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Pesquisa : A03.556.124.369.290 [Categoria DeCS]
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[PMID]:29202487
[Au] Autor:Sarabia-Sainz HM; Mata Haro V; Sarabia Sainz JA; Vázquez-Moreno L; Montfort GR
[Ad] Endereço:Laboratorio de Bioquímica de Proteínas y Glicanos Coordinación de Ciencia de los Alimentos, Centro de Investigación en Alimentación y Desarrollo A.C., Hermosillo, Sonora 83304, México.
[Ti] Título:Maillard neoglycans as inhibitors for in vitro adhesion of F4 enterotoxigenic Escherichia coli to piglet intestinal cells.
[So] Source:Acta Biochim Pol;64(4):679-686, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Adhesion of enterotoxigenic (ETEC) E. coli to host intestinal cells is mediated by lectin-like fimbriae that bind to specific glycan moieties on the surfaces of enterocytes. To prevent in vitro binding of E. coli F4 fimbriae (F4 ETEC ) to piglet enterocytes, neoglycans were synthesized by the Maillard reaction conjugating lactose (Lac), galacto-oligosaccharides (GOS) or chitin oligosaccharides (Ochit) to porcine serum albumin (PSA). Neoglycans were characterized by SDS-PAGE, intrinsic tryptophan fluorescence and recognition by plant lectins, as well as by F4 ETEC variants. Electrophoretic patterns suggested the binding to PSA of 63, 13 and 2 molecules of Lac, GOS and Ochit, respectively. All neoglycans displayed quenching of tryptophan fluorescence consistent with the degree of glycation estimated by SDS-PAGE. Plant lectins recognized the neoglycans according to their specificity, whereas antigenic variants of F4 ETEC (ab, ac and ad) recognized PSA-Ochit and PSA-Lac with higher affinity than that for GOS. Neoglycans partially hindered the in vitro binding of F4 ETEC to piglet enterocytes in a dose-dependent manner. The most effective blocking was observed with PSA-Lac that partially inhibited the adhesion of bacteria to enterocytes in a dose dependent manner, as quantified by flow cytometry. Increased production of the cytokines IL-6 and TNF-α was observed in response to F4 ETEC infection of enterocytes and production was reduced in the presence of PSA-Ochit and PSA-GOS. These results suggest that neoglycans synthesized by the Maillard reaction could be useful in the prophylaxis of diarrhea in piglets.
[Mh] Termos MeSH primário: Enterócitos/efeitos dos fármacos
Enterócitos/microbiologia
Escherichia coli Enterotoxigênica/efeitos dos fármacos
Polissacarídeos/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antibacterianos/química
Antibacterianos/farmacologia
Aderência Bacteriana/efeitos dos fármacos
Eletroforese em Gel de Poliacrilamida
Escherichia coli Enterotoxigênica/patogenicidade
Infecções por Escherichia coli/tratamento farmacológico
Infecções por Escherichia coli/microbiologia
Infecções por Escherichia coli/veterinária
Produtos Finais de Glicação Avançada/química
Intestinos/citologia
Intestinos/microbiologia
Suínos
Doenças dos Suínos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Glycation End Products, Advanced); 0 (Polysaccharides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_2199


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[PMID]:27771159
[Au] Autor:Schall KA; Holoyda KA; Isani M; Lien CL; Al Alam D; Grikscheit TC
[Ad] Endereço:Division of Pediatric Surgery and Developmental Biology and Regenerative Medicine, Saban Research Institute, Children's Hospital Los Angeles and USC Keck School of Medicine, Los Angeles, CA.
[Ti] Título:Inhibition of Fgf signaling in short bowel syndrome increases weight loss and epithelial proliferation.
[So] Source:Surgery;161(3):694-703, 2017 03.
[Is] ISSN:1532-7361
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Signaling by fibroblast growth factor is critical for epithelial proliferation, differentiation, and the development of many organs, including the intestine. Fibroblast growth factor 10 and fibroblast growth factor 2c are upregulated after massive bowel resection during intestinal adaptation. This pathway is conserved highly. We hypothesized that inhibition of fibroblast growth factor signaling would impair intestinal adaptation in the zebrafish model of short bowel syndrome and allow insight into the negative regulation of this pathway. METHODS: Short bowel syndrome equivalent to a high jejunostomy was generated in adult male hsp70:dnfgfr1-GFP zebrafish, wildtype fish exposed to tyrosine-kinase inhibitor, and wildtype fish in absence of tyrosine-kinase inhibitor. Heat shock in hsp70:dnfgfr1-GFP fish decreases fgf 1 expression. Parameters including weight, proliferation, and differentiation were evaluated after harvest in experimental and control groups. RESULTS: Although short bowel syndrome zebrafish lost more weight relative to sham zebrafish in both groups, heat shock fish with short bowel syndrome lost more weight compared with non-heat shock fish with short bowel syndrome. In the non-heat shock controls, the villus epithelial perimeter increased in short bowel syndrome compared with sham fish, but this did not occur in heat shock fish. Non-heat shock fish with short bowel syndrome fish had significantly increased Bromodeoxyuridine(+) proliferative cells per hemivillus compared with non-heat shock-sham, while heat shock-short bowel syndrome had a more substantial increase in Bromodeoxyuridine(+) cells compared with HS-sham. Non-heat shock-short bowel syndrome demonstrated a significantly increased percentage of Alcian blue(+) goblet cells per hemivillus compared with non-heat shock-sham, while the heat shock-short bowel syndrome demonstrated decreased Alcian blue(+) cells compared with non-heat shock-short bowel syndrome. In contrast, SU5402 inhibited epithelial proliferation while increasing weight loss. CONCLUSION: Inhibition of fibroblast growth factor-1 signaling in short bowel syndrome decreases epithelial adaptation, increases Bromodeoxyuridine-labeled cells at 2 weeks, and exacerbates weight loss while decreasing epithelial goblet cells.
[Mh] Termos MeSH primário: Proliferação Celular/fisiologia
Enterócitos/fisiologia
Fator 1 de Crescimento de Fibroblastos/fisiologia
Síndrome do Intestino Curto/patologia
Perda de Peso/fisiologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Intestino Delgado/metabolismo
Intestino Delgado/patologia
Masculino
Síndrome do Intestino Curto/etiologia
Síndrome do Intestino Curto/metabolismo
Transdução de Sinais/fisiologia
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
104781-85-3 (Fibroblast Growth Factor 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29320535
[Au] Autor:Franz J; Grünebaum J; Schäfer M; Mulac D; Rehfeldt F; Langer K; Kramer A; Riethmüller C
[Ad] Endereço:Faculty of Physics, Georg-August-Universität, Göttingen, Germany.
[Ti] Título:Rhombic organization of microvilli domains found in a cell model of the human intestine.
[So] Source:PLoS One;13(1):e0189970, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Symmetry is rarely found on cellular surfaces. An exception is the brush border of microvilli, which are essential for the proper function of transport epithelia. In a healthy intestine, they appear densely packed as a 2D-hexagonal lattice. For in vitro testing of intestinal transport the cell line Caco-2 has been established. As reported by electron microscopy, their microvilli arrange primarily in clusters developing secondly into a 2D-hexagonal lattice. Here, atomic force microscopy (AFM) was employed under aqueous buffer conditions on Caco-2 cells, which were cultivated on permeable filter membranes for optimum differentiation. For analysis, the exact position of each microvillus was detected by computer vision; subsequent Fourier transformation yielded the type of 2D-lattice. It was confirmed, that Caco-2 cells can build a hexagonal lattice of microvilli and form clusters. Moreover, a second type of arrangement was discovered, namely a rhombic lattice, which appeared at sub-maximal densities of microvilli with (29 ± 4) microvilli / µm2. Altogether, the findings indicate the existence of a yet undescribed pattern in cellular organization.
[Mh] Termos MeSH primário: Enterócitos/ultraestrutura
Microvilosidades/ultraestrutura
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Técnicas de Cultura de Células/instrumentação
Linhagem Celular Tumoral
Neoplasias do Colo/patologia
Análise de Fourier
Seres Humanos
Microscopia de Força Atômica
Microscopia Eletrônica de Varredura
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189970


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[PMID]:27771295
[Au] Autor:Park SH; Yu M; Kim J; Moon Y
[Ad] Endereço:Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences, Medical Research Institute, Pusan National University School of Medicine, Yangsan, 50612, South Korea.
[Ti] Título:C/EBP homologous protein promotes NSAID-activated gene 1-linked pro-inflammatory signals and enterocyte invasion by enteropathogenic Escherichia coli.
[So] Source:Microbes Infect;19(2):110-121, 2017 02.
[Is] ISSN:1769-714X
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:NSAID-activated Gene 1 (NAG-1) is a prognostic indicator of chronic inflammatory diseases and aggressive tumors. Among the stress sentinels in response to infection by enteropathogenic Escherichia coli (EPEC) or other pathogenic E. coli, C/EBP homologous protein (CHOP), a representative stress-regulated transcription factor, was prominently increased and assessed for its involvement in NAG-1-mediated pathogenic cellular responses. NAG-1 expression was transcriptionally upregulated by CHOP, which promoted chemokine production through sustained NF-κB activation. Mechanistically, NF-κB activation by NAG-1 was due to TGFß-activated kinase 1 (TAK-1)-mediated pathway rather than SMAD-associated signals. Moreover, CHOP and subsequent TAK-1-linked signals were also involved in bacterial invasion into human cells. Therefore, CHOP as an infection-induced sentinel played crucial roles in induction of NAG-1 and subsequent prolonged activation of pro-inflammatory responses to EPEC infection or related chronic pathogenic states.
[Mh] Termos MeSH primário: Endocitose
Enterócitos/microbiologia
Escherichia coli Enteropatogênica/patogenicidade
Fator 15 de Diferenciação de Crescimento/metabolismo
Fator de Transcrição CHOP/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GDF15 protein, human); 0 (Growth Differentiation Factor 15); 147336-12-7 (Transcription Factor CHOP)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


  5 / 2616 MEDLINE  
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[PMID]:29197592
[Au] Autor:Bao Q; Li C; Xu C; Zhang R; Zhao K; Duan Z
[Ad] Endereço:Key Laboratory of Adaptation and Evolution of Plateau Biota, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining 810001, China; Laboratory of Plateau Fish Evolutionary and Functional Genomics, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining 810001,
[Ti] Título:Porcine enterocyte protein Btnl5 negatively regulates NF-kappa B pathway by interfering p65 nuclear translocation.
[So] Source:Gene;646:47-55, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Porcine butyrophilin-like 5 (Btnl5) is a novel member of the butyrophilin family, which consists of immune regulators. The expression pattern and the function of this gene remain unclear. In this study, Btnl5 is identified as a negative regulator of the NF-κB pathway. Our study indicates that Btnl5 is mainly expressed in intestinal epithelial cells (IECs) and expressed in membrane systems. Btnl5 inhibits MyD88-mediated activation of the NF-κB pathway. Btnl5 interacts with TNF receptor-associated factor 2 (TRAF2) and transcription factor p65. Besides, Btnl5 inhibits p65-mediated activation of the NF-κB pathway and inhibits nuclear translocation of p65. These results suggest that Btnl5 may inhibit NF-κB pathway through binding and interfere nuclear translocation of p65.
[Mh] Termos MeSH primário: Butirofilinas/metabolismo
Núcleo Celular/metabolismo
Enterócitos/metabolismo
Fator de Transcrição RelA/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Enterócitos/citologia
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Intestino Delgado/metabolismo
Transporte Proteico
Transdução de Sinais
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrophilins); 0 (Transcription Factor RelA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


  6 / 2616 MEDLINE  
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[PMID]:29211815
[Au] Autor:Berger AK; Yi H; Kearns DB; Mainou BA
[Ad] Endereço:Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia, United States of America.
[Ti] Título:Bacteria and bacterial envelope components enhance mammalian reovirus thermostability.
[So] Source:PLoS Pathog;13(12):e1006768, 2017 Dec.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enteric viruses encounter diverse environments as they migrate through the gastrointestinal tract to infect their hosts. The interaction of eukaryotic viruses with members of the host microbiota can greatly impact various aspects of virus biology, including the efficiency with which viruses can infect their hosts. Mammalian orthoreovirus, a human enteric virus that infects most humans during childhood, is negatively affected by antibiotic treatment prior to infection. However, it is not known how components of the host microbiota affect reovirus infectivity. In this study, we show that reovirus virions directly interact with Gram positive and Gram negative bacteria. Reovirus interaction with bacterial cells conveys enhanced virion thermostability that translates into enhanced attachment and infection of cells following an environmental insult. Enhanced virion thermostability was also conveyed by bacterial envelope components lipopolysaccharide (LPS) and peptidoglycan (PG). Lipoteichoic acid and N-acetylglucosamine-containing polysaccharides enhanced virion stability in a serotype-dependent manner. LPS and PG also enhanced the thermostability of an intermediate reovirus particle (ISVP) that is associated with primary infection in the gut. Although LPS and PG alter reovirus thermostability, these bacterial envelope components did not affect reovirus utilization of its proteinaceous cellular receptor junctional adhesion molecule-A or cell entry kinetics. LPS and PG also did not affect the overall number of reovirus capsid proteins σ1 and σ3, suggesting their effect on virion thermostability is not mediated through altering the overall number of major capsid proteins on the virus. Incubation of reovirus with LPS and PG did not significantly affect the neutralizing efficiency of reovirus-specific antibodies. These data suggest that bacteria enhance reovirus infection of the intestinal tract by enhancing the thermal stability of the reovirus particle at a variety of temperatures through interactions between the viral particle and bacterial envelope components.
[Mh] Termos MeSH primário: Bacillus subtilis/fisiologia
Enterócitos/virologia
Escherichia coli K12/fisiologia
Infecções por Reoviridae/virologia
Reoviridae/fisiologia
[Mh] Termos MeSH secundário: Acetilglucosamina/análogos & derivados
Acetilglucosamina/metabolismo
Acetilglucosamina/toxicidade
Bacillus subtilis/metabolismo
Bacillus subtilis/ultraestrutura
Bacillus subtilis/virologia
Células CACO-2
Endotoxinas/metabolismo
Endotoxinas/toxicidade
Enterócitos/efeitos dos fármacos
Enterócitos/microbiologia
Enterócitos/patologia
Escherichia coli K12/metabolismo
Escherichia coli K12/ultraestrutura
Escherichia coli K12/virologia
Microbioma Gastrointestinal
Células HeLa
Temperatura Alta
Seres Humanos
Lipopolissacarídeos/metabolismo
Lipopolissacarídeos/toxicidade
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Microscopia Eletrônica de Transmissão
Peptidoglicano/metabolismo
Peptidoglicano/toxicidade
RNA/metabolismo
Estabilidade de RNA/efeitos dos fármacos
Proteínas Recombinantes/metabolismo
Reoviridae/química
Reoviridae/efeitos dos fármacos
Reoviridae/patogenicidade
Infecções por Reoviridae/metabolismo
Infecções por Reoviridae/microbiologia
Infecções por Reoviridae/patologia
Ácidos Teicoicos/metabolismo
Ácidos Teicoicos/toxicidade
Vírion/química
Vírion/patogenicidade
Vírion/fisiologia
Ligação Viral/efeitos dos fármacos
Internalização do Vírus/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endotoxins); 0 (Lipopolysaccharides); 0 (Luminescent Proteins); 0 (Peptidoglycan); 0 (RNA, recombinant); 0 (Recombinant Proteins); 0 (Teichoic Acids); 0 (red fluorescent protein); 56411-57-5 (lipoteichoic acid); 63231-63-0 (RNA); 67924-63-4 (endotoxin, Escherichia coli); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006768


  7 / 2616 MEDLINE  
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[PMID]:29198708
[Au] Autor:Lepage M; Seltana A; Thibault MP; Tremblay É; Beaulieu JF
[Ad] Endereço:Laboratory of Intestinal Physiopathology, Department of Anatomy and Cell Biology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, Canada.
[Ti] Título:Knockdown of laminin α5 stimulates intestinal cell differentiation.
[So] Source:Biochem Biophys Res Commun;495(1):1510-1515, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interactions between cells and the extracellular matrix regulate a wide range of cell processes such as proliferation and differentiation. Laminins are major components of the basement membrane that actively participate in most biological functions via their interactions with a variety of specific cell receptors. The α5-containing laminins (LAMA5) are one of the three main types of laminins identified at the epithelial basal lamina in the adult intestine. The aim of the present study was to investigate the role of α5-containing laminins on intestinal cell proliferation and differentiation. Using an shRNA targeting approach, the effects of knocking down the expression of LAMA5 were investigated in the enterocytic-like Caco-2/15 cell line, a well-characterized model for intestinal cell differentiation. Surprisingly, the abolition of the laminin α5 chain resulted in a drastic increase in the differentiation marker sucrase-isomaltase which was correctly expressed at the apical pole of the cells as observed by indirect immunofluorescence. Transient increases of dipeptidylpeptidase IV, villin, CDX2, HNF-1α, HNF-4α and transepithelial resistance as well as an apparent redistribution of the junctional components ZO-1 and E-cadherin were also observed at early stages of differentiation but no specific effect was observed on cell proliferation as evaluated by BrdU incorporation. Taken together, these data suggest that α5-containing laminins repress intestinal differentiation in its early stages.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Enterócitos/citologia
Enterócitos/fisiologia
Proteínas da Matriz Extracelular/metabolismo
Intestinos/citologia
Laminina/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CACO-2
Proliferação Celular/fisiologia
Técnicas de Silenciamento de Genes
Seres Humanos
Intestinos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Laminin); 0 (laminin alpha5)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  8 / 2616 MEDLINE  
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[PMID]:28455446
[Au] Autor:Wang C; Sun M; Yuan X; Ji L; Jin Y; Cardona CJ; Xing Z
[Ad] Endereço:From the Medical School and Jiangsu Provincial Key Laboratory of Medicine, Nanjing University, Nanjing 210008, China.
[Ti] Título:Enterovirus 71 suppresses interferon responses by blocking Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling through inducing karyopherin-α1 degradation.
[So] Source:J Biol Chem;292(24):10262-10274, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enterovirus 71 (EV71) has emerged as one of the most important enteroviruses since the eradication of poliovirus, and it causes severe neurological symptoms for which no effective antiviral drugs are available. Type I interferons (IFN) α/ß have been used clinically as antiviral therapy as the first line of defense against virus infections successfully for decades. However, treatment with type I interferons has not been effective in patients with EV71 infection. In this study, we found that in cells pretreated with IFN-ß, EV71 infection could still lead to a cytopathic effect, and the viral replication was not affected. The mechanism by which EV71 antagonizes interferon signaling, however, has been controversial. Our study indicated that EV71 infection did not inhibit phosphorylation of STAT1/2 induced by IFN-ß stimulation, but p-STAT1/2 transport into the nucleus was significantly blocked. We showed that EV71 infection reduced the formation of STAT/karyopherin-α1 (KPNA1) complex upon interferon stimulation and that the virus down-regulated the expression of KPNA1, a nuclear localization signal receptor for p-STAT1. Using specific caspase inhibitors and siRNA for caspase-3, we demonstrated that EV71 infection induced degradation of cellular KPNA1 in a caspase-3-dependent manner, which led to decreased induction of interferon-inducible genes and IFN response. Viral 2A and 3C proteases did not degrade KPNA1, inhibit the activity of ISRE or suppress the transcription of interferon-inducible genes induced by IFN-ß. Our study demonstrates a novel mechanism by which antiviral signaling is suppressed through degradation of KPNA1 by activated caspase-3 induced in an enteroviral infection.
[Mh] Termos MeSH primário: Caspase 3/metabolismo
Enterócitos/virologia
Enterovirus Humano A/fisiologia
Interferon beta/metabolismo
Janus Quinase 1/metabolismo
Transdução de Sinais
alfa Carioferinas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Caspase 3/química
Caspase 3/genética
Cercopithecus aethiops
Enterócitos/imunologia
Enterócitos/metabolismo
Enterovirus Humano A/crescimento & desenvolvimento
Células HT29
Células HeLa
Seres Humanos
Interferon beta/genética
Janus Quinase 1/genética
Fosforilação
Processamento de Proteína Pós-Traducional
Proteólise
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT2/metabolismo
Células Vero
Replicação Viral
alfa Carioferinas/genética
alfa Carioferinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KPNA1 protein, human); 0 (Recombinant Fusion Proteins); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT2 Transcription Factor); 0 (STAT2 protein, human); 0 (alpha Karyopherins); 77238-31-4 (Interferon-beta); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.745729


  9 / 2616 MEDLINE  
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[PMID]:29190745
[Au] Autor:Thomas DM; Bell B; Papillon S; Delaplain P; Lim J; Golden J; Bowling J; Wang J; Wang L; Grishin AV; Ford HR
[Ad] Endereço:Division of Pediatric Surgery, Children's Hospital Los Angeles, Los Angeles, California, United States of America.
[Ti] Título:Colonization with Escherichia coli EC 25 protects neonatal rats from necrotizing enterocolitis.
[So] Source:PLoS One;12(11):e0188211, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Necrotizing enterocolitis (NEC) is a significant cause of morbidity and mortality in premature infants; yet its pathogenesis remains poorly understood. To evaluate the role of intestinal bacteria in protection against NEC, we assessed the ability of naturally occurring intestinal colonizer E. coli EC25 to influence composition of intestinal microbiota and NEC pathology in the neonatal rat model. Experimental NEC was induced in neonatal rats by formula feeding/hypoxia, and graded histologically. Bacterial populations were characterized by plating on blood agar, scoring colony classes, and identifying each class by sequencing 16S rDNA. Binding of bacteria to, and induction of apoptosis in IEC-6 enterocytes were examined by plating on blood agar and fluorescent staining for fragmented DNA. E. coli EC 25, which was originally isolated from healthy rats, efficiently colonized the intestine and protected from NEC following introduction to newborn rats with formula at 106 or 108 cfu. Protection did not depend significantly on EC25 inoculum size or load in the intestine, but positively correlated with the fraction of EC25 in the microbiome. Introduction of EC25 did not prevent colonization with other bacteria and did not significantly alter bacterial diversity. EC25 neither induced cultured enterocyte apoptosis, nor protected from apoptosis induced by an enteropathogenic strain of Cronobacter muytjensii. Our results show that E. coli EC25 is a commensal strain that efficiently colonizes the neonatal intestine and protects from NEC.
[Mh] Termos MeSH primário: Animais Recém-Nascidos
Enterocolite Necrosante/prevenção & controle
Escherichia coli/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Enterocolite Necrosante/microbiologia
Enterocolite Necrosante/patologia
Enterócitos/patologia
Feminino
Microbiota
Gravidez
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188211


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[PMID]:28548701
[Au] Autor:Tonucci FM; Ferretti A; Almada E; Cribb P; Vena R; Hidalgo F; Favre C; Tyska MJ; Kaverina I; Larocca MC
[Ad] Endereço:Instituto de Fisiología Experimental, Consejo de Investigaciones Científicas y Técnicas, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Rosario, Argentina.
[Ti] Título:Microtubules regulate brush border formation.
[So] Source:J Cell Physiol;233(2):1468-1480, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most epithelial cells contain apical membrane structures associated to bundles of actin filaments, which constitute the brush border. Whereas microtubule participation in the maintenance of the brush border identity has been characterized, their contribution to de novo microvilli organization remained elusive. Hereby, using a cell model of individual enterocyte polarization, we found that nocodazole induced microtubule depolymerization prevented the de novo brush border formation. Microtubule participation in brush border actin organization was confirmed in polarized kidney tubule MDCK cells. We also found that centrosome, but not Golgi derived microtubules, were essential for the initial stages of brush border development. During this process, microtubule plus ends acquired an early asymmetric orientation toward the apical membrane, which clearly differs from their predominant basal orientation in mature epithelia. In addition, overexpression of the microtubule plus ends associated protein CLIP170, which regulate actin nucleation in different cell contexts, facilitated brush border formation. In combination, the present results support the participation of centrosomal microtubule plus ends in the activation of the polarized actin organization associated to brush border formation, unveiling a novel mechanism of microtubule regulation of epithelial polarity.
[Mh] Termos MeSH primário: Colo/fisiologia
Enterócitos/fisiologia
Células Epiteliais/fisiologia
Rim/fisiologia
Microtúbulos/fisiologia
Microvilosidades/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/fisiologia
Animais
Polaridade Celular
Centrômero/fisiologia
Colo/efeitos dos fármacos
Colo/metabolismo
Colo/ultraestrutura
Cães
Enterócitos/efeitos dos fármacos
Enterócitos/metabolismo
Enterócitos/ultraestrutura
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Células Epiteliais/ultraestrutura
Seres Humanos
Rim/efeitos dos fármacos
Rim/ultraestrutura
Células Madin Darby de Rim Canino
Proteínas Associadas aos Microtúbulos/metabolismo
Microtúbulos/efeitos dos fármacos
Microtúbulos/metabolismo
Microvilosidades/efeitos dos fármacos
Microvilosidades/metabolismo
Nocodazol/farmacologia
Fatores de Tempo
Moduladores de Tubulina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins); 0 (Tubulin Modulators); SH1WY3R615 (Nocodazole)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26033



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