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[PMID]:28457919
[Au] Autor:Ma L; Su L; Liu H; Zhao F; Zhou D; Duan D
[Ad] Endereço:Key Laboratory for Sustainable Utilization of Marine Fisheries Resources, Ministry of Agriculture, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Qingdao, Shandong, 266071, China; Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy o
[Ti] Título:Norovirus contamination and the glycosphingolipid biosynthesis pathway in Pacific oyster: A transcriptomics study.
[So] Source:Fish Shellfish Immunol;66:26-34, 2017 Jul.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Noroviruses are the primary pathogens associated with shellfish-borne gastroenteritis outbreaks. These viruses remain stable in oysters, suggesting an active mechanism for virus concentration. In this study, a deep RNA sequencing technique was used to analyze the transcriptome profiles of Pacific oysters at different time points after inoculation with norovirus (GII.4). We obtained a maximum of 65, 294, 698 clean sample reads. When aligned to the reference genome, the average mapping ratio of clean data was approximately 65%. In the samples harvested at 12, 24, and 48 h after contamination, 2,223, 2,990, and 2020 genes, respectively, were differentially expressed in contaminated and non-contaminated oyster digestive tissues, including 500, 1748, and 1039 up-regulated and 1723, 1242, and 981 down-regulated genes, respectively. In particular, FUT2 and B3GNT4, genes encoding the signaling components of glycosphingolipid biosynthesis, were significantly up-regulated in contaminated samples. In addition, we found up-regulation of some immune- and disease-related genes in the MHC I pathway (PA28, HSP 70, HSP90, CANX, BRp57, and CALR) and MHC II pathway (GILT, CTSBLS, RFX, and NFY), although NoVs did not cause diseases in the oysters. We detected two types of HBGA-like molecules with positive-to-negative ratios similar to type A and H1 HBGA-like molecules in digestive tissues that were significantly higher in norovirus-contaminated than in non-contaminated oysters. Thus, our transcriptome data analysis indicated that a human pathogen (GII.4 Norovirus) was likely concentrated in the digestive tissues of oysters via HBGA-like molecules that were synthesized by the glycosphingolipid biosynthesis pathway. The identified differentially expressed genes also provide potential candidates for functional analysis to identify genes involved in the accumulation of noroviruses in oysters.
[Mh] Termos MeSH primário: Crassostrea/metabolismo
Crassostrea/virologia
Glicoesfingolipídeos/metabolismo
Norovirus/fisiologia
Transcriptoma
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Vias Biossintéticas
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycosphingolipids)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28671252
[Au] Autor:Qin WY; Gan LN; Xia RW; Dong WH; Sun SY; Zhu GQ; Wu SL; Bao WB
[Ad] Endereço:Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, , , China.
[Ti] Título:Promoter identification and analysis of key glycosphingolipid biosynthesis-globo series pathway genes in piglets.
[So] Source:Genet Mol Res;16(2), 2017 Jun 29.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Glycosphingolipid biosynthesis-globo series pathway genes (FUT1, FUT2, ST3GAL1, HEXA, HEXB, B3GALNT1, and NAGA) play an important regulatory role in the defense against Escherichia coli F18 in piglets. In this study, we identified the transcription initiation site and promoter of this gene cluster by mined previous RNA-seq results using bioinformatics tools. The FUT1 transcription initiation region included five alternative splicing sites and two promoter regions, whereas each of the six other genes had one promoter. Dual luciferase reporter results revealed significantly higher transcriptional activity by FUT1 promoter 2, indicating that it played a more important role in transcription. The promoters of glycosphingolipid biosynthesis genes identified contained a CpG island within the first 500 bp, except for the B3GALNT1 promoter which included fewer CpG sites. These results provide a deeper insight into methylation and the regulatory mechanisms of glycosphingolipid biosynthesis-globo series pathway genes in piglets.
[Mh] Termos MeSH primário: Fucosiltransferases/genética
Glicoesfingolipídeos/biossíntese
Regiões Promotoras Genéticas
Suínos/genética
[Mh] Termos MeSH secundário: Animais
Ilhas de CpG
Metilação de DNA
Fucosiltransferases/metabolismo
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycosphingolipids); EC 2.4.1.- (Fucosyltransferases); EC 2.4.1.69 (galactoside 2-alpha-L-fucosyltransferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.4238/gmr16029574


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[PMID]:28645851
[Au] Autor:Tóth EA; Oszvald Á; Péter M; Balogh G; Osteikoetxea-Molnár A; Bozó T; Szabó-Meleg E; Nyitrai M; Derényi I; Kellermayer M; Yamaji T; Hanada K; Vígh L; Matkó J
[Ad] Endereço:Department of Immunology, Eötvös Lorand University, Budapest, Hungary.
[Ti] Título:Nanotubes connecting B lymphocytes: High impact of differentiation-dependent lipid composition on their growth and mechanics.
[So] Source:Biochim Biophys Acta;1862(9):991-1000, 2017 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Nanotubes (NTs) are thin, long membranous structures forming novel, yet poorly known communication pathways between various cell types. Key mechanisms controlling their growth still remained poorly understood. Since NT-forming capacity of immature and mature B cells was found largely different, we investigated how lipid composition and molecular order of the membrane affect NT-formation. Screening B cell lines with various differentiation stages revealed that NT-growth linearly correlates with membrane ganglioside levels, while it shows maximum as a function of cholesterol level. NT-growth of B lymphocytes is promoted by raftophilic phosphatidylcholine and sphingomyelin species, various glycosphingolipids, and docosahexaenoic acid-containing inner leaflet lipids, through supporting membrane curvature, as demonstrated by comparative lipidomic analysis of mature versus immature B cell membranes. Targeted modification of membrane cholesterol and sphingolipid levels altered NT-forming capacity confirming these findings, and also highlighted that the actual lipid raft number may control NT-growth via defining the number of membrane-F-actin coupling sites. Atomic force microscopic mechano-manipulation experiments further proved that mechanical properties (elasticity or bending stiffness) of B cell NTs also depend on the actual membrane lipid composition. Data presented here highlight importance of the lipid side in controlling intercellular, nanotubular, regulatory communications in the immune system.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Diferenciação Celular/fisiologia
Microdomínios da Membrana/fisiologia
Esfingolipídeos/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Linhagem Celular
Membrana Celular/metabolismo
Colesterol/metabolismo
Gangliosídeos/metabolismo
Glicoesfingolipídeos/metabolismo
Fluidez de Membrana/fisiologia
Microdomínios da Membrana/metabolismo
Camundongos
Nanotubos
Fosfatidilcolinas/metabolismo
Esfingomielinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Gangliosides); 0 (Glycosphingolipids); 0 (Phosphatidylcholines); 0 (Sphingolipids); 0 (Sphingomyelins); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


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[PMID]:28586101
[Au] Autor:Huang X; Schurman N; Handa K; Hakomori S
[Ad] Endereço:Division of Biomembrane Research, Pacific Northwest Research Institute, Seattle, WA, USA.
[Ti] Título:Functional role of glycosphingolipids in contact inhibition of growth in a human mammary epithelial cell line.
[So] Source:FEBS Lett;591(13):1918-1928, 2017 Jul.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have demonstrated previously the involvement of certain glycosphingolipids (GSLs) in 'contact inhibition' (dependent on cell-to-cell contact) of cell growth. Here, we examined the roles of specific GSLs in contact inhibition of the human epithelial cell line MCF10A. Contact-inhibited cells show increased expression of the ganglioside GD3 and the globo-series GSL Gb3, and of the mRNAs for the corresponding sialyltransferases ST8SIA1 (GD3 synthase) and galactosyltransferase A4GALT (Gb3 synthase). siRNA knockdown (KD) of ST8SIA1 and/or A4GALT significantly suppresses contact inhibition. Exogenous addition of GD3 or Gb3 inhibits proliferation of low-density cells. Our findings suggest that GSLs play functional roles in contact inhibition of these cells and that Merlin/NF2, a tumor suppressor protein, is involved in the GSL function.
[Mh] Termos MeSH primário: Inibição de Contato
Glicoesfingolipídeos/metabolismo
Glândulas Mamárias Humanas/citologia
[Mh] Termos MeSH secundário: Contagem de Células
Linhagem Celular Tumoral
Proliferação Celular
Galactosiltransferases/deficiência
Galactosiltransferases/genética
Regulação da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
Sialiltransferases/deficiência
Sialiltransferases/genética
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Glycosphingolipids); 0 (RNA, Messenger); 0 (RNA, Small Interfering); EC 2.4.1.- (Galactosyltransferases); EC 2.4.1.- (UDP-galactose-lactosylceramide alpha 1-4-galactosyltransferase); EC 2.4.99.- (Sialyltransferases); EC 2.4.99.8 (alpha-N-acetylneuraminate alpha-2,8-sialyltransferase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12709


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[PMID]:28551069
[Au] Autor:Dany M; Elston D
[Ad] Endereço:Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston, South Carolina.
[Ti] Título:Gene expression of sphingolipid metabolism pathways is altered in hidradenitis suppurativa.
[So] Source:J Am Acad Dermatol;77(2):268-273.e6, 2017 Aug.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hidradenitis suppurativa (HS) is a debilitating skin disease characterized by painful recurrent nodules and abscesses caused by chronic inflammation. Early events in the development of HS are believed to occur in the folliculopilosebaceous unit; however, the signaling pathways behind this mechanism are unknown. Sphingolipids, such as ceramide, are essential components of the skin and appendages and have important structural and signaling roles. OBJECTIVE: We sought to explore whether the gene expression of enzymes involved in sphingolipid metabolic pathways is altered in HS. METHODS: A microarray data set including 30 samples was used to compare the expression of sphingolipid-related enzymes in inflammatory skin lesions from HS patients (n = 17) with the expression in clinically healthy skin tissue (n = 13). Differential expression of sphingolipid metabolism-related genes was analyzed using Gene Expression Omnibus 2R. RESULTS: HS lesional skin samples have significantly decreased expression of enzymes generating ceramide and sphingomyelin, increased expression of enzymes catabolizing ceramide to sphingosine, and increased expression of enzymes converting ceramide to galactosylceramide and gangliosides. LIMITATIONS: Limitations of this study include assessing the expression of sphingolipid-related enzymes without assessing the levels of the related sphingolipids. CONCLUSION: Our study suggests that sphingolipid metabolism is altered in HS lesional skin compared with normal skin.
[Mh] Termos MeSH primário: Expressão Gênica
Hidradenite Supurativa/enzimologia
Hidradenite Supurativa/genética
Perilipinas/genética
Pele/enzimologia
Esfingolipídeos/metabolismo
[Mh] Termos MeSH secundário: Ceramidase Alcalina/genética
Estudos de Casos e Controles
Ceramidas/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/genética
Glucosilceramidase/genética
Glucosiltransferases/genética
Glicoesfingolipídeos/metabolismo
Hexosaminidases/genética
Seres Humanos
Lisofosfolipídeos/metabolismo
Proteínas de Membrana/genética
Redes e Vias Metabólicas/genética
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Serina C-Palmitoiltransferase/genética
Transdução de Sinais/genética
Esfingolipídeos/biossíntese
Esfingomielina Fosfodiesterase/genética
Esfingomielinas/metabolismo
Esfingosina/análogos & derivados
Esfingosina/metabolismo
Esfingosina N-Aciltransferase/genética
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ceramides); 0 (Glycosphingolipids); 0 (Lysophospholipids); 0 (Membrane Proteins); 0 (Perilipins); 0 (Sphingolipids); 0 (Sphingomyelins); 0 (Tumor Suppressor Proteins); 26993-30-6 (sphingosine 1-phosphate); EC 2.3.1.24 (CERS2 protein, human); EC 2.3.1.24 (CERS5 protein, human); EC 2.3.1.24 (Sphingosine N-Acyltransferase); EC 2.3.1.50 (Serine C-Palmitoyltransferase); EC 2.4.1.- (Glucosyltransferases); EC 2.4.1.80 (ceramide glucosyltransferase); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.91 (sphingosine kinase 2, human); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase); EC 3.2.1.- (Hexosaminidases); EC 3.2.1.45 (Glucosylceramidase); EC 3.5.1.23 (Alkaline Ceramidase); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


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[PMID]:28399449
[Au] Autor:Cheng S; Wu P; Han J; Wang Y; Cui Y; Zhang Z; Yamagata T; Li X
[Ad] Endereço:CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Chaoyang District, Beijing 100101, China.
[Ti] Título:Synthesis and biological evaluation of neoglycosphingolipids.
[So] Source:Eur J Med Chem;134:43-51, 2017 Jul 07.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Various neoglycosphingolipids were efficiently synthesized in a one-step reaction by the coupling of free sugars with an N-alkylaminooxy-functionalized ceramide analogue. The bioactivity studies demonstrated that most of these compounds could upregulate the expression of matrix metalloproteinase-9 (MMP-9, extracellular matrix proteins associated with tumor migration) in murine melanoma B16 cells in a similar manner to the natural ganglioside monosialodihexosylganglioside (GM3), which highlights the potential use of these neoglycosphingolipids as inhibitors of tumor migration.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Glicoesfingolipídeos/química
Glicoesfingolipídeos/farmacologia
Metaloproteinase 9 da Matriz/genética
Melanoma Experimental/tratamento farmacológico
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Linhagem Celular Tumoral
Glicoesfingolipídeos/síntese química
Melanoma Experimental/genética
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Glycosphingolipids); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE


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[PMID]:28369040
[Au] Autor:Boland S; Schmidt U; Zagoriy V; Sampaio JL; Fritsche RF; Czerwonka R; Lübken T; Reimann J; Penkov S; Knölker HJ; Kurzchalia TV
[Ad] Endereço:MPI of Molecular Cell Biology and Genetics, Dresden, Germany.
[Ti] Título:Phosphorylated glycosphingolipids essential for cholesterol mobilization in Caenorhabditis elegans.
[So] Source:Nat Chem Biol;13(6):647-654, 2017 Jun.
[Is] ISSN:1552-4469
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nematode Caenorhabditis elegans requires exogenous cholesterol to survive and its depletion leads to early developmental arrest. Thus, tight regulation of cholesterol storage and distribution within the organism is indispensable. Here, we present a novel class of C. elegans phosphorylated glycosphingolipids, phosphoethanolamine glucosylceramides (PEGCs), capable of rescuing larval arrest induced by sterol starvation. We describe the total synthesis of a major PEGC species and demonstrate that the PEGC synthetic counterpart suppresses the dauer-constitutive phenotype of Niemann-Pick C1 (NPC1) and DAF-7/TGF-ß mutant worms caused by impaired intracellular sterol trafficking. PEGC biosynthesis depends on functional NPC1 and TGF-ß, indicating that these proteins control larval development at least partly through PEGC. Furthermore, glucosylceramide deficiency dramatically reduced PEGC amounts. However, the resulting developmental arrest could be rescued by oversaturation of food with cholesterol. Taken together, these data show that PEGC is essential for C. elegans development through its regulation of sterol mobilization.
[Mh] Termos MeSH primário: Caenorhabditis elegans/metabolismo
Colesterol/metabolismo
Glicoesfingolipídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans/genética
Caenorhabditis elegans/crescimento & desenvolvimento
Cromatografia Líquida
Espectrometria de Massas
Estrutura Molecular
Mutação
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycosphingolipids); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1038/nchembio.2347


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[PMID]:28345149
[Au] Autor:Olmos-Ortiz LM; Barajas-Mendiola MA; Barrios-Rodiles M; Castellano LE; Arias-Negrete S; Avila EE; Cuéllar-Mata P
[Ad] Endereço:Departamento de Biología, Universidad de Guanajuato, Guanajuato, Mexico.
[Ti] Título:Trichomonas vaginalis exosome-like vesicles modify the cytokine profile and reduce inflammation in parasite-infected mice.
[So] Source:Parasite Immunol;39(6), 2017 Jun.
[Is] ISSN:1365-3024
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Trichomonas vaginalis (Tv) is a flagellated parasite commonly spread through sexual transmission. This protozoan initiates a severe inflammatory process, inducing nitric oxide, interleukin-6 (IL-6), IL-8, IL-10, IL-17 and IL-22 production by host immune cells. The parasites elicit these responses by releasing surface lipophosphoglycan, small extracellular vesicles (exosomes) and other factors. Tv exosomes are similar to mammalian exosomes and have been implicated in the modulation of IL-8 secretion by epithelial cells. Here, we report that exosome-like vesicles from T. vaginalis (Tv-ELVs) induced a more than 15-fold increase in IL-10 expression in RAW264.7 macrophages but only a two fold increase in IL-6 and TNF-α expression levels measured by RT-PCR. Because Tv-ELVs modulated the macrophage response, we also explored the effect of Tv-ELVs in a murine model of infection. Pretreatment with Tv-ELVs significantly increased IL-10 production as measured in vaginal washes by days 8 and 16 post-infection. Remarkably, Tv-ELVs-pretreated mice exhibited a decrease in IL-17 production and a significant decrease in vulvar inflammation. In addition, IL-6 and IL-13 were decreased during infection. Our results suggest that Tv-ELVs have an immunomodulatory role on the cytokine profile induced by the parasite and promote a decrease in the inflammatory process in mice infected with T. vaginalis.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Vaginite por Trichomonas/imunologia
Trichomonas vaginalis/imunologia
[Mh] Termos MeSH secundário: Animais
Células Epiteliais/imunologia
Exossomos/imunologia
Feminino
Glicoesfingolipídeos
Inflamação/imunologia
Inflamação/metabolismo
Inflamação/parasitologia
Ativação de Macrófagos
Macrófagos/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Óxido Nítrico/metabolismo
Células RAW 264.7
Vulva/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Glycosphingolipids); 0 (lipophosphonoglycan); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1111/pim.12426


  9 / 3941 MEDLINE  
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[PMID]:28294600
[Au] Autor:Nasir W; Frank M; Kunze A; Bally M; Parra F; Nyholm PG; Höök F; Larson G
[Ad] Endereço:Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska Academy, University of Gothenburg , Gothenburg, Sweden.
[Ti] Título:Histo-Blood Group Antigen Presentation Is Critical for Binding of Norovirus VLP to Glycosphingolipids in Model Membranes.
[So] Source:ACS Chem Biol;12(5):1288-1296, 2017 May 19.
[Is] ISSN:1554-8937
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Virus entry depends on biomolecular recognition at the surface of cell membranes. In the case of glycolipid receptors, these events are expected to be influenced by how the glycan epitope close to the membrane is presented to the virus. This presentation of membrane-associated glycans is more restricted than that of glycans in solution, particularly because of orientational constraints imposed on the glycolipid through its lateral interactions with other membrane lipids and proteins. We have developed and employed a total internal reflection fluorescence microscopy-based binding assay and a scheme for molecular dynamics (MD) membrane simulations to investigate the consequences of various glycan presentation effects. The system studied was histo-blood group antigen (HBGA) epitopes of membrane-bound glycosphingolipids (GSLs) derived from small intestinal epithelium of humans (type 1 chain) and dogs (type 2 chain) interacting with GII.4 norovirus-like particles. Our experimental results showed strong binding to all lipid-linked type 1 chain HBGAs but no or only weak binding to the corresponding type 2 chain HBGAs. This is in contrast to results derived from STD experiments with free HBGAs in solution where binding was observed for Lewis x. The MD data suggest that the strong binding to type 1 chain glycolipids was due to the well-exposed (1,2)-linked α-l-Fucp and (1,4)-linked α-l-Fucp residues, while the weaker binding or lack of binding to type 2 chain HBGAs was due to the very restricted accessibility of the (1,3)-linked α-l-Fucp residue when the glycolipid is embedded in a phospholipid membrane. Our results not only contribute to a general understanding of protein-carbohydrate interactions on model membrane surfaces, particularly in the context of virus binding, but also suggest a possible role of human intestinal GSLs as potential receptors for norovirus uptake.
[Mh] Termos MeSH primário: Apresentação do Antígeno/fisiologia
Antígenos de Grupos Sanguíneos/imunologia
Glicoesfingolipídeos/metabolismo
Norovirus/fisiologia
Ligação Viral
[Mh] Termos MeSH secundário: Animais
Cães
Seres Humanos
Mucosa Intestinal
Simulação de Dinâmica Molecular
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Group Antigens); 0 (Glycosphingolipids)
[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:170316
[St] Status:MEDLINE
[do] DOI:10.1021/acschembio.7b00152


  10 / 3941 MEDLINE  
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[PMID]:28277984
[Au] Autor:Tuzcu H; Unal B; Kirac E; Konuk E; Ozcan F; Elpek GO; Demir N; Aslan M
[Ad] Endereço:a Department of Medical Biochemistry , Akdeniz University Faculty of Medicine , Antalya , Turkey.
[Ti] Título:Neutral sphingomyelinase inhibition alleviates apoptosis, but not ER stress, in liver ischemia-reperfusion injury.
[So] Source:Free Radic Res;51(3):253-268, 2017 Mar.
[Is] ISSN:1029-2470
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previous studies have revealed the activation of neutral sphingomyelinase (N-SMase)/ceramide pathway in hepatic tissue following warm liver ischemia reperfusion (IR) injury. Excessive ceramide accumulation is known to potentiate apoptotic stimuli and a link between apoptosis and endoplasmic reticulum (ER) stress has been established in hepatic IR injury. Thus, this study determined the role of selective N-SMase inhibition on ER stress and apoptotic markers in a rat model of liver IR injury. Selective N-SMase inhibitor was administered via intraperitoneal injections. Liver IR injury was created by clamping blood vessels supplying the median and left lateral hepatic lobes for 60 min, followed by 60 min reperfusion. Levels of sphingmyelin and ceramide in liver tissue were determined by an optimized multiple reactions monitoring (MRM) method using ultrafast-liquid chromatography (UFLC) coupled with tandem mass spectrometry (MS/MS). Spingomyelin levels were significantly increased in all IR groups compared with controls. Treatment with a specific N-SMase inhibitor significantly decreased all measured ceramides in IR injury. A significant increase was observed in ER stress markers C/EBP-homologous protein (CHOP) and 78 kDa glucose-regulated protein (GRP78) in IR injury, which was not significantly altered by N-SMase inhibition. Inhibition of N-SMase caused a significant reduction in phospho-NF-kB levels, hepatic TUNEL staining, cytosolic cytochrome c, and caspase-3, -8, and -9 activities which were significantly increased in IR injury. Data herein confirm the role of ceramide in increased apoptotic cell death and highlight the protective effect of N-SMase inhibition in down-regulation of apoptotic stimuli responses occurring in hepatic IR injury.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Inibidores Enzimáticos/administração & dosagem
Fígado/efeitos dos fármacos
Traumatismo por Reperfusão/tratamento farmacológico
Esfingomielina Fosfodiesterase/genética
[Mh] Termos MeSH secundário: Animais
Vasos Sanguíneos/efeitos dos fármacos
Vasos Sanguíneos/patologia
Caspases/biossíntese
Ceramidas/metabolismo
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Glicoesfingolipídeos/metabolismo
Proteínas de Choque Térmico/biossíntese
Seres Humanos
Fígado/lesões
Fígado/patologia
Ratos
Esfingomielina Fosfodiesterase/antagonistas & inibidores
Fator de Transcrição CHOP/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ceramides); 0 (Ddit3 protein, rat); 0 (Enzyme Inhibitors); 0 (Glycosphingolipids); 0 (Heat-Shock Proteins); 0 (Hspa5 protein, rat); 147336-12-7 (Transcription Factor CHOP); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/10715762.2017.1298103



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