Search results for "ASTROCYTES"

showing 10 items of 171 documents

Adrenergic modulation of astroglial phospholipase D activity and cell proliferation.

1999

As phospholipase D (PLD) activation has been associated with mitogenic signalling in several cell types, we tested an association between adrenergic activation of PLD and cellular proliferation in primary cultures of rat cortical astrocytes. In 2-week old cultures, PLD activation by noradrenaline (EC50: 0.49 microM) was inhibited by prazosin, a specific antagonist at alpha1-adrenergic receptors (IC50: 0.23 microM). Adrenergic PLD activation was not affected by genistein, an inhibitor of tyrosine kinases, or by Ro 31-8220, an inhibitor of protein kinase C (PKC), but was dose-dependently depressed in the presence of brefeldin A (1-100 microg/ml), an inhibitor of ARF activation. In experiments…

medicine.medical_specialtyAdrenergic AntagonistsAdrenergicBiologyPharmacologychemistry.chemical_compoundNorepinephrineGTP-Binding ProteinsIsoprenalineInternal medicinemedicineAdrenergic antagonistPrazosinPhospholipase DPhospholipase D activityAnimalsMolecular BiologyProtein kinase CCells CulturedBrefeldin APhospholipase DGeneral NeurosciencePrazosinBrefeldin AAdrenergic AgonistsPropranololRatsReceptors AdrenergicEndocrinologychemistryAlcoholsAstrocyteslipids (amino acids peptides and proteins)Neurology (clinical)Cell DivisionDevelopmental Biologymedicine.drugSignal TransductionBrain research
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Estradiol or genistein prevent Alzheimer's disease-associated inflammation correlating with an increase PPAR gamma expression in cultured astrocytes.

2009

Inflammation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). The main inflammatory players in AD are the glial cells which initiate the inflammatory response. One of the earliest neuropathological changes in AD is the accumulation of astrocytes at sites of A beta deposition. It is desirable to find methods of tipping the balance towards anti-inflammatory state. Estrogenic compounds have shown anti-inflammatory and also antioxidant activity. Astrocytes were pretreated with 17-beta estradiol or with genistein, and 48 h later treated with 5 microM amyloid beta (A beta) for 24 h. We found that A beta induces inflammatory mediators, such as cyclooxygenase 2 (…

medicine.medical_specialtyAmyloid betaInterleukin-1betaGenisteinPeroxisome proliferator-activated receptorNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsMolecular BiologyProtein Kinase InhibitorsCells Culturedchemistry.chemical_classificationCerebral CortexAmyloid beta-PeptidesbiologyDose-Response Relationship DrugEstradiolTumor Necrosis Factor-alphaGeneral NeuroscienceInterleukinEstrogensGenisteinPeptide FragmentsRatsPPAR gammaEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationCyclooxygenase 2Astrocytesbiology.proteinNeurogliaTumor necrosis factor alphaNeurology (clinical)medicine.symptomDevelopmental BiologyAstrocyteBrain research
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Transient focal cerebral ischemia significantly alters not only EAATs but also VGLUTs expression in rats: relevance of changes in reactive astroglia

2010

The involvement of plasma membrane glutamate transporters (EAATs - excitatory aminoacid transporters) in the pathophysiology of ischemia has been widely studied, but little is known about the role of vesicular glutamate transporters (VGLUTs) in the ischemic process. We analyzed the expression of VGLUT1-3 in the cortex and caudate-putamen of rats subjected to transient middle cerebral artery occlusion. Western blot and immunohistochemistry revealed an increase of VGLUT1 signal in cortex and caudate-putamen until 3 days of reperfusion followed by a reduction 7 days after the ischemic insult. By contrast, VGLUT2 and 3 were drastically reduced. Confocal microscopy revealed an increase in VGLUT2…

medicine.medical_specialtyBlotting WesternIschemiaFluorescent Antibody TechniqueGlutamic AcidBiologyBiochemistryBrain ischemiaGlutamate Plasma Membrane Transport ProteinsCellular and Molecular NeuroscienceCell MovementInternal medicineNeuroblast migrationCortex (anatomy)Vesicular Glutamate Transport ProteinsmedicineAnimalsCerebral CortexMicroscopy ConfocalNeuronal PlasticityCell DeathNeurogenesisPutamenGlutamate receptorInfarction Middle Cerebral Arterymedicine.diseaseImmunohistochemistryRatsEndocrinologymedicine.anatomical_structureIschemic Attack TransientAstrocytesReperfusion InjuryExcitatory postsynaptic potentialCaudate NucleusNeurogliaReperfusion injuryNeuroscienceJournal of Neurochemistry
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Neurological impairment in experimental antiphospholipid syndrome is associated with increased ligand binding to hippocampal and cortical serotonergi…

2013

The antiphospholipid syndrome (APS) is an autoimmune disease where the presence of high titers of circulating autoantibodies causes thrombosis with consecutive infarcts. In experimental APS (eAPS), a mouse model of APS, behavioral abnormalities develop in the absence of vessel occlusion or infarcts. Using brain hemispheres of control and eAPS mice with documented neurological and cognitive deficits, we checked for lymphocytic infiltration, activation of glia and macrophages, as well as alterations of ligand binding densities of various neurotransmitter receptors to unravel the molecular basis of this abnormal behavior. Lymphocytic infiltrates were immunohistochemically characterized using a…

medicine.medical_specialtyImmunologyHippocampusAMPA receptorBiologySerotonergicHippocampusMiceNeurotransmitter receptorInternal medicinemedicineAnimalsImmunology and AllergyLymphocytesReceptor5-HT receptorAutoantibodiesBehavior AnimalMicrogliaGABAA receptorMacrophagesSomatosensory CortexHematologyAntiphospholipid SyndromeAntigens DifferentiationUp-RegulationDisease Models Animalmedicine.anatomical_structureEndocrinologynervous systemAstrocytesReceptor Serotonin 5-HT1ANervous System DiseasesImmunobiology
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Aquaporin-4 distribution in control and stressed astrocytes in culture and in the cerebrospinal fluid of patients with traumatic brain injuries

2012

Distribution of aquaporin-4 (AQP4) was studied by western analysis and immunofluorescence in rat astrocytes exposed to either hypothermic (30 °C) or hyperosmolar (0.45 M sucrose) stress, and in the cerebrospinal fluid (CSF) of patients who suffered traumatic brain injury (TBI). CSF was obtained from 5 healthy subjects and from 20 patients suffering from severe TBI. CSF samples were taken at admission and on days 3 and 5-7. Here we report that, in response to both hypothermia and hyperosmolar stress, AQP4 was markedly reduced in cultured astrocytes. We also found that AQP4 significantly increased in patients with severe brain injury in respect to healthy subjects (P < 0.002). AQP4 in CSF rem…

medicine.medical_specialtyPathologyNeurologyTraumatic brain injuryaquaporin-4DermatologyImmunofluorescencecerebrospinal fluidCerebrospinal fluidStress PhysiologicalSettore BIO/10 - BiochimicamedicineAnimalsHumansDistribution (pharmacology)Settore BIO/06 - Anatomia Comparata E CitologiaRats WistarCells CulturedAquaporin 4medicine.diagnostic_testbusiness.industrytraumatic brain injuryCultured astrocyteGeneral MedicineHypothermiamedicine.diseaseRatsPsychiatry and Mental healthAquaporin 4AstrocytesBrain InjuriesAnesthesiasense organsNeurology (clinical)Neurosurgerymedicine.symptombusinessNeurological Sciences
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Ethanol inhibits astroglial cell proliferation by disruption of phospholipase D-mediated signaling.

2002

The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD-mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol-induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum-deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1-2%) suppressed the FCS-induced, PLD-mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration…

medicine.medical_specialtyPlatelet-derived growth factorIndolestert-Butyl Alcoholmedicine.medical_treatmentButanolsBecaplerminPhosphatidic AcidsNerve Tissue ProteinsBiologyBiochemistryCulture Media Serum-FreeCellular and Molecular Neurosciencechemistry.chemical_compound1-ButanolInternal medicineLysophosphatidic acidmedicinePhospholipase DAnimalsPhosphorylationProtein kinase APlatelet-Derived Growth FactorEndothelin-1EthanolPhospholipase DCell growthGrowth factorPhosphatidic acidDNAProto-Oncogene Proteins c-sisProtein-Tyrosine KinasesGenisteinGrowth InhibitorsCell biologyRatsEndocrinologychemistryFetal Alcohol Spectrum DisordersAstrocyteslipids (amino acids peptides and proteins)Signal transductionVanadatesProtein Processing Post-TranslationalCell DivisionSignal TransductionJournal of neurochemistry
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Age-Related Changes in Astrocytic and Ependymal Cells of the Subventricular Zone

2014

Neurogenesis persists in the adult subventricular zone (SVZ) of the mammalian brain. During aging, the SVZ neurogenic capacity undergoes a progressive decline, which is attributed to a decrease in the population of neural stem cells (NSCs). However, the behavior of the NSCs that remain in the aged brain is not fully understood. Here we performed a comparative ultrastructural study of the SVZ niche of 2-month-old and 24-month-old male C57BL/6 mice, focusing on the NSC population. Using thymidine-labeling, we showed that residual NSCs in the aged SVZ divide less frequently than those in young mice. We also provided evidence that ependymal cells are not newly generated during senescence, as ot…

nervous systemagingastrocytesependymal cellssubventricular zoneultrastructureneural stem cells
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Dataset related to article "Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures"

2020

This dataset is related to the article entitled: Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures. This article is published in the Journal GLIA. Bres EE et al. Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures. Glia. 2020;1&ndash;33.

nervous systemradial glia stem cellsreactive astrocytesastrocytesepilepsylipoprotein receptor-related proteinseizures
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NEURONS AND ASTROCYTES SHED EXTRACELLULAR VESICLES THAT SEEM TO VEHICLE ANGIOGENIC FACTORS

2007

neuronsastrocytes extracellular vesicleangiogenic factors
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Activation of astroglial phospholipase D activity by phorbol ester involves ARF and Rho proteins.

2000

Primary cultures of rat cortical astrocytes express phospholipase D (PLD) isoforms 1 and 2 as determined by RT-PCR and Western blot. Basal PLD activity was strongly (10-fold) increased by 4beta-phorbol-12beta,13alpha-dibutyrate (PDB) (EC(50): 56 nM), an effect which was inhibited by Ro 31-8220 (0.1-1 microM), an inhibitor of protein kinase C (PKC), and by brefeldin A (10-100 microg/ml), an inhibitor of ADP-ribosylating factor (ARF) activation. Pretreatment of the cultures with Clostridium difficile toxin B-10463 (0.1-1 ng/ml), which inactivates small G proteins of the Rho family, led to a breakdown of the astroglial cytoskeleton; concomitantly, PLD activation by PDB was reduced by up to 50%…

rho GTP-Binding ProteinsIndolesADP ribosylation factorBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologyRats Sprague-Dawleychemistry.chemical_compoundWestern blotBacterial ProteinsPhorbol EstersmedicinePhospholipase DPhospholipase D activityAnimalsEnzyme InhibitorsMolecular BiologyProtein kinase CCells CulturedProtein Kinase CProtein Synthesis InhibitorsBrefeldin Amedicine.diagnostic_testPhospholipase DADP-Ribosylation FactorsSerum Albumin BovineCell BiologyBrefeldin AMolecular biologyRatsEnzyme ActivationchemistryAstrocyteslipids (amino acids peptides and proteins)Biochimica et biophysica acta
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