and DTT significantly inhibited the effects of Ang II. What is more, proteins involved in caveolae-mediated transcytosis, including LDL receptor (LDLR), caveolin-1 and cavin-1, were associated with Ang II-induced LDL transcytosis across the ECs. Nevertheless, this process was independent of clathrin in our study. Of note, ROS inhibitor, DTT, markedly decreased the expression levels of those proteins. Consequently, ROS are critical mediators in Ang II-induced LDL transcytosis. Hopefully, these findings will provide novel insight into the crosstalk between dyslipidemia and RAS in atherogenesis.
[Mh] Termos MeSH primário: Angiotensina II/metabolismo
Células Endoteliais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transcitose
[Mh] Termos MeSH secundário: Angiotensina II/farmacologia
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Lipoproteínas LDL/metabolismo
Transcitose/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoproteins, LDL); 0 (Reactive Oxygen Species); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.3892/ijmm.2017.2887



página 1 de 34 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