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[PMID]:28949968
[Au] Autor:Soo JY; Orgeig S; McGillick EV; Zhang S; McMillen IC; Morrison JL
[Ad] Endereço:Early Origins of Adult Health Research Group, School of Pharmacy & Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia.
[Ti] Título:Normalisation of surfactant protein -A and -B expression in the lungs of low birth weight lambs by 21 days old.
[So] Source:PLoS One;12(9):e0181185, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intrauterine growth restriction (IUGR) induced by placental restriction (PR) in the sheep negatively impacts lung and pulmonary surfactant development during fetal life. Using a sheep model of low birth weight (LBW), we found that there was an increase in mRNA expression of surfactant protein (SP)-A, -B and -C in the lung of LBW lambs but no difference in the protein expression of SP-A or -B. LBW also resulted in increased lysosome-associated membrane glycoprotein (LAMP)-3 mRNA expression, which may indicate an increase in either the density of type II Alveolar epithelial cells (AEC) or maturity of type II AECs. Although there was an increase in glucocorticoid receptor (GR) and 11ß-hydroxysteroid dehydrogenase (11ßHSD)-1 mRNA expression in the lung of LBW lambs, we found no change in the protein expression of these factors, suggesting that the increase in SP mRNA expression is not mediated by increased GC signalling in the lung. The increase in SP mRNA expression may, in part, be mediated by persistent alterations in hypoxia signalling as there was an increase in lung HIF-2α mRNA expression in the LBW lamb. The changes in the hypoxia signalling pathway that persist within the lung after birth may be involved in maintaining SP production in the LBW lamb.
[Mh] Termos MeSH primário: Recém-Nascido de Baixo Peso
Pulmão/metabolismo
Proteína A Associada a Surfactante Pulmonar/metabolismo
Proteína B Associada a Surfactante Pulmonar/metabolismo
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenases/genética
11-beta-Hidroxiesteroide Desidrogenases/metabolismo
Animais
Peso Corporal
Ensaio de Imunoadsorção Enzimática
Feminino
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Tamanho do Órgão
Proteína A Associada a Surfactante Pulmonar/genética
Proteína B Associada a Surfactante Pulmonar/genética
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysosome-Associated Membrane Glycoproteins); 0 (Pulmonary Surfactant-Associated Protein A); 0 (Pulmonary Surfactant-Associated Protein B); 0 (RNA, Messenger); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181185


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[PMID]:28823833
[Au] Autor:Tang F; Yang TL; Zhang Z; Li XG; Zhong QQ; Zhao TT; Gong L
[Ad] Endereço:Department of Cardiology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, PR China; Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, Guizhou, PR China.
[Ti] Título:MicroRNA-21 suppresses ox-LDL-induced human aortic endothelial cells injuries in atherosclerosis through enhancement of autophagic flux: Involvement in promotion of lysosomal function.
[So] Source:Exp Cell Res;359(2):374-383, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is a common pathological basis of cardiovascular disease and remains the leading cause of mortality. Endothelial cell (EC) injury and autophagy dysfunction have been proved to contribute to the development of atherosclerosis. Recently, accumulating evidence confirms that microRNAs (miRNAs) have emerged as vital regulators and fine-tuners of various pathophysiological cellular impacts and molecular signaling pathways involved in atherosclerosis. Herein, the objective of the present study was to explore the biological function of miR-21 in oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cells (HAECs) injury and the underlying molecular mechanism. The results showed that ox-LDL treatment significantly decreased HAECs viability, increased caspase-3 activity, apoptosis ratio and Bax protein expression, and reduced Bcl-2 protein expression resulting in EC injuries. Simultaneously, ox-LDL treatment obviously reduced miR-21 level in a time-and dose-dependent manner. Notably, ox-LDL-induced EC injuries were abolished by miR-21 mimics transfection. In addition, miR-21 mimics alleviated ox-LDL-induced impaired autophagic flux as illustrated by the increases in LC3-II/LC3-I ratio and Beclin-1 protein expression, and the decrease in p62 protein expression in HAECs. Moreover, ox-LDL suppressed the expressions of lysosomal membrane protein (LAMP1) and cathepsin D proteins, and attenuated cathepsin D activity in HAECs, leading to lysosomal dysfunction, while these effects were also blocked by miR-21 mimics. These findings indicated that miR-21 restored impaired autophagic flux and lysosomal dysfunction, thereby attenuating ox-LDL-induced HAECs injuries.
[Mh] Termos MeSH primário: Autofagia/genética
Células Endoteliais/efeitos dos fármacos
Lipoproteínas LDL/farmacologia
MicroRNAs/genética
[Mh] Termos MeSH secundário: Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Autofagia/efeitos dos fármacos
Beclina-1/genética
Beclina-1/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Catepsina D/genética
Catepsina D/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Lisossomos/efeitos dos fármacos
Lisossomos/metabolismo
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Mimetismo Molecular
Oligorribonucleotídeos/genética
Oligorribonucleotídeos/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteína Sequestossoma-1/genética
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2 protein, human); 0 (BECN1 protein, human); 0 (Beclin-1); 0 (LAMP1 protein, human); 0 (Lipoproteins, LDL); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (MAP1LC3A protein, human); 0 (MIRN21 microRNA, human); 0 (MicroRNAs); 0 (Microtubule-Associated Proteins); 0 (Oligoribonucleotides); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (SQSTM1 protein, human); 0 (Sequestosome-1 Protein); 0 (light chain 3, human); 0 (oxidized low density lipoprotein); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.23.5 (CTSD protein, human); EC 3.4.23.5 (Cathepsin D)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE


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[PMID]:28720501
[Au] Autor:Sun H; Liu Y; Zhang L; Shao X; Liu K; Ding Z; Liu X; Jiang C; Li H; Li H
[Ad] Endereço:Shenzhen Key Laboratory for Molecular Biology of Neural Development, Guangdong Key Laboratory of Nanomedicine, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China; University of Chinese Academy of Scie
[Ti] Título:Numb positively regulates autophagic flux via regulating lysosomal function.
[So] Source:Biochem Biophys Res Commun;491(3):780-786, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autophagy is a lysosome-dependent catabolic process involving in the degradation and recycling of unnecessary or damaged proteins and organelles. Emerging evidence indicates that autophagy dysfunction is closely related to various human diseases including cancer, aging, myopathies and neurodegenerative disorders. Here, using genetic knockdown, we uncover the role of Numb, an endocytic adaptor protein, in regulating the late steps of autophagy. We found that Numb depletion led to the accumulation of autophagic vacuole, as verified by RFP-LC3 staining combined with transmission electron microscopy. Further investigation indicated that Numb depletion impaired autophagic degradation through inhibiting the activities of lysosomal enzymes (Cathepsin D, ß-glucuronidase and ß-glucosidase). Moreover, Numb depletion induced elevation of lysosomal pH values and decrease of glycosylated lysosome-associated membrane proteins. We further observed that Rab7 activity was inhibited in Numb-depleted cells. Together, our findings revealed a novel function of Numb and its likely mechanism in regulation of autophagy events.
[Mh] Termos MeSH primário: Autofagia
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Lisossomos/metabolismo
Proteínas de Membrana/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Proteínas rab de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Regulação Enzimológica da Expressão Gênica
Seres Humanos
Concentração de Íons de Hidrogênio
Lisossomos/química
Células MCF-7
Proteínas de Membrana/química
Proteínas do Tecido Nervoso/química
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysosome-Associated Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Numb protein, human); 152989-05-4 (rab7 protein); EC 3.6.5.2 (rab GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


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[PMID]:28679759
[Au] Autor:Acciani M; Alston JT; Zhao G; Reynolds H; Ali AM; Xu B; Brindley MA
[Ad] Endereço:Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA.
[Ti] Título:Mutational Analysis of Lassa Virus Glycoprotein Highlights Regions Required for Alpha-Dystroglycan Utilization.
[So] Source:J Virol;91(18), 2017 Sep 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lassa virus (LASV) is an enveloped RNA virus endemic to West Africa and responsible for severe cases of hemorrhagic fever. Virus entry is mediated by the glycoprotein complex consisting of a stable-signal peptide, a receptor-binding subunit, GP1, and a viral-host membrane fusion subunit, GP2. Several cellular receptors can interact with the GP1 subunit and mediate viral entry, including alpha-dystroglycan (αDG) and lysosome-associated membrane protein 1 (LAMP1). In order to define the regions within GP1 that interact with the cellular receptors, we implemented insertional mutagenesis, carbohydrate shielding, and alanine scanning mutagenesis. Eighty GP constructs were engineered and evaluated for GP1-GP2 processing, surface expression, and the ability to mediate cell-to-cell fusion after low-pH exposure. To examine virus-to-cell entry, 49 constructs were incorporated onto vesicular stomatitis virus (VSV) pseudoparticles and transduction efficiencies were monitored in HAP1 and HAP1-ΔDAG1 cells that differentially produce the αDG cell surface receptor. Seven constructs retained efficient transduction in HAP1-ΔDAG1 cells yet poorly transduced HAP1 cells, suggesting that they are involved in αDG utilization. Residues H141, N146, F147, and Y150 cluster at the predicted central core of the trimeric interface and are important for GP-αDG interaction. Additionally, H92A-H93A, 150HA, 172HA, and 230HA displayed reduced transduction in both HAP1 and HAP1-ΔDAG1 cells, despite efficient cell-to-cell fusion activity. These mutations may interfere with interactions with the endosomal receptor LAMP1 or interfere at another stage in entry that is common to both cell lines. Insight gained from these data can aid in the development of more-effective entry inhibitors by blocking receptor interactions. Countries in which Lassa virus is endemic, such as Nigeria, Sierra Leone, Guinea, and Liberia, usually experience a seasonal outbreak of the virus from December to March. Currently, there is neither a preventative vaccine nor a therapeutic available to effectively treat severe Lassa fever. One way to thwart virus infection is to inhibit interaction with cellular receptors. It is known that the GP1 subunit of the Lassa glycoprotein complex plays a critical role in receptor recognition. Our results highlight a region within the Lassa virus GP1 protein that interacts with the cellular receptor alpha-dystroglycan. This information may be used for future development of new Lassa virus antivirals.
[Mh] Termos MeSH primário: Distroglicanas/metabolismo
Vírus Lassa/genética
Vírus Lassa/metabolismo
Receptores Virais/metabolismo
Proteínas do Envelope Viral/genética
Proteínas do Envelope Viral/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Análise Mutacional de DNA
Seres Humanos
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Mutagênese Insercional
Mutagênese Sítio-Dirigida
Proteínas Mutantes/genética
Proteínas Mutantes/metabolismo
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Transdução Genética
Vesiculovirus/genética
Vesiculovirus/fisiologia
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LAMP1 protein, human); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Mutant Proteins); 0 (Receptors, Virus); 0 (Recombinant Proteins); 0 (Viral Envelope Proteins); 0 (glycoprotein gp1, lassa virus); 146888-27-9 (Dystroglycans)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE


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[PMID]:28673965
[Au] Autor:Button RW; Roberts SL; Willis TL; Hanemann CO; Luo S
[Ad] Endereço:From the Peninsula Schools of Medicine and Dentistry, Institute of Translational and Stratified Medicine, University of Plymouth, Research Way, Plymouth PL6 8BU, United Kingdom.
[Ti] Título:Accumulation of autophagosomes confers cytotoxicity.
[So] Source:J Biol Chem;292(33):13599-13614, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autophagy comprises the processes of autophagosome synthesis and lysosomal degradation. In certain stress conditions, increased autophagosome synthesis may be associated with decreased lysosomal activity, which may result in reduced processing of the excessive autophagosomes by the rate-limiting lysosomal activity. Thus, the excessive autophagosomes in such situations may be largely unfused to lysosomes, and their formation/accumulation under these conditions is assumed to be futile for autophagy. The role of cytotoxicity in accumulating autophagosomes (representing synthesis of autophagosomes subsequently unfused to lysosomes) has not been investigated previously. Here, we found that accumulation of autophagosomes compromised cell viability, and this effect was alleviated by depletion of autophagosome machinery proteins. We tested whether reduction in autophagosome synthesis could affect cell viability in cell models expressing mutant huntingtin and α-synuclein, given that both of these proteins cause increased autophagosome biogenesis and compromised lysosomal activity. Importantly, partial depletion of autophagosome machinery proteins Atg16L1 and Beclin 1 significantly ameliorated cell death in these conditions. Our data suggest that production/accumulation of autophagosomes subsequently unfused to lysosomes (or accumulation of autophagosomes) directly induces cellular toxicity, and this process may be implicated in the pathogenesis of neurodegenerative diseases. Therefore, lowering the accumulation of autophagosomes may represent a therapeutic strategy for tackling such diseases.
[Mh] Termos MeSH primário: Autofagossomos/metabolismo
Lisossomos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/metabolismo
Proteínas Qa-SNARE/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Proteínas de Transporte Vesicular/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagossomos/patologia
Autofagossomos/ultraestrutura
Linhagem Celular Tumoral
Sobrevivência Celular
Células Cultivadas
Embrião de Mamíferos/citologia
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Proteína 2 de Membrana Associada ao Lisossomo/genética
Proteína 2 de Membrana Associada ao Lisossomo/metabolismo
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Lisossomos/patologia
Lisossomos/ultraestrutura
Camundongos
Camundongos Knockout
Microscopia Eletrônica de Transmissão
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/genética
Neurônios/patologia
Neurônios/ultraestrutura
Proteínas Qa-SNARE/antagonistas & inibidores
Proteínas Qa-SNARE/genética
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Serina-Treonina Quinases TOR/antagonistas & inibidores
Serina-Treonina Quinases TOR/genética
Células Tumorais Cultivadas
Proteínas de Transporte Vesicular/antagonistas & inibidores
Proteínas de Transporte Vesicular/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lamp1 protein, mouse); 0 (Lysosomal-Associated Membrane Protein 2); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Nerve Tissue Proteins); 0 (Qa-SNARE Proteins); 0 (Recombinant Fusion Proteins); 0 (STX17 protein, human); 0 (VPS33A protein, human); 0 (Vesicular Transport Proteins); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.782276


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[PMID]:28639285
[Au] Autor:Korsak B; Almeida GM; Rocha S; Pereira C; Mendes N; Osório H; Pereira PMR; Rodrigues JMM; Schneider RJ; Sarmento B; Tomé JPC; Oliveira C
[Ad] Endereço:Instituto de Investigação e Inovação em Saúde- i3S, Universidade do Porto, Portugal.
[Ti] Título:Porphyrin modified trastuzumab improves efficacy of HER2 targeted photodynamic therapy of gastric cancer.
[So] Source:Int J Cancer;141(7):1478-1489, 2017 Oct 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gastric cancer (GC) is the 3rd deadliest cancer worldwide, due to limited treatment options and late diagnosis. Human epidermal growth factor receptor-2 (HER2) is overexpressed in ∼20% of GC cases and anti-HER2 antibody trastuzumab in combination with conventional chemotherapy, is recognized as standard therapy for HER2-positive metastatic GC. This strategy improves GC patients' survival by 2-3 months, however its optimal results in breast cancer indicate that GC survival may be improved. A new photoimmunoconjugate was developed by conjugating a porphyrin with trastuzumab (Trast:Porph) for targeted photodynamic therapy in HER2-positive GC. Using mass spectrometry analysis, the lysine residues in the trastuzumab structure most prone for porphyrin conjugation were mapped. The in vitro data demonstrates that Trast:Porph specifically binds to HER2-positive cells, accumulates intracellularly, co-localizes with lysosomal marker LAMP1, and induces massive HER2-positive cell death upon cellular irradiation. The high selectivity and cytotoxicity of Trast:Porph based photoimmunotherapy is confirmed in vivo in comparison with trastuzumab alone, using nude mice xenografted with a HER2-positive GC cell line. In the setting of human disease, these data suggest that repetitive cycles of Trast:Porph photoimmunotherapy may be used as an improved treatment strategy in HER2-positive GC patients.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Morte Celular
Imunoterapia/métodos
Fotoquimioterapia/métodos
Porfirinas/uso terapêutico
Receptor ErbB-2
Neoplasias Gástricas/tratamento farmacológico
Trastuzumab/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacocinética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Lisina/química
Glicoproteínas de Membrana Associadas ao Lisossomo/farmacocinética
Masculino
Espectrometria de Massas
Camundongos Nus
Porfirinas/química
Porfirinas/farmacocinética
Distribuição Aleatória
Neoplasias Gástricas/metabolismo
Trastuzumab/química
Trastuzumab/farmacocinética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (LAMP1 protein, human); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Porphyrins); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); K3Z4F929H6 (Lysine); P188ANX8CK (Trastuzumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30844


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[PMID]:28591131
[Au] Autor:Baharom F; Thomas OS; Lepzien R; Mellman I; Chalouni C; Smed-Sörensen A
[Ad] Endereço:Immunology and Allergy Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Visualization of early influenza A virus trafficking in human dendritic cells using STED microscopy.
[So] Source:PLoS One;12(6):e0177920, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Influenza A viruses (IAV) primarily target respiratory epithelial cells, but can also replicate in immune cells, including human dendritic cells (DCs). Super-resolution microscopy provides a novel method of visualizing viral trafficking by overcoming the resolution limit imposed by conventional light microscopy, without the laborious sample preparation of electron microscopy. Using three-color Stimulated Emission Depletion (STED) microscopy, we visualized input IAV nucleoprotein (NP), early and late endosomal compartments (EEA1 and LAMP1 respectively), and HLA-DR (DC membrane/cytosol) by immunofluorescence in human DCs. Surface bound IAV were internalized within 5 min of infection. The association of virus particles with early endosomes peaked at 5 min when 50% of NP+ signals were also EEA1+. Peak association with late endosomes occurred at 15 min when 60% of NP+ signals were LAMP1+. At 30 min of infection, the majority of NP signals were in the nucleus. Our findings illustrate that early IAV trafficking in human DCs proceeds via the classical endocytic pathway.
[Mh] Termos MeSH primário: Células Dendríticas/ultraestrutura
Interações Hospedeiro-Patógeno
Vírus da Influenza A/ultraestrutura
Vírion/ultraestrutura
[Mh] Termos MeSH secundário: Células Dendríticas/metabolismo
Células Dendríticas/virologia
Endossomos/virologia
Células Epiteliais/ultraestrutura
Células Epiteliais/virologia
Antígenos HLA-DR/isolamento & purificação
Seres Humanos
Vírus da Influenza A/genética
Vírus da Influenza A/isolamento & purificação
Vírus da Influenza A/patogenicidade
Glicoproteínas de Membrana Associadas ao Lisossomo/isolamento & purificação
Microscopia
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/isolamento & purificação
Proteínas de Transporte Vesicular/isolamento & purificação
Proteínas do Core Viral/genética
Proteínas do Core Viral/isolamento & purificação
Vírion/genética
Vírion/patogenicidade
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-DR Antigens); 0 (LAMP1 protein, human); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (NP protein, Influenza A virus); 0 (RNA-Binding Proteins); 0 (Vesicular Transport Proteins); 0 (Viral Core Proteins); 0 (early endosome antigen 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177920


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[PMID]:28586379
[Au] Autor:Couto NF; Pedersane D; Rezende L; Dias PP; Corbani TL; Bentini LC; Oliveira ACS; Kelles LF; Castro-Gomes T; Andrade LO
[Ad] Endereço:Department of Morphology/Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:LAMP-2 absence interferes with plasma membrane repair and decreases T. cruzi host cell invasion.
[So] Source:PLoS Negl Trop Dis;11(6):e0005657, 2017 Jun.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trypanosoma cruzi enters host cells by subverting the mechanism of cell membrane repair. In this process, the parasite induces small injuries in the host cell membrane leading to calcium entry and lysosomal exocytosis, which are followed by compensatory endocytosis events that drive parasites into host cells. We have previously shown that absence of both LAMP-1 and 2, major components of lysosomal membranes, decreases invasion of T. cruzi into host cells, but the mechanism by which they interfere with parasite invasion has not been described. Here we investigated the role of these proteins in parasitophorous vacuole morphology, host cell lysosomal exocytosis, and membrane repair ability. First, we showed that cells lacking only LAMP-2 present the same invasion phenotype as LAMP1/2-/- cells, indicating that LAMP-2 is an important player during T. cruzi invasion process. Second, neither vacuole morphology nor lysosomal exocytosis was altered in LAMP-2 lacking cells (LAMP2-/- and LAMP1/2-/- cells). We then investigated the ability of LAMP-2 deficient cells to perform compensatory endocytosis upon lysosomal secretion, the mechanism by which cells repair their membrane and T. cruzi ultimately enters cells. We observed that these cells perform less endocytosis upon injury when compared to WT cells. This was a consequence of impaired cholesterol traffic in cells lacking LAMP-2 and its influence in the distribution of caveolin-1 at the cell plasma membrane, which is crucial for plasma membrane repair. The results presented here show the major role of LAMP-2 in caveolin traffic and membrane repair and consequently in T. cruzi invasion.
[Mh] Termos MeSH primário: Membrana Celular/fisiologia
Fibroblastos/parasitologia
Proteína 2 de Membrana Associada ao Lisossomo/metabolismo
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Trypanosoma cruzi/fisiologia
[Mh] Termos MeSH secundário: Animais
Caveolina 1/genética
Caveolina 1/metabolismo
Endocitose
Fibroblastos/metabolismo
Fibroblastos/ultraestrutura
Regulação da Expressão Gênica/fisiologia
Proteína 2 de Membrana Associada ao Lisossomo/genética
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolin 1); 0 (Lamp1 protein, mouse); 0 (Lysosomal-Associated Membrane Protein 2); 0 (Lysosome-Associated Membrane Glycoproteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005657


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[PMID]:28447294
[Au] Autor:Zhang X; Yang P; Wang N; Zhang J; Li J; Guo H; Yin X; Rao Z; Wang X; Zhang L
[Ad] Endereço:Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
[Ti] Título:The binding of a monoclonal antibody to the apical region of SCARB2 blocks EV71 infection.
[So] Source:Protein Cell;8(8):590-600, 2017 Aug.
[Is] ISSN:1674-8018
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Entero virus 71 (EV71) causes hand, foot, and mouth disease (HFMD) and occasionally leads to severe neurological complications and even death. Scavenger receptor class B member 2 (SCARB2) is a functional receptor for EV71, that mediates viral attachment, internalization, and uncoating. However, the exact binding site of EV71 on SCARB2 is unknown. In this study, we generated a monoclonal antibody (mAb) that binds to human but not mouse SCARB2. It is named JL2, and it can effectively inhibit EV71 infection of target cells. Using a set of chimeras of human and mouse SCARB2, we identified that the region containing residues 77-113 of human SCARB2 contributes significantly to JL2 binding. The structure of the SCARB2-JL2 complex revealed that JL2 binds to the apical region of SCARB2 involving α-helices 2, 5, and 14. Our results provide new insights into the potential binding sites for EV71 on SCARB2 and the molecular mechanism of EV71 entry.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/química
Enterovirus Humano A/efeitos dos fármacos
Fragmentos Fab das Imunoglobulinas/química
Glicoproteínas de Membrana Associadas ao Lisossomo/química
Receptores Depuradores/química
Receptores Virais/química
Proteínas Recombinantes de Fusão/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Anticorpos Monoclonais/genética
Anticorpos Monoclonais/metabolismo
Sítios de Ligação
Linhagem Celular
Cristalografia por Raios X
Enterovirus Humano A/genética
Enterovirus Humano A/crescimento & desenvolvimento
Enterovirus Humano A/imunologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/virologia
Expressão Gênica
Células HEK293
Seres Humanos
Fragmentos Fab das Imunoglobulinas/genética
Fragmentos Fab das Imunoglobulinas/metabolismo
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
Glicoproteínas de Membrana Associadas ao Lisossomo/imunologia
Camundongos
Modelos Moleculares
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Receptores Depuradores/genética
Receptores Depuradores/imunologia
Receptores Virais/genética
Receptores Virais/imunologia
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Células Sf9
Spodoptera
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Immunoglobulin Fab Fragments); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Receptors, Scavenger); 0 (Receptors, Virus); 0 (Recombinant Fusion Proteins); 0 (SCARB2 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1007/s13238-017-0405-7


  10 / 1350 MEDLINE  
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[PMID]:28423002
[Au] Autor:Baranova IN; Souza ACP; Bocharov AV; Vishnyakova TG; Hu X; Vaisman BL; Amar MJ; Chen Z; Remaley AT; Patterson AP; Yuen PST; Star RA; Eggerman TL
[Ad] Endereço:Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America.
[Ti] Título:Human SR-BII mediates SAA uptake and contributes to SAA pro-inflammatory signaling in vitro and in vivo.
[So] Source:PLoS One;12(4):e0175824, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Serum amyloid A (SAA) is an acute phase protein with cytokine-like and chemotactic properties, that is markedly up-regulated during various inflammatory conditions. Several receptors, including FPRL-1, TLR2, TLR4, RAGE, class B scavenger receptors, SR-BI and CD36, have been identified as SAA receptors. This study provides new evidence that SR-BII, splice variant of SR-BI, could function as an SAA receptor mediating its uptake and pro-inflammatory signaling. The uptake of Alexa Fluor488 SAA was markedly (~3 fold) increased in hSR-BII-expressing HeLa cells when compared with mock-transfected cells. The levels of SAA-induced interleukin-8 secretion by hSR-BII-expressing HEK293 cells were also significantly (~3-3.5 fold) higher than those detected in control cells. Moderately enhanced levels of phosphorylation of all three mitogen-activated protein kinases, ERK1/2, and p38 and JNK, were observed in hSR-BII-expressing cells following SAA stimulation when compared with control wild type cells. Transgenic mice with pLiv-11-directed liver/kidney overexpression of hSR-BI or hSR-BII were used to assess the in vivo role of each receptor in SAA-induced pro-inflammatory response in these organs. Six hours after intraperitoneal SAA injection both groups of transgenic mice demonstrated markedly higher (~2-5-fold) expression levels of inflammatory mediators in the liver and kidney compared to wild type mice. Histological examinations of hepatic and renal tissue from SAA-treated mice revealed moderate level of damage in the liver of both transgenic but not in the wild type mice. Activities of plasma transaminases, biomarkers of liver injury, were also moderately higher in hSR-B transgenic mice when compared to wild type mice. Our findings identify hSR-BII as a functional SAA receptor that mediates SAA uptake and contributes to its pro-inflammatory signaling via the MAPKs-mediated signaling pathways.
[Mh] Termos MeSH primário: Rim/metabolismo
Fígado/metabolismo
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Receptores Depuradores/metabolismo
Proteína Amiloide A Sérica/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Corantes Fluorescentes/metabolismo
Fluorbenzenos/metabolismo
Regulação da Expressão Gênica
Células HEK293
Células HeLa
Seres Humanos
Inflamação/induzido quimicamente
Inflamação/genética
Inflamação/metabolismo
Inflamação/patologia
Rim/efeitos dos fármacos
Rim/patologia
Fígado/efeitos dos fármacos
Fígado/patologia
Glicoproteínas de Membrana Associadas ao Lisossomo/genética
MAP Quinase Quinase 4/genética
MAP Quinase Quinase 4/metabolismo
Camundongos
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Receptores Depuradores/genética
Proteína Amiloide A Sérica/genética
Proteína Amiloide A Sérica/farmacologia
Transdução de Sinais
Transfecção
Transgenes
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Fluorobenzenes); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Receptors, Scavenger); 0 (SCARB2 protein, human); 0 (Serum Amyloid A Protein); EC 2.7.11.24 (Mapk1 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 2.7.12.2 (MAP Kinase Kinase 4)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175824



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