Search results for "oligodendrocyte"

showing 10 items of 104 documents

Involvement of Kv3.1 potassium chanels in 7-ketocholesterol, 24S-hydroxycholesterol and C24 : 0-induced lipotoxicity on 158N and BV-2 cells : relatio…

2017

Potassium (K+) is involved in the regulation of cellular excitability, cell cycle regulation, cell viability, neuroprotection and maintenance of microglial and oligodendrocytic functions. Potassium dysfunction, described in several neurodegenerative diseases such as Alzheimer's Disease (AD), multiple sclerosis (MS), Parkinson's disease and Huntington's disease, may be a potential therapeutic target. The underlying toxic mechanisms of these neurodegenerative pathologies involve oxysterols, which are oxidized cholesterol derivatives, and fatty acids including those associated with peroxisomal metabolism. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0),…

Cellules microgliales murines BV-2Oligodengrocytes murins 158N158N murine oligodendrocytesCanaux KvKv3.1b7-cétocholestérolNeurodégénérescenceMaladie d’Alzheimer24S-hydroxycholesterolTetracosanoic acid (C24:0)24S-hydroxycholestérolPotassium[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAcide tétracosanoïque (C24:0)NeurodegenerationMurine microglial BV-2 cellsAlzheimer’s disease7-ketocholesterolKv channels
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NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling

2018

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIKΔT) mice. Despite showing normal development of lymphoid organs, NIKΔT mice were resistant to induction of CNS autoimmunity. T cells from NIKΔT mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK-/- T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dy…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesT cellPrimary Cell CultureImmunologyReceptors Antigen T-CellPriming (immunology)Protein Serine-Threonine KinasesBiologyLymphocyte ActivationImmunological synapseMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsImmunology and AllergyProtein kinase BAdaptor Proteins Signal TransducingMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinasePhospholipase C gammaGene Expression ProfilingZAP70T-cell receptorMembrane ProteinsPhosphoproteinsActinsPeptide FragmentsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisMyelin-Oligodendrocyte GlycoproteinLymph NodesSignal transductionT-Box Domain ProteinsProto-Oncogene Proteins c-aktSpleenSignal TransductionJournal of Autoimmunity
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IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous system

2011

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by …

Central Nervous SystemBlotting WesternIκB kinaseBiologyddc:616.07Myelin assemblyMicroglia/cytology/metabolismNerve Regeneration/physiologyDemyelinating Diseases/chemically induced/metabolism03 medical and health sciencesMyelinCuprizoneMice0302 clinical medicineCentral Nervous System/cytology/metabolismmedicineAnimalsRemyelinationCHUKMyelin Sheath030304 developmental biologyAstrocytes/cytology/metabolismMyelin Sheath/metabolism0303 health sciencesReverse Transcriptase Polymerase Chain ReactionSignal Transduction/physiologyI-Kappa-B KinaseNF-kappa BI-kappa B Kinase/metabolismOriginal ArticlesOligodendrocyte3. Good healthCell biologyI-kappa B KinaseNerve RegenerationOligodendrogliamedicine.anatomical_structureOligodendroglia/metabolismAstrocytesNF-kappa B/metabolismNeurogliaNeurology (clinical)MicrogliaNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesSignal Transduction
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NG2-positive cells in CNS function and the pathological role of antibodies against NG2 in demyelinating diseases

2005

NG2 is expressed by a variety of immature glia in the CNS including oligodendrocyte progenitor cells, paranodal astrocytes and perisynaptic glia. The protein has a large extracellular domain with two LNS/Lam G domains at the N-terminus and a short intracellular tail with a PDZ-recognition domain at the C-terminus. Experiments suggest that the protein plays a role in migration. The PDZ protein GRIP was identified as an intracellular binding partner of NG2 in immature glial cells. A complex is formed between GRIP, NG2 and the AMPA class of glutamate receptors: this may position these glial receptors towards sites of neuronal glutamate release at synapses and during myelination. Identification…

Central Nervous SystemCentral nervous systemPDZ domainGlutamate receptorAMPA receptorBiologyModels BiologicalAntibodiesOligodendrocytemedicine.anatomical_structurenervous systemNeurologySynapsesmedicineAnimalsHumansNeurogliaProteoglycansNeurology (clinical)AntigensRemyelinationReceptorNeurogliaNeuroscienceDemyelinating DiseasesJournal of the Neurological Sciences
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Oligodendrogliogenic and neurogenic adult subependymal zone neural stem cells constitute distinct lineages and exhibit differential responsiveness to…

2012

The adult mouse subependymal zone (SEZ) harbours adult neural stem cells (aNSCs) that give rise to neuronal and oligodendroglial progeny. However it is not known whether the same aNSC can give rise to neuronal and oligodendroglial progeny or whether these distinct progenies constitute entirely separate lineages. Continuous live imaging and single-cell tracking of aNSCs and their progeny isolated from the mouse SEZ revealed that aNSCs exclusively generate oligodendroglia or neurons, but never both within a single lineage. Moreover, activation of canonical Wnt signalling selectively stimulated proliferation within the oligodendrogliogenic lineage, resulting in a massive increase in oligodendr…

Central Nervous SystemMaleReceptor Platelet-Derived Growth Factor alphaWnt signallingNerve Tissue ProteinsBiologyWnt3 ProteinMiceNeural Stem CellsLive cell imagingSubependymal zoneBasic Helix-Loop-Helix Transcription FactorsAnimalsCell LineageWnt Signaling PathwayCells CulturedProgenitorCell ProliferationCell CycleWnt signaling pathwayCell DifferentiationCell BiologyOligodendrocyte Transcription Factor 2Neural stem cellCell biologyMice Inbred C57BLOligodendrogliaFemaleCell DivisionNature cell biology
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A critical role for the cholesterol-associated proteolipids PLP and M6B in myelination of the central nervous system.

2012

The formation of central nervous system myelin by oligodendrocytes requires sterol synthesis and is associated with a significant enrichment of cholesterol in the myelin membrane. However, it is unknown how oligodendrocytes concentrate cholesterol above the level found in nonmyelin membranes. Here, we demonstrate a critical role for proteolipids in cholesterol accumulation. Mice lacking the most abundant myelin protein, proteolipid protein (PLP), are fully myelinated, but PLP-deficient myelin exhibits a reduced cholesterol content. We therefore hypothesized that "high cholesterol" is not essential in the myelin sheath itself but is required for an earlier step of myelin biogenesis that is f…

Central Nervous SystemProteolipid protein 1Nerve Tissue ProteinsBiologyCell Line03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundMyelinMice0302 clinical medicineimmune system diseasesmedicineEvoked Potentials Auditory Brain StemAnimalsMyelin Proteolipid ProteinMyelin Sheath030304 developmental biology0303 health sciencesMembrane GlycoproteinsCholesterolProteolipidsLeukodystrophyPelizaeus–Merzbacher diseasemedicine.diseaseOligodendrocytenervous system diseasesMyelin proteolipid proteinmedicine.anatomical_structureCholesterolnervous systemNeurologychemistryBiochemistryEvoked Potentials Visuallipids (amino acids peptides and proteins)Vomeronasal Organ030217 neurology & neurosurgeryGlia
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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Role of the cellular prion protein in oligodendrocyte precursor cell proliferation and differentiation in the developing and adult mouse CNS

2012

There are numerous studies describing the signaling mechanisms that mediate oligodendrocyte precursor cell (OPC) proliferation and differentiation, although the contribution of the cellular prion protein (PrP c) to this process remains unclear. PrP c is a glycosyl-phosphatidylinositol (GPI)-anchored glycoprotein involved in diverse cellular processes during the development and maturation of the mammalian central nervous system (CNS). Here we describe how PrP c influences oligodendrocyte proliferation in the developing and adult CNS. OPCs that lack PrP c proliferate more vigorously at the expense of a delay in differentiation, which correlates with changes in the expression of oligodendrocyt…

Central Nervous SystemTelencephalonMouseCellular differentiationanimal diseasesGene ExpressionHippocampusMice0302 clinical medicineNeural Stem CellsGene expressionMolecular Cell BiologyNeurobiology of Disease and RegenerationCell proliferationNeuronsCerebral CortexMice Knockout0303 health sciencesProliferació cel·lularMultidisciplinaryNeurogenesisQRCell DifferentiationAnimal ModelsNeural stem cell3. Good healthCell biologyOligodendrogliamedicine.anatomical_structureKnockout mouseMedicineFemaleBiologia del desenvolupamentCellular TypesCell DivisionResearch ArticlePrionsNeurogenesisScienceBiologyModels BiologicalCell Growth03 medical and health sciencesModel OrganismsDevelopmental NeuroscienceNeuroglial Developmentmental disordersDevelopmental biologymedicineAnimalsPrPC ProteinsBiology030304 developmental biologyCell ProliferationCell growthLineage markersMolecular DevelopmentOligodendrocytenervous system diseasesMice Inbred C57BLImmunologyOrganism Development030217 neurology & neurosurgeryDevelopmental BiologyNeuroscience
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Myelin Proteome Analysis: Methods and Implications for the Myelin Cytoskeleton

2012

Myelin, the multilayered membrane that enwraps and insulates neuronal axons for fast signal propagation, is a plasma membrane specialization of oligodendrocytes and Schwann cells in the central and peripheral nervous system, respectively. Here we provide our lab protocols for the puri fi cation of myelin from mouse brains and for gel-based and gel-free proteomic applications, as well as a brief discussion with respect to our current knowledge of the myelin cytoskeleton.

ChemistryLeukodystrophySchwann cellmedicine.diseaseProteomicsOligodendrocyteMyelinmedicine.anatomical_structurenervous systemPeripheral nervous systemProteomemedicineCytoskeletonNeuroscience
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Chromatin remodelling factor Mll1 is essential for neurogenesis from postnatal neural stem cells

2009

Epigenetic mechanisms that maintain neurogenesis throughout adult life remain poorly understood(1). Trithorax group (trxG) and Polycomb group (PcG) gene products are part of an evolutionarily conserved chromatin remodelling system that activate or silence gene expression, respectively(2). Although PcG member Bmi1 has been shown to be required for postnatal neural stem cell self-renewal(3,4), the role of trxG genes remains unknown. Here we show that the trxG member Mll1 (mixed-lineage leukaemia 1) is required for neurogenesis in the mouse postnatal brain. Mll1-deficient subventricular zone neural stem cells survive, proliferate and efficiently differentiate into glial lineages; however, neur…

Chromatin ImmunoprecipitationEpigenetic regulation of neurogenesisCell SurvivalNeurogenesisCellular differentiationSubventricular zoneNerve Tissue ProteinsBiologyMethylationArticleHistonesMiceBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsCell LineageCells CulturedCell ProliferationGliogenesisHomeodomain ProteinsNeuronsMultidisciplinaryStem CellsNeurogenesisCell DifferentiationHistone-Lysine N-MethyltransferaseOligodendrocyte Transcription Factor 2Chromatin Assembly and DisassemblyOlfactory BulbMolecular biologyChromatinNeural stem cellCell biologyChromatinmedicine.anatomical_structureAnimals NewbornStem cellNeurogliaMyeloid-Lymphoid Leukemia ProteinTranscription Factors
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