0000000000414308

AUTHOR

José Castillo

showing 3 related works from this author

Iron-loaded transferrin (Tf) is detrimental whereas iron-free Tf confers protection against brain ischemia by modifying blood Tf saturation and subse…

2018

Despite transferrin being the main circulating carrier of iron in body fluids, and iron overload conditions being known to worsen stroke outcome through reactive oxygen species (ROS)-induced damage, the contribution of blood transferrin saturation (TSAT) to stroke brain damage is unknown. The objective of this study was to obtain evidence on whether TSAT determines the impact of experimental ischemic stroke on brain damage and whether iron-free transferrin (apotransferrin, ATf)-induced reduction of TSAT is neuroprotective. We found that experimental ischemic stroke promoted an early extravasation of circulating iron-loaded transferrin (holotransferrin, HTf) to the ischemic brain parenchyma.…

0301 basic medicineU-PAGE urea-polyacrylamide gel electrophoresisMaleClinical BiochemistryExperimental strokeBiochemistryBrain IschemiaBrain ischemia0302 clinical medicineADC apparent diffusion coefficientApotransferrinDWI diffusion-weighted imagingTANDEM-1 Thrombolysis and Deferoxamine in Middle Cerebral Artery Occlusion clinical trialrHTf rat HTfrATf rat ATflcsh:QH301-705.5chemistry.chemical_classificationNeuronslcsh:R5-920ChemistryTransferrinExtravasationNS21 a medium supplement to grow neuronspDAPK-1 phosphorylated anti-death-associated protein kinase 1NeuroprotectionStrokeWB Western blotFemalemedicine.symptomlcsh:Medicine (General)Research PaperhHTf human HTfPC12 cell line derived from a pheochromocytoma of the rat adrenal medullamedicine.medical_specialtyIron OverloadBBB blood-brain barrierNMDAR N-methyl-D-aspartate receptorDCF dihydrofluoresceinIronWGA wheat germ agglutininHTf holotransferrinTransferrin receptorBrain damageTfR transferrin receptorDeferoxamineNeuroprotectionPI propidium iodide03 medical and health sciencesBrain damageCM conditioned mediumROS reactive oxygen speciesInternal medicine4-HNE 4-hydroxynonenalTf transferrinReceptors TransferrinmedicineFeRhoNoxTM-1 probe to detect Fe2+AnimalsHumansATf apotransferrinCM-H2DCFDA 5-chloromethyl-27-dichlorodihydrofluorescein diacetateMCAO middle cerebral artery occlusionDMT-1 divalent metal transporterB-27 a medium supplement to grow neuronsReactive oxygen speciesNMDA N-methyl-D-aspartateTSAT blood transferrin saturationTransferrin saturationBlood transferrin saturation (TSAT)Organic ChemistryNIR near infraredReactive oxygen species (ROS)medicine.diseasepMCAO permanent middle cerebral artery occlusionRatsPWI perfusion-weighted imaging030104 developmental biologyEndocrinologylcsh:Biology (General)TransferrinDAPK-1 anti-death-associated protein kinaseOGD oxygen/glucose deprivationTTC 235-triphenyl-tetrazolium chlorideLipid PeroxidationMCA middle cerebral arteryApoproteinsReactive Oxygen SpeciesMRI magnetic resonance imagingtMCAO transient middle cerebral artery occlusion030217 neurology & neurosurgeryhATf human ATf
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Inhibition of iNOS activity by 1400W decreases glutamate release and ameliorates stroke outcome after experimental ischemia

2005

Background and purpose. It has been shown that the reversed operation of glutamate transporters when ATP levels fall accounts for most glutamate release induced by severe cerebral ischemia. Nitric oxide (NO) is formed after ischemia and causes ATP depletion. Our purpose is to test if NO release from inducible NO synthase (iNOS) after stroke may cause a delayed glutamate release due to ATP depletion that might underlie progression of the ischemic infarct. We have studied the effect of the highly selective inhibitor of iNOS activity 1400W on brain ATP levels, extracellular glutamate, and stroke outcome after transient focal cerebral ischemia in rats. Methods. To induce focal ischemia, the mid…

MaleBenzylaminesAmino Acid Transport System X-AGIschemiaAmidinesInfarctionDown-RegulationGlutamic AcidNitric Oxide Synthase Type IIL-argininePharmacologyNeuroprotectionNitric oxidelcsh:RC321-571chemistry.chemical_compoundAdenosine TriphosphateWestern blotmedicine.arteryStroke outcomeMedicineAnimalscardiovascular diseasesEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedicine.diagnostic_testbusiness.industryGlutamate receptorBrainInfarction Middle Cerebral ArteryNitric oxideCerebral Infarctionmedicine.diseaseNeuroprotectionRatsATPStrokeDisease Models AnimalNeuroprotective AgentsTreatment OutcomeNeurologychemistryCytoprotectionIschemic Attack TransientAnesthesiaMiddle cerebral arteryNitric Oxide SynthaseGlutamatebusinessNeurobiology of Disease
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Delayed post-ischemic administration of CDP-choline increases EAAT2 association to lipid rafts and affords neuroprotection in experimental stroke

2007

Glutamate transport is the only mechanism for maintaining extracellular glutamate concentrations below excitotoxic levels. Among glutamate transporters, EAAT2 is responsible for up to 90% of all glutamate transport and has been reported to be associated to lipid rafts. In this context, we have recently shown that CDP-choline induces EAAT2 translocation to the membrane. Since CDP-choline preserves membrane stability by recovering levels of sphingomyelin, a glycosphingolipid present in lipid rafts, we have decided to investigate whether CDP-choline increases association of EAAT2 transporter to lipid rafts. Flotillin-1 was used as a marker of lipid rafts due to its known association to these m…

MaleCytidine Diphosphate CholineTime FactorsIschemiaGlutamic AcidContext (language use)PharmacologyBiologyCell FractionationNeuroprotectionlcsh:RC321-571chemistry.chemical_compoundMembrane MicrodomainsIschemiamedicineAnimalsCholineLipid raftlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGlutamate transportersGlutamate receptorInfarction Middle Cerebral ArteryGlutamic acidmedicine.diseaseRats Inbred F344Ratscarbohydrates (lipids)Disease Models AnimalNeuroprotective AgentsExcitatory Amino Acid Transporter 2Gene Expression RegulationNeurologyBiochemistrychemistrylipids (amino acids peptides and proteins)GlutamateSphingomyelinNeurobiology of Disease
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