Search results for "ASTROCYTES"

showing 10 items of 171 documents

Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβ

2019

Aspirin has been used as anti-inflammatory and anti-aggregate for decades but the precise mechanism(s) of action after the presence of the toxic peptide Aβ1-42 in cultured astrocytes remains poorly resolved. Here we use low-doses of aspirin (10-7 M) in astrocytes in primary culture in presence or absence of Aβ1-42 toxic peptide. We noted an increase of cell viability and proliferation with or without Aβ1-42 peptide presence in aspirin treated cells. In addition, a decrease in apoptosis, determined by Caspase 3 activity and the expression of Cyt c and Smac/Diablo, were detected. Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-β and TNF-α) and NF-ᴋB prot…

InflammationAmyloid beta-PeptidesAspirinDose-Response Relationship DrugCell SurvivalTumor Necrosis Factor-alphaInterleukin-1betaPrimary Cell CultureNF-kappa BAlzheimer's diseasePeptide FragmentsRatsOxidative StressGene Expression RegulationAlzheimer DiseaseAstrocytesAnimalsHumansAmyloid-βCell ProliferationResearch PaperInternational journal of medical sciences
researchProduct

Correction to: Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute …

2019

Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI."Depletion of regulatory T cell" (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological, protein, and gene expressio…

InflammationGeneral NeuroscienceImmunologyCorrectionBrainT-Lymphocytes Regulatorylcsh:RC346-429Lymphocyte DepletionCellular and Molecular NeuroscienceDisease Models AnimalInterferon-gammaMiceNeurologyAstrocytesBrain Injuries TraumaticAnimalsGliosislcsh:Neurology. Diseases of the nervous systemJournal of Neuroinflammation
researchProduct

Na+ dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) in primary astrocyte cultures: effect of oxidative stress.

2001

Abstract The Na + -dependent l -glutamate transporters EAAT1(GLAST), EAAT2 (GLT-1) and EAAT3 (EAAC1) are expressed in primary astrocyte cultures, showing that the EAAT3 transporter is not neuron-specific. The presence of these three transporters was evaluated by RT–PCR, immunoblotting, immunocytochemical techniques, and transport activity. When primary astrocyte cultures were incubated with l -buthionine-( S , R )-sulfoximine (BSO), a selective inhibitor of γ-glutamylcysteine synthetase, the GSH concentration was significantly lower than in control cultures, but the expression and amount of protein of EAAT1, EAAT2 and EAAT3 and transport of l -glutamate was unchanged. Oxidative stress was c…

InsecticidesAmino Acid Transport System X-AGImmunoblottingGlutamic AcidOxidative phosphorylationBiologymedicine.disease_causeDDTchemistry.chemical_compoundGlutamate Plasma Membrane Transport ProteinsLactate dehydrogenasemedicineAnimalsRNA MessengerRats WistarMolecular BiologyCells CulturedBrain ChemistryL-Lactate DehydrogenaseSymportersReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceSodiumGlutamate receptorTransporterGlutathioneGlutathioneImmunohistochemistryRatsExcitatory Amino Acid Transporter 1Oxidative Stressmedicine.anatomical_structureExcitatory Amino Acid Transporter 3BiochemistrychemistryAnimals NewbornExcitatory Amino Acid Transporter 2Microscopy FluorescenceAstrocytesNeurogliaElectrophoresis Polyacrylamide GelNeurology (clinical)Carrier ProteinsOxidative stressDevelopmental BiologyAstrocyteBrain research
researchProduct

Intracellular Na+ concentration influences short-term plasticity of glutamate transporter-mediated currents in neocortical astrocytes.

2012

Fast synaptic transmission requires a rapid clearance of the released neurotransmitter from the extracellular space. Glial glutamate transporters (excitatory amino acid transporters, EAATs) strongly contribute to glutamate removal. In this work, we investigated the paired-pulse plasticity of synaptically activated, glutamate transporter-mediated currents (STCs) in cortical layer 2/3 astrocytes. STCs were elicited by local electrical stimulation in layer 4 in the presence of ionotropic glutamate (AMPA and NMDA), GABAA, and GABAB receptor antagonists. In experiments with low [Na+]i (5 mM) intrapipette solution, STCs elicited by paired-pulse stimulation demonstrated paired-pulse facilitation (…

Intracellular FluidPatch-Clamp TechniquesAmino Acid Transport System X-AGBiophysicsNipecotic AcidsAction PotentialsNeocortexAMPA receptorTetrodotoxinBiologyGABAB receptorAnisolesIn Vitro TechniquesSynaptic TransmissionGABA AntagonistsCellular and Molecular NeuroscienceMiceCadmium ChlorideEthers CyclicOximesmedicineGABA transporterAnimalsgamma-Aminobutyric AcidBenzofuransAspartic AcidNeuronal PlasticityGABAA receptorRhodaminesSodiumGlutamate receptorCalcium Channel BlockersElectric StimulationMice Inbred C57BLmedicine.anatomical_structureNeurologyAnimals NewbornAstrocytesExcitatory postsynaptic potentialBiophysicsbiology.proteinNMDA receptorNeuroscienceExcitatory Amino Acid AntagonistsAstrocyteSodium Channel BlockersGlia
researchProduct

Requirement of caveolae microdomains in extracellular signal-regulated kinase and focal adhesion kinase activation induced by endothelin-1 in primary…

1999

Endothelin-1 (ET-1) mitogenic activity in astrocytes is mediated by the activation of the extracellular signal-regulated kinase (ERK) pathway together with the Rho-dependent activation of the focal adhesion kinase (FAK) pathway. To clarify the mechanisms responsible for the coordinate activation of both pathways in the ET-1 signal propagation, the involvement of caveolae microdomains, suggested to play a role in signal transduction, was evaluated. In this study, it is reported that caveolae of primary astrocytes are enriched in endothelin receptor (ETB-R). Furthermore, signaling molecules such as the adaptor proteins Shc and Grb2, and the small G protein Rho, also reside within these microd…

MAPK/ERK pathwayCaveolin 1BiologyBiochemistryCaveolinsFocal adhesionCellular and Molecular Neurosciencechemistry.chemical_compoundCaveolaeCell AdhesionAnimalsFilipinPhosphorylationCells CulturedCytoskeletonMitogen-Activated Protein Kinase 1Endothelin-1Signal transducing adaptor proteinMembrane ProteinsTyrosine phosphorylationProtein-Tyrosine KinasesActinsCell biologyAnti-Bacterial AgentsCell CompartmentationRatsEnzyme ActivationchemistryAstrocytesFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesCaveolin 1Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinTyrosineGRB2Signal transductionExtracellular SpaceCell Adhesion MoleculesSignal TransductionJournal of neurochemistry
researchProduct

Effect of oxidative stress on UDP-glucuronosyltransferases in rat astrocytes.

2012

WOS:000309170300003; International audience; The present work reports data regarding effects of an induced oxidative stress on the mainly expressed isoforms of UDP-glucuronosyltransferases (UGTs) in the brain. UGT1A6 and UGT1A7 expression and enzymatic activities toward the 1-naphthol were analyzed in rat cultured astrocytes following the exposure for 48 h to redox-cycling xenobiotic compounds such as quinones and bipyridinium ions. The expression of NADPH:cytochrome P450 reductase and NAD(P)H:quinone oxidoreductase 1 (NQO1) was also investigated. Oxidative stress induced significant deleterious changes in astrocyte morphology, decreased cell viability and inhibited catalytic function of UG…

MESH : Oxidative StressMESH : RNA MessengerAntioxidantTranscription Geneticmedicine.medical_treatmentToxicologyNAD(P)H:quinone oxidoreductase 1MESH: GlucuronosyltransferaseAntioxidantsSubstrate SpecificityRats Sprague-Dawley0302 clinical medicineMESH: NADPH-Ferrihemoprotein ReductaseMESH: GlucuronidesNAD(P)H Dehydrogenase (Quinone)MESH : CatalysisMESH: AnimalsMESH : NAD(P)H Dehydrogenase (Quinone)GlucuronosyltransferaseCells Culturedchemistry.chemical_classificationMESH : Cell Survival0303 health sciencesMESH : Substrate SpecificityMESH : Animals NewbornCytochrome P450 reductaseGeneral MedicineMESH: Cell SurvivalMESH: Pyridinium CompoundsMESH : AntioxidantsMESH: Cells CulturedOxidative phosphorylationGene Expression Regulation EnzymologicMESH : QuinonesMESH : Glucuronides03 medical and health sciencesRNA MessengerCell ShapeNADPH-Ferrihemoprotein ReductaseMESH : Oxidation-ReductionMESH : Pyridinium CompoundsMESH: NaphtholsMESH : GlucuronosyltransferaseMESH: AntioxidantsMESH: CatalysischemistryOxidative stressAstrocytesReactive Oxygen Species030217 neurology & neurosurgeryMESH: Oxidation-ReductionTime Factors[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMESH : Reactive Oxygen SpeciesNADPH:cytochrome P450 reductasePyridinium CompoundsNaphtholsMESH: Rats Sprague-DawleyProtein oxidationmedicine.disease_causeMESH: Animals NewbornMESH: NAD(P)H Dehydrogenase (Quinone)Protein CarbonylationMESH : OxidantsMESH: OxidantsMelatoninMESH: MelatoninMESH: Oxidative StressMESH : MelatoninMESH : RatsMESH: Gene Expression Regulation EnzymologicQuinonesMESH: Reactive Oxygen SpeciesOxidantsBiochemistryMESH : Protein CarbonylationOxidation-ReductionUDP-glucuronosyltransferaseMESH : Time FactorsMESH: Protein CarbonylationMESH: RatsCell SurvivalMESH : NaphtholsBiologyCatalysisMESH: QuinonesMESH : Gene Expression Regulation EnzymologicGlucuronidesMESH : Cells CulturedmedicineAnimalsMESH: Cell Shape030304 developmental biologyMESH: RNA MessengerReactive oxygen speciesMESH: Transcription GeneticMESH: Time FactorsMESH : AstrocytesMESH : Transcription GeneticNAD(P)H Dehydrogenase (Quinone)MESH : Rats Sprague-DawleyRatsMESH: AstrocytesAnimals NewbornMESH : NADPH-Ferrihemoprotein ReductaseMESH: Substrate SpecificityMESH : AnimalsNAD+ kinaseMESH : Cell Shape[SDV.AEN]Life Sciences [q-bio]/Food and NutritionOxidative stress
researchProduct

MK801 blocks hypoxic blood-brain-barrier disruption and leukocyte adhesion.

2008

The aim of the present study was to examine the signaling pathways of hypoxia followed by reoxygenation (H/R)-induced disruption of the blood-brain-barrier (BBB) in a co-culture of astrocytes and brain endothelial cells (BEC) in vitro. We analyzed the possible stabilizing effect of MK801, a highly selective N-methyl-d-aspartate receptor (NMDAR) antagonist, on BBB integrity. Levels of reactive oxygen species (ROS), glutamate (Glut) release and monocyte adhesion were measured under normoxia and H/R. BBB integrity was monitored measuring the trans-endothelial electrical resistance (TEER). TEER values dropped under H/R conditions which was abolished by MK801. Glut release from astrocytes, but n…

Macrocyclic CompoundsSwineGlutamic AcidBiologyBlood–brain barrierchemistry.chemical_compoundmedicineExtracellularCell AdhesionElectric ImpedanceLeukocytesAnimalsEnzyme InhibitorsOxazolesCells Culturedchemistry.chemical_classificationReactive oxygen speciesRyanodine receptorRyanodineGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorAcetophenonesBrainEndothelial CellsCell HypoxiaCoculture TechniquesCell biologyOxygenmedicine.anatomical_structurechemistryBlood-Brain BarrierAstrocytesApocyninCalciumNAD+ kinaseDizocilpine MaleateReactive Oxygen SpeciesExcitatory Amino Acid AntagonistsNeuroscience letters
researchProduct

Neuroprotective action of diazepam at very low and moderate doses in Alzheimer's disease model rats

2018

Abstract Early manifestations of Alzheimer's disease (AD) include neuroinflammation, disrupted neurotransmission and cognitive deficits. Impairment of the GABAergic system is essentially involved in the pathogenesis of AD. Traditionally, agonists of GABAA receptors at doses above 1 mg/kg are known to possess memory impairing effects. However, we have previously found that GABAA receptor GABA site ligand muscimol at very low doses acted contrary – enhanced spatial learning/memory, as well as prevented neuroinflammation and augmented neurotransmission in AD model rats. Therefore, in the present study we focused on the assessment of the effects of non-sedative – very low (0.05 mg/kg) and moder…

Male0301 basic medicineAllosteric modulatormedicine.drug_classSynaptophysinNeurotransmissionPharmacologyHippocampusNeuroprotectionRandom Allocation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineAlzheimer DiseasemedicineAnimalsGliosisRats Wistargamma-Aminobutyric AcidCerebral CortexPharmacologyMemory DisordersBenzodiazepineDiazepamDose-Response Relationship DrugGlutamate DecarboxylaseGABAA receptorAcetylcholineNeuroprotective Agents030104 developmental biologyGene Expression RegulationMuscimolchemistryAstrocytesSynaptic plasticityGABAergic030217 neurology & neurosurgeryNeuropharmacology
researchProduct

β1 integrin signaling promotes neuronal migration along vascular scaffolds in the post-stroke brain

2017

Cerebral ischemic stroke is a main cause of chronic disability. However, there is currently no effective treatment to promote recovery from stroke-induced neurological symptoms. Recent studies suggest that after stroke, immature neurons, referred to as neuroblasts, generated in a neurogenic niche, the ventricular-subventricular zone, migrate toward the injured area, where they differentiate into mature neurons. Interventions that increase the number of neuroblasts distributed at and around the lesion facilitate neuronal repair in rodent models for ischemic stroke, suggesting that promoting neuroblast migration in the post-stroke brain could improve efficient neuronal regeneration. To move t…

Male0301 basic medicineChain migrationlcsh:MedicineExtracellular matrixNeural Stem CellsCell MovementLamininCells CulturedMice KnockoutNeuronslcsh:R5-920Mice Inbred ICRMicroscopy ConfocalTissue ScaffoldsbiologyIntegrin beta1BrainCell migrationGeneral MedicineCell biologyStrokeVasculature-guided migrationFemaleBlood vesselmedicine.symptomlcsh:Medicine (General)Signal TransductionResearch Paperanimal structuresIntegrinMice TransgenicGeneral Biochemistry Genetics and Molecular BiologyLesion03 medical and health sciencesNeuroblastβ1 integrinNeuroblast migrationmedicineAnimalsRegeneration (biology)lcsh:RCoculture TechniquesMicroscopy Electron030104 developmental biologynervous systemAstrocytesImmunologybiology.proteinBlood VesselsLamininEBioMedicine
researchProduct

Astrocytic Calcium Waves Signal Brain Injury to Neural Stem and Progenitor Cells

2017

Summary Brain injuries, such as stroke or trauma, induce neural stem cells in the subventricular zone (SVZ) to a neurogenic response. Very little is known about the molecular cues that signal tissue damage, even over large distances, to the SVZ. Based on our analysis of gene expression patterns in the SVZ, 48 hr after an ischemic lesion caused by middle cerebral artery occlusion, we hypothesized that the presence of an injury might be transmitted by an astrocytic traveling calcium wave rather than by diffusible factors or hypoxia. Using a newly established in vitro system we show that calcium waves induced in an astrocytic monolayer spread to neural stem and progenitor cells and increase th…

Male0301 basic medicineTime FactorsNotch signaling pathwaySubventricular zonechemistry.chemical_elementBiologyCalciumcalcium signalingBiochemistryArticleMice03 medical and health sciencesAdenosine TriphosphateNeural Stem CellsDownregulation and upregulationCell MovementGeneticsmedicineAnimalsCell Self RenewalProgenitor celllcsh:QH301-705.5Cells CulturedCalcium signalinglcsh:R5-920Gene Expression ProfilingastrocytesGap JunctionsCell DifferentiationCell BiologyAnatomyHypoxia (medical)strokeNeural stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)chemistryBrain InjuriesCalciummedicine.symptomFunction and Dysfunction of the Nervous Systemlcsh:Medicine (General)TranscriptomeNeurosciencenotchDevelopmental BiologyStem Cell Reports
researchProduct