Search results for "ASTROCYTES"

showing 10 items of 171 documents

Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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Mitogenic effects of phospholipase D and phosphatidic acid in transiently permeabilized astrocytes: effects of ethanol.

2003

Investigations of lipid-mediated signalling pathways are often limited by a lack of methods for the intracellular delivery of lipid messengers. We established a procedure for the transient permeabilization of astrocytes by an oxygen-insensitive mutant of streptolysin-O (SLO) to investigate the participation of the phospholipase D (PLD) signalling pathway in astroglial cell proliferation. Exogenous PLD, when incubated in the presence of SLO, caused an increase in DNA synthesis (measured by thymidine incorporation) which was completely suppressed by ethanol (0.3%, v/v). In parallel experiments, phosphatidic acid also induced a dose-dependent mitogenic response which, however, was not affected…

Cell Membrane PermeabilityIndolesmedicine.drug_classPhosphatidic AcidsBiologyBiochemistryDiglyceridesCellular and Molecular Neurosciencechemistry.chemical_compoundBacterial ProteinsmedicinePhospholipase DAnimalsEnzyme InhibitorsProtein kinase ACells CulturedDiacylglycerol kinaseDNA synthesisDose-Response Relationship DrugEthanolPhospholipase DPhosphatidic acidDNAProtein kinase inhibitorRatschemistryBiochemistryAstrocytesStreptolysinslipids (amino acids peptides and proteins)Signal transductionMitogensIntracellularCell DivisionSignal TransductionJournal of neurochemistry
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Unraveling In vivo brain transport of protein‐coated fluorescent nanodiamonds

2019

The blood–brain barrier is the biggest hurdle to overcome for the treatment of neurological disorders. Here, protein‐coated nanodiamonds are delivered to the brain and taken up by neurovascular unit cells after intravenous injection. Thus, for the first time, nanodiamonds with their unique properties and a flexible protein coating for the attachment of therapeutics emerge as a potential platform for nanotheranostics of neurological disorders.Nanotheranostics, combining diagnostics and therapy, has the potential to revolutionize treatment of neurological disorders. But one of the major obstacles for treating central nervous system diseases is the blood–brain barrier (BBB) preventing systemic…

Cell SurvivalCentral nervous systemnanotheranosticsTunneling (Physics)Serum Albumin Human02 engineering and technology010402 general chemistryBlood–brain barrier01 natural sciencesFluorescencePolyethylene GlycolsNanodiamondsBiomaterialstunneling nanotubesMiceIn vivoCell MovementmedicineAnimalsBlut-Hirn-SchrankeGeneral Materials Scienceddc:610Blood-brain barrierNeuronsNanotubesChemistryBrainEndothelial CellsBiological TransportGeneral ChemistryHospitals Drug distribution systems021001 nanoscience & nanotechnologyHuman serum albuminPhotobleachingIn vitroEndocytosis0104 chemical sciencesmedicine.anatomical_structureTranscytosisBlood-Brain BarrierNanoröhreAstrocytesDrug deliverydrug deliveryBiophysics0210 nano-technologyDDC 610 / Medicine & healthBiotechnologymedicine.drug
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The effect of cadmium on brain cells in culture

2009

Cadmium is a long-living heavy metal, abundantly present in the environment, which accumulates in the body. In this study, we investigated the effects of cadmium on the expression of molecular chaperones, and of certain cell-specific proteins, in a variety of brain cell types in culture, namely primary cultures of rat cortical neurons and astrocytes, a brain capillary endothelial cell line (RB4E.B cells), and pheochromocytoma cells (PC12), induced or not to differentiate by NGF treatment. The metal induces a dose-dependent increase of Hsp70 in all cell types. Responses to the metal are cell-specific in the case of Hsc70 and Hsp90: i) in astrocytes, as well as in PC12 cells, cadmium has no s…

Cell typecadmium brain cells molecular chaperones PIPPinCell SurvivalCellBlotting Westernchemistry.chemical_elementNerve Tissue ProteinsBiologyPC12 CellsSettore BIO/10 - BiochimicaNerve Growth FactorGeneticsmedicineAnimalsCytoskeletonCell ShapeCells CulturedFluorescent DyesCerebral CortexNeuronsCadmiumBrainEndothelial CellsRNA-Binding ProteinsCell DifferentiationGeneral MedicineCell cycleMolecular biologyHsp70Cell biologyRatsEndothelial stem cellmedicine.anatomical_structurechemistryApoptosisAstrocytesCadmiumMolecular Chaperones
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EGF converts transit-amplifying neurogenic precursors in the adult brain into multipotent stem cells.

2002

AbstractNeural stem cells in the subventricular zone (SVZ) continue to generate new neurons in the adult brain. SVZ cells exposed to EGF in culture grow to form neurospheres that are multipotent and self-renewing. We show here that the majority of these EGF-responsive cells are not derived from relatively quiescent stem cells in vivo, but from the highly mitotic, Dlx2+, transit-amplifying C cells. When exposed to EGF, C cells downregulate Dlx2, arrest neuronal production, and become highly proliferative and invasive. Killing Dlx2+ cells dramatically reduces the in vivo response to EGF and neurosphere formation in vitro. Furthermore, purified C cells are 53-fold enriched for neurosphere gene…

Cellular differentiationNeuroscience(all)Mice TransgenicBiology03 medical and health sciencesMice0302 clinical medicineCell MovementNeurosphereSpheroids CellularAnimalsCell LineageCells Cultured030304 developmental biologyHomeodomain ProteinsNeurons0303 health sciencesEpidermal Growth FactorGeneral NeuroscienceStem CellsBrainCell DifferentiationImmunohistochemistryNeural stem cellCell biologyUp-RegulationNeuroepithelial cellEndothelial stem cellErbB ReceptorsMicroscopy ElectronPhenotypenervous systemMultipotent Stem CellAstrocytesStem cellNeuroscience030217 neurology & neurosurgeryCell DivisionAdult stem cellTranscription FactorsNeuron
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Symmetric expansion of neural stem cells from the adult olfactory bulb is driven by astrocytes via WNT7A.

2012

Adult neural stem cells (NSCs) located in the subventricular zone (SVZ) persistently produce new neurons destined to the olfactory bulb (OB). Recent research suggests that the OB is also a source of NSCs that remains largely unexplored. Using single/dual-labeling procedures, we address the existence of NSCs in the innermost layers of the OB. In vivo, these cells are more quiescent that their SVZ counterparts, but after in vitro expansion, they behave similarly. Self-renewal and proliferation assays in co-culture with niche astrocytes indicate that OB-glia restricts NSC activity whereas SVZ-glia has the opposite effect. Gene expression profiling identifies WNT7A as a key SVZ-glial factor lac…

Cellular differentiationSubventricular zoneCell Growth ProcessesBiologyMiceNeural Stem CellsIn vivomedicineAnimalsHumansreproductive and urinary physiologyWnt signaling pathwayCell DifferentiationCell BiologyAnatomyOlfactory BulbNeural stem cellnervous system diseasesOlfactory bulbCell biologyGene expression profilingWnt ProteinsWNT7Amedicine.anatomical_structurenervous systemAstrocytesMolecular Medicinebiological phenomena cell phenomena and immunityDevelopmental BiologyStem cells (Dayton, Ohio)
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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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Caveolin and GLT-1 gene expression is reciprocally regulated in primary astrocytes: Association of GLT-1 with non-caveolar lipid rafts

2004

Caveolae represent membrane microdomains acting as integrators of cellular signaling and functional processes. Caveolins are involved in the biogenesis of caveolae and regulate the activity of caveolae-associated proteins. Although caveolin proteins are found in the CNS, the regulation of caveolins in neural cells is poorly described. In the present study, we investigated different modes and mechanisms of caveolin gene regulation in primary rat astrocytes. We demonstrated that activation of cAMP-dependent signaling pathways led to a marked reduction in protein levels of caveolin-1/-2 in cortical astrocytes. Application of transforming growth factor-alpha (TGF-alpha) also resulted in a decre…

Central Nervous SystemCaveolin 2Caveolin 1Down-RegulationGlutamic AcidBiologyCaveolinsHistone DeacetylasesChromatin remodelingRats Sprague-DawleyPhosphatidylinositol 3-KinasesCellular and Molecular NeuroscienceAstrocyte differentiationMembrane MicrodomainsCaveolaeCaveolinCyclic AMPAnimalsRNA MessengerLipid raftCerebral CortexRegulation of gene expressionTransforming Growth Factor alphaRatsCell biologyCaveolin 2Animals NewbornExcitatory Amino Acid Transporter 2Gene Expression RegulationNeurologyAstrocytesCaveolin 1Signal TransductionGlia
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Pharmacological Suppression of CNS Scarring by Deferoxamine Reduces Lesion Volume and Increases Regeneration in an In Vitro Model for Astroglial-Fibr…

2015

Lesion-induced scarring is a major impediment for regeneration of injured axons in the central nervous system (CNS). The collagen-rich glial-fibrous scar contains numerous axon growth inhibitory factors forming a regeneration-barrier for axons. We demonstrated previously that the combination of the iron chelator 2,2'-bipyridine-5,5'-decarboxylic acid (BPY-DCA) and 8-Br-cyclic AMP (cAMP) inhibits scar formation and collagen deposition, leading to enhanced axon regeneration and partial functional recovery after spinal cord injury. While BPY-DCA is not a clinical drug, the clinically approved iron chelator deferoxamine mesylate (DFO) may be a suitable alternative for anti-scarring treatment (A…

Central Nervous SystemCollagen Type IVmedicine.medical_specialtyNeuriteCentral nervous systemlcsh:MedicineBiologyPharmacologyDeferoxamineIn Vitro TechniquesIron Chelating AgentsCicatrixIn vivoTransforming Growth Factor betamedicineCyclic AMPNeuritesAnimalsHumansRNA MessengerAxonRats Wistarlcsh:ScienceSpinal cord injurySpinal Cord InjuriesMultidisciplinaryDeferoxamine mesylatelcsh:RFibroblastsSpinal cordmedicine.diseaseAxonsSurgeryNerve RegenerationRatsDeferoxamineDisease Models Animalmedicine.anatomical_structureAstrocyteslcsh:QFemalemedicine.drugResearch ArticlePloS one
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