Search results for "oligodendrocyte"

showing 10 items of 104 documents

Cytoprotective organoselenium compounds for oligodendrocytes

2021

Abstract Herein we report the synthesis of peptide-like and tetrazole-based organoselenium compounds via Ugi and Ugi-azide reactions, respectively. The organoselenium compounds' intrinsic cytoprotective and antioxidant capacities were evaluated in 158 N and 158JP murine oligodendrocytes. Furthermore, their redox properties were theoretically evaluated using Molecular Operating Environment-docking studies. Most of the compounds did not exhibit any cytotoxicity against the 158JP and 158 N cells. Among the tested compounds, the tetrazole- (e.g., 6, 7, and 9) and the pseudopeptide-based organoselenium compounds (e.g., 11, 15, and 17) displayed antioxidant properties. On the other hand, the quin…

AntioxidantCytoprotectiveGeneral Chemical Engineeringmedicine.medical_treatmentOrganoselenium02 engineering and technology010402 general chemistry01 natural sciencesRedoxlcsh:Chemistrychemistry.chemical_compoundOrganoselenium CompoundmedicineTetrazoleCytotoxicityTetrazoleOligodendrocytesGeneral Chemistry021001 nanoscience & nanotechnologyCombinatorial chemistry0104 chemical sciencesUgi reactionchemistrylcsh:QD1-999Antioxidant0210 nano-technologyArabian Journal of Chemistry
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B7‐H1 and CD8+Treg: The enigmatic role of B7‐H1 in peripheral tolerance

2009

The interaction between B7-H1 (PD-L1) expressed on APC with PD-1 expressed by T cells was shown previously to result in inhibition of T-cell activation and autoimmune diseases. A paper in this issue of the European Journal of Immunology demonstrates that DC B7-H1 expression can in fact enhance autoimmunity, rather than suppress it. Using a model of direct injection of self antigen-loaded DC into the CNS, the authors demonstrate that DC with intact B7-H1 expression exacerbate CNS autoimmune disease. Importantly, the improved disease outcome in animals treated with B7-H1(-/-) DC is a result of a population of CD8(+) Treg cells that expand at the site of autoimmune inflammation.

Autoimmune diseaseeducation.field_of_studybiologyImmunologyPopulationPeripheral tolerancemedicine.diseasemedicine.disease_causeAutoimmunityMyelin oligodendrocyte glycoproteinAntigenImmunologymedicinebiology.proteinImmunology and AllergyeducationCD8B7-H1 AntigenEuropean Journal of Immunology
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The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses.

2011

Abstract Lymphnode swelling during immune responses is a transient, finely regulated tissue rearrangement, accomplished with the participation of the extracellular matrix. Here we show that murine and human reactive lymph nodes express SPARC in the germinal centres. Defective follicular dendritic cell networking in SPARC-deficient mice is accompanied by a severe delay in the arrangement of germinal centres and development of humoral autoimmunity, events that are linked to Th17 development. SPARC is required for the optimal and rapid differentiation of Th17 cells, accordingly we show delayed development of experimental autoimmune encephalomyelitis whose pathogenesis involves Th17. Not only h…

Autoimmune diseases; Extracellular matrix; Germinal centre reaction; Th17 cellsEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyCell CommunicationBiologyfollicular dendritic cellExtracellular matrixAnimals Genetically ModifiedMiceImmune systemSPARC; follicular dendritic cell; Th17Autoimmune diseasemedicinegerminal centre reactionImmunology and AllergyAnimalsHumansautoimmune diseasesOsteonectinMice KnockoutB-LymphocytesCD40Follicular dendritic cellsExperimental autoimmune encephalomyelitisMatricellular proteinGerminal centerSPARCCell Differentiationmedicine.diseaseCell biologyExtracellular MatrixImmunity HumoralMice Inbred C57BLCrosstalk (biology)Disease Models AnimalImmunologybiology.proteinDisease ProgressionTh17 CellsImmunizationMyelin-Oligodendrocyte GlycoproteinTh17autoimmune diseases; extracellular matrix; germinal centre reaction; th17 cellsDendritic Cells FollicularMyelin ProteinsJournal of autoimmunity
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A low repeat length in oligodendrocyte chromatin

1985

Abstract: The behavior of oligodendrocyte chromatin after micrococcal nuclease digestion of nuclei was assayed in brains of rats of four different ages. During oligodendrocyte differentiation, a decreasing sensitivity of the chromatin to enzymatic attack was observed. On the other hand, the nucleosomal repeat length showed a slight tendency to increase during development. It is worth noting that even the highest values reported here for “oligodendrocyte’ chromatin repeat lengths are significantly lower than 200 base pairs, the value previously reported by others for “non‐astrocytic glia.” Copyright © 1985, Wiley Blackwell. All rights reserved

Base pairCellular differentiationFluorescent Antibody TechniqueOligodendrocyte differentiationBiochemistryCellular and Molecular NeuroscienceSettore BIO/10 - BiochimicamedicineAnimalsMicrococcal NucleaseNucleosomeRepetitive Sequences Nucleic AcidElectrophoresis Agar GelGeneticsNucleosomal Repeat LengthbiologyAge FactorsOligodendrocyte differentiationDNAMolecular biologyChromatinOligodendrocyteNucleosomesRatsChromatinOligodendrogliamedicine.anatomical_structureLiverbiology.proteinSettore MED/26 - NeurologiaNucleosomal repeat lengthNeurogliaBrain StemMicrococcal nuclease
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The role of CD8+ T cells and their local interaction with CD4+ T cells in myelin oligodendrocyte glycoprotein35-55-induced experimental autoimmune en…

2013

Abstract T cells have an essential role in the induction of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Although for CD4+ T cells it is well established that they contribute to the disease, less is known about the role of CD8+ T cells. Our aim was to determine the individual contribution of CD4+ and CD8+ T cells in myelin oligodendrocyte glycoprotein (MOG)35–55–induced EAE. We investigated MOG35–55–activated CD8+ T cells to clarify their potential to induce or attenuate EAE. We monitored the behavior of CD8+ T cells and their interaction with CD4+ T cells directly at the site of inflammation in the CNS using intravital imaging of the brainstem of…

CD4-Positive T-LymphocytesCentral Nervous SystemEncephalomyelitis Autoimmune ExperimentalT cellImmunologyMedizinCell CommunicationCD8-Positive T-LymphocytesLymphocyte ActivationInterleukin 21MiceCell MovementmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorInflammationMice KnockoutCD40biologyCD28Molecular biologyPeptide FragmentsMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinInterleukin 12Myelin-Oligodendrocyte GlycoproteinCD8Journal of immunology (Baltimore, Md. : 1950)
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Cross-recognition of a myelin peptide by CD8+ T cells in the CNS is not sufficient to promote neuronal damage.

2015

Multiple sclerosis (MS) is an inflammatory disease of the CNS thought to be driven by CNS-specific T lymphocytes. Although CD8+T cells are frequently found in multiple sclerosis lesions, their distinct role remains controversial because direct signs of cytotoxicity have not been confirmedin vivo. In the present work, we determined that murine ovalbumin-transgenic (OT-1) CD8+T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40–54 (MOG40–54) bothin vitroandin vivo. The aim of this study was to investigate whether such cross-recognizing CD8+T cells are capable of inducing CNS damagein vivo. Using intravital two-photon microscopy in the mouse model of multiple sclerosis, …

CD4-Positive T-LymphocytesCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisAutoimmunityMice TransgenicCD8-Positive T-Lymphocytesmedicine.disease_causeMyelin oligodendrocyte glycoproteinMyelinMiceIn vivomedicineCytotoxic T cellAnimalsCells CulturedCell ProliferationbiologyCell DeathGeneral NeuroscienceMultiple sclerosisArticlesmedicine.diseaseMolecular mimicrymedicine.anatomical_structureImmunologyNerve Degenerationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinCD8Intravital microscopyThe Journal of neuroscience : the official journal of the Society for Neuroscience
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A novel plasmid DNA electroporation method allows transfection of murine DC.

2007

Under steady state conditions dendritic cells (DC) exert tolerogenic function, but acquire potent immunogenic function due to strong upregulation of costimulatory molecules and proinflammatory cytokines. In numerous studies the potential of modified DC to induce tolerance or immune reactions towards a distinct antigen has been demonstrated. However, DC are refractory to transfection with plasmid DNA by non-viral methods. In this study we have tested the suitability of a newly developed electroporation device to transfect immature murine bone-marrow derived DC (BM-DC). Transfected BM-DC expressed reporter molecules at considerable extent which renders this method suitable to perform all kind…

CD4-Positive T-LymphocytesvirusesTransgeneT cellImmunologyGenetic VectorsGene ExpressionMice TransgenicBiologyTransfectionProinflammatory cytokineMyelin oligodendrocyte glycoproteinMicemedicineImmunology and AllergyAnimalsTransgenesCells CulturedCell ProliferationMice Inbred BALB CExpression vectorElectroporationTransfectionDendritic cellDendritic CellsMolecular biologyInterleukin-10Mice Inbred C57BLMyelin-Associated Glycoproteinmedicine.anatomical_structureElectroporationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPlasmidsJournal of immunological methods
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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Multiple sclerosis patient-derived CSF induces transcriptional changes in proliferating oligodendrocyte progenitors.

2014

Background: Cerebrospinal fluid (CSF) is in contact with brain parenchyma and ventricles, and its composition might influence the cellular physiology of oligodendrocyte progenitor cells (OPCs) thereby contributing to multiple sclerosis (MS) disease pathogenesis. Objective: To identify the transcriptional changes that distinguish the transcriptional response induced in proliferating rat OPCs upon exposure to CSF from primary progressive multiple sclerosis (PPMS) or relapsing remitting multiple sclerosis (RRMS) patients and other neurological controls. Methods: We performed gene microarray analysis of OPCs exposed to CSF from neurological controls, or definitive RRMS or PPMS disease course. R…

Cell physiologyAdultPathologymedicine.medical_specialtyTranscription GeneticGalectin 3GalectinsImmunocytochemistryBiologyArticleCerebrospinal fluidMultiple Sclerosis Relapsing-RemittingNeural Stem CellsmedicineAnimalsHumansProgenitor cellCells CulturedCell ProliferationCerebrospinal FluidMultiple sclerosisBrainHuman brainBlood ProteinsMultiple Sclerosis Chronic Progressivemedicine.diseaseMicroarray AnalysisNeural stem cellOligodendrocyteRatsUp-RegulationOligodendrogliamedicine.anatomical_structureNeurologyNeurology (clinical)Multiple sclerosis (Houndmills, Basingstoke, England)
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In Vivo Imaging of Partially Reversible Th17 Cell-Induced Neuronal Dysfunction in the Course of Encephalomyelitis

2010

SummaryNeuronal damage in autoimmune neuroinflammation is the correlate for long-term disability in multiple sclerosis (MS) patients. Here, we investigated the role of immune cells in neuronal damage processes in animal models of MS by monitoring experimental autoimmune encephalomyelitis (EAE) by using two-photon microscopy of living anaesthetized mice. In the brainstem, we detected sustained interaction between immune and neuronal cells, particularly during disease peak. Direct interaction of myelin oligodendrocyte glycoprotein (MOG)-specific Th17 and neuronal cells in demyelinating lesions was associated with extensive axonal damage. By combining confocal, electron, and intravital microsc…

Cell signalingPathologymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalEncephalomyelitisImmunologyApoptosisCell CommunicationBiologyReceptors N-Methyl-D-AspartateMyelin oligodendrocyte glycoproteinMiceImmune systemCell MovementmedicineAnimalsImmunology and AllergyNeuroinflammationCells CulturedNeuronsMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukin-17T-Lymphocytes Helper-Inducermedicine.diseaseAxonsCell biologyMice Inbred C57BLInfectious Diseasesnervous systemSynapsesbiology.proteinCalciumIntravital microscopyImmunity
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