Search results for "neuron"

showing 10 items of 2611 documents

Swelling and death of neuronal cells by lactic acid.

1993

Lactacidosis occurring in cerebral ischemia or trauma is a major mechanism of cytotoxic brain edema and brain damage. Respective effects of lactacidosis were currently analyzed in vitro by employment of the murine neuronal cell line, Neuro-2A, in order to obtain a better understanding of specific mechanisms underlying cell swelling and cell death in comparison with glial cells. The cells were suspended in a physiological medium in the presence of lactic acid at increasing concentrations. Levels of acidosis reaching from pH 6.8-5.6 were obtained while other parameters, such as osmolarity and electrolyte concentrations, were maintained in the physiological range. Assessment of cell swelling a…

Programmed cell deathPathologymedicine.medical_specialtyBiologyFlow cytometryAndrologychemistry.chemical_compoundMiceNeuroblastomamedicineTumor Cells CulturedAnimalsViability assayPropidium iodideLactic AcidAcidosisNeuronsOsmotic concentrationmedicine.diagnostic_testCell DeathOsmolar ConcentrationHydrogen-Ion ConcentrationFlow CytometryCulture MediaNeurologychemistryCell cultureLactatesNeurology (clinical)medicine.symptomSwellingNeurogliaJournal of the neurological sciences
researchProduct

Toxic effects on astrocytes of extracellular vesicles from CSF of multiple sclerosis patients: a pilot in vitro study.

2020

Multiple sclerosis (MS) is an autoimmune and degenerative disorder of the central nervous system (CNS) that causes a progressive loss of motor and cognitive perfor-mances. Moreover, since the earlier phases, axonal loss as well as neuronal degener-ation and a failure of oligodendrocytes to promote myelin repair have been demon-strated. In previous studies, it has been shown that the treatment of rat neuronal primary cultures with serum from MS patients can be toxic for neurons. Here we report a pilot investigation showing that CSF from patients contains extracellular vesicles (EVs) able to induce cell death in rat cultured astrocytes. Although these data are still preliminary, they suggest …

Programmed cell deathPathologymedicine.medical_specialtyMultiple SclerosisDegenerative DisorderCentral nervous systemAxonal lossExtracellular vesiclesPathology and Forensic MedicineMyelinExtracellular VesiclesSettore BIO/10 - BiochimicamedicineAnimalsHumansSettore BIO/06 - Anatomia Comparata E CitologiaNeuronsbusiness.industryMultiple sclerosisRGeneral Medicinemedicine.diseaseRatsmedicine.anatomical_structureAstrocytesToxicityMedicineSettore MED/26 - NeurologiabusinessBiomarkersPolish journal of pathology : official journal of the Polish Society of Pathologists
researchProduct

A new technique for real-time analysis of caspase-3 dependent neuronal cell death

2007

Several markers are available to identify cells undergoing programmed cell death, but so far they are only applicable on fixed material. Therefore, no information on the kinetics of apoptosis can be obtained, although apoptosis is a dynamic cell process. Here, we describe a new technique that allows the real-time observation of the onset of apoptosis in primary neurons. Neurons are transfected with a plasmid that codes for a fluorescent protein localized in the soma. Upon activation of caspase-3, which represents the point-of-no-return in the apoptosis process, the fusion protein is cleaved and as a consequence translocates into the nucleus. The onset of apoptosis is thus visualized by tran…

Programmed cell deathRecombinant Fusion ProteinsCellApoptosisCaspase 3BiologyMiceComputer SystemsmedicineAnimalsCells CulturedNeuronsMice Inbred BALB CTUNEL assayStaining and LabelingCaspase 3General NeuroscienceImage EnhancementFusion proteinCell biologymedicine.anatomical_structureAnimals NewbornMicroscopy FluorescenceApoptosisSomaNucleusJournal of Neuroscience Methods
researchProduct

Coffee Silverskin and Spent Coffee Suitable as Neuroprotectors against Cell Death by Beauvericin and α-Zearalenol: Evaluating Strategies of Treatment

2021

Coffee silverskin and spent coffee have been evaluated in a neuroblastoma cell line (SH-SY5Y cells) against beauvericin (BEA) and α-zearalenol (α-ZEL)-induced cytotoxicity with different strategies of treatment. First, the direct treatment of mycotoxins and coffee by-products extracts in SH-SY5Y cells was assayed. IC50 values for α-ZEL were 20.8 and 14.0 µM for 48 h and 72 h, respectively and, for BEA only at 72 h, it was 2.5 µM. Afterwards, the pre-treatment with spent coffee obtained by boiling water increased cell viability for α-ZEL at 24 h and 48 h from 10% to 16% and from 25% to 30%, respectively

Programmed cell deathTime Factors030309 nutrition & dieteticsHealth Toxicology and Mutagenesislcsh:MedicineToxicologyCoffeeArticleSH-SY5Y cells03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500404 agricultural biotechnologyCell Line TumorDepsipeptidesIc50 valuesHumansViability assayFood scienceCytotoxicityMycotoxinNeuroblastoma cell linespent coffeeNeurons0303 health sciencesCell DeathDose-Response Relationship DrugPlant Extractslcsh:Rbeauvericin04 agricultural and veterinary sciences040401 food scienceCytoprotectionBeauvericinNeuroprotective AgentschemistryCytoprotectionSeedsZeranolα-zearalenolcoffee silverskinToxins
researchProduct

Prevention by Dietary Polyphenols (Resveratrol, Quercetin, Apigenin) Against 7-Ketocholesterol-Induced Oxiapoptophagy in Neuronal N2a Cells: Potentia…

2020

The Mediterranean diet is associated with health benefits due to bioactive compounds such as polyphenols. The biological activities of three polyphenols (quercetin (QCT), resveratrol (RSV), apigenin (API)) were evaluated in mouse neuronal N2a cells in the presence of 7-ketocholesterol (7KC), a major cholesterol oxidation product increased in patients with age-related diseases, including neurodegenerative disorders. In N2a cells, 7KC (50 &micro

Programmed cell deathanimal diseasesSOD2N2a cellsApoptosisresveratrolmedicine.disease_causeoxiapoptophagyArticleCell LinequercetinMiceage-related diseasesmedicineAutophagyPeroxisomesAnimalsHumansApigeninlcsh:QH301-705.5Ketocholesterols7-ketocholesterolchemistry.chemical_classificationNeuronsReactive oxygen speciesDose-Response Relationship DrugChemistryfood and beveragesPolyphenolsNeurodegenerative DiseasesGeneral MedicinePeroxisomeMolecular biologyMitochondriaOxidative StresspolyphenolMitochondrial biogenesislcsh:Biology (General)ApoptosisACOX1Reactive Oxygen SpeciesoxysterolOxidative stressCells
researchProduct

Cell cycle independent role of Cyclin E during neural cell fate specification in Drosophila is mediated by its regulation of Prospero function

2009

AbstractDuring development, neural progenitor cells or neuroblasts generate a great intra- and inter-segmental diversity of neuronal and glial cell types in the nervous system. In thoracic segments of the embryonic central nervous system of Drosophila, the neuroblast NB6-4t undergoes an asymmetric first division to generate a neuronal and a glial sublineage, while abdominal NB6-4a divides once symmetrically to generate only 2 glial cells. We had earlier reported a critical function for the G1 cyclin, CyclinE (CycE) in regulating asymmetric cell division in NB6-4t. Here we show that (i) this function of CycE is independent of its role in cell cycle regulation and (ii) the two functions are m…

ProsperoNerve Tissue ProteinsStem cellsCyclinEBiologyCell fate determinationNeuroblastNeuroblastsCyclin EAsymmetric cell divisionAnimalsDrosophila ProteinsCell LineageMolecular BiologyNeural cellCell ProliferationSequence DeletionNeuronsCell fate determinationCell CycleNuclear ProteinsCell DifferentiationCell BiologyCell cycleNeural stem cellUp-RegulationCell biologyProtein TransportDrosophila melanogasternervous systemDrosophilaCNSStem cellGanglion mother cellBiomarkersProtein BindingTranscription FactorsDevelopmental BiologyDevelopmental Biology
researchProduct

The Cleavage Product of Amyloid-β Protein Precursor sAβPPα Modulates BAG3-Dependent Aggresome Formation and Enhances Cellular Proteasomal Activity

2015

Alzheimer's disease (AD) is the major age-associated form of dementia characterized by gradual cognitive decline. Aberrant cleavage of the amyloid-β protein precursor (AβPP) is thought to play an important role in the pathology of this disease. Two principal AβPP processing pathways exist: amyloidogenic cleavage of AβPP resulting in production of the soluble N-terminal fragment sAβPPβ, amyloid-β (Aβ), which accumulates in AD brain, and the AβPP intracellular domain (AICD) sAβPPα, p3 and AICD are generated in the non-amyloidogenic pathway. Prevalence of amyloidogenic versus non-amyloidogenic processing leads to depletion of sAβPPα and an increase in Aβ. Although sAβPPα is a well-accepted neu…

Proteasome Endopeptidase ComplexTime FactorsCell SurvivalLeupeptinsGreen Fluorescent ProteinsCysteine Proteinase InhibitorsProtein degradationProtein aggregationBiologyTransfectionBAG3Rats Sprague-DawleyAmyloid beta-Protein PrecursorAnimalsHumansRNA MessengerRNA Small InterferingProtein precursorCells CulturedAdaptor Proteins Signal TransducingNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGeneral NeuroscienceHEK 293 cellsBrainGeneral MedicineFibroblastsEmbryo MammalianRatsCell biologyPsychiatry and Mental healthClinical PsychologyHEK293 CellsProteostasisAggresomeGene Expression RegulationBiochemistryProteasomeProteolysisAmyloid Precursor Protein SecretasesGeriatrics and GerontologyApoptosis Regulatory ProteinsJournal of Alzheimer's Disease
researchProduct

Activation of the p75 neurotrophin receptor through conformational rearrangement of disulphide-linked receptor dimers.

2009

Ligand-mediated dimerization has emerged as a universal mechanism of growth factor receptor activation. Recent structural studies have shown that neurotrophins interact with dimers of the p75 neurotrophin receptor (p75NTR), but the actual mechanism of receptor activation has remained elusive. Here we show that p75NTR forms disulphide-linked dimers independently of neurotrophin binding through the highly conserved Cys257 in its transmembrane domain. Mutation of Cys257 abolished neurotrophin-dependent receptor activity but did not affect downstream signaling by the p75NTR/NgR/Lingo-1 complex in response to MAG, indicating the existence of distinct, ligand-specific activation mechanisms for p7…

Protein ConformationMutantNeuronesReceptor Nerve Growth FactorMiceProtein structureChlorocebus aethiopsNerve Growth FactorLow-affinity nerve growth factor receptorRNA Small InterferingReceptorskin and connective tissue diseasesReceptors neuralsCells CulturedNeuronsCell DeathGeneral NeuroscienceNF-kappa BCell biologyTransmembrane domainSIGNALINGOligopeptidesNeurotrophinProtein BindingSignal Transductionmusculoskeletal diseasesPROTEINSNeuroscience(all)Green Fluorescent ProteinsNerve Tissue ProteinsReceptors Nerve Growth FactorSuperior Cervical GanglionBiologyTransfectionMOLNEUROArticleGrowth factor receptorAnimalsHumansProtein Interaction Domains and MotifsReceptors Growth FactorCysteineBinding SitesMembrane Proteinsbiological factorsRatsnervous systemAnimals NewbornNeurotrophin bindingMutationbiology.proteinsense organsProtein MultimerizationrhoA GTP-Binding ProteinProteïnesNeuron
researchProduct

BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.

2010

Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates …

Protein FoldingRecombinant Fusion ProteinsDyneinGreen Fluorescent ProteinsAggrephagyMice TransgenicBAG3BiochemistryMiceJUNQ and IPODChlorocebus aethiopsGeneticsAutophagyAnimalsHumansPoint MutationHSP70 Heat-Shock ProteinsMolecular BiologyAdaptor Proteins Signal TransducingSequence DeletionInclusion BodiesMotor NeuronsbiologySuperoxide DismutaseAutophagyScientific ReportsDyneinsTransport proteinCell biologyProtein TransportAggresomeHEK293 CellsSpinal CordChaperone (protein)COS Cellsbiology.proteinApoptosis Regulatory ProteinsProteasome InhibitorsEMBO reports
researchProduct

Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells.

2012

PURPOSE: Previous studies show significantly specifically changed autoantibody reactions against retinal antigens in the serum of glaucoma and ocular hypertension (OHT) patients in comparison to healthy people. As pathogenesis of glaucoma still is unknown the aim of this study was to analyze if the serum and antibodies of glaucoma patients interact with neuroretinal cells. METHODS: R28 cells were incubated with serum of patients suffering from primary open angle glaucoma (POAG), normal tension glaucoma (NTG) or OHT, POAG serum after antibody removal and serum from healthy people for 48 h under a normal or an elevated pressure of 15000 Pa (112 mmHg). RGC5 cells were additionally incubated wi…

ProteomicsRetinal Ganglion CellsSerumProteomegenetic structuresOcular hypertensionGlaucomalcsh:MedicineAutoimmunityPathogenesischemistry.chemical_compoundMolecular Cell Biologylcsh:ScienceCellular Stress ResponsesMultidisciplinarySpectrometric Identification of ProteinsbiologyNeurodegenerative DiseasesBlood proteinsSignaling CascadesNeurologyMedicineRetinal DisordersElectrophoresis Polyacrylamide GelAntibodyGlaucoma Open-AngleRetinal NeuronsSignal TransductionResearch ArticleSpectrometry Mass Electrospray IonizationImmunologyImmunoglobulinsPeptide MappingAntibodiesStress Signaling CascadeCell LineAntigenmedicinePressureAnimalsHumansBiologylcsh:RAutoantibodyRetinalGlaucomamedicine.diseaseeye diseasesRatsOphthalmologychemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationImmunologybiology.proteinOcular HypertensionClinical Immunologylcsh:Qsense organsChromatography LiquidPLoS ONE
researchProduct