0000000000591390

AUTHOR

Juan R. Ureña-peralta

showing 4 related works from this author

TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles

2019

Background Current evidence indicates that extracellular vesicles (EVs) participate in intercellular signaling, and in the regulation and amplification of neuroinflammation. We have previously shown that ethanol activates glial cells through Toll-like receptor 4 (TLR4) by triggering neuroinflammation. Here, we evaluate if ethanol and the TLR4 response change the release and inflammatory content of astrocyte-derived EVs, and whether these vesicles are capable of communicating with neurons by spreading neuroinflammation. Methods Cortical neurons and astrocytes in culture were used. EVs were isolated from the extracellular medium of the primary culture of the WT and TLR4-KO astrocytes treated …

0301 basic medicineImmunologyInflammationlcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineWestern blotNeuroinflammationGlial cellsExtracellularmedicineAnimalsProtein Interaction MapsReceptorNeuroinflammationCells Culturedlcsh:Neurology. Diseases of the nervous systemInflammationMice KnockoutNeuronsmedicine.diagnostic_testEthanolChemistryGeneral NeuroscienceResearchExtracellular vesiclesCell biologyMice Inbred C57BLToll-Like Receptor 4030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTLR4medicine.symptom030217 neurology & neurosurgeryIntracellularAstrocyteJournal of Neuroinflammation
researchProduct

Role of mTOR-regulated autophagy in spine pruning defects and memory impairments induced by binge-like ethanol treatment in adolescent mice.

2021

Abstract Adolescence is a brain maturation developmental period during which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. Different mechanism participates in adolescent brain maturation, including autophagy that plays a role in synaptic development and plasticity. Alcohol is a neurotoxic compound and its abuse in adolescence induces neuroinflammation, synaptic and myelin alterations, neural damage and behavioral impairments. Changes in synaptic plasticity and its regulation by mTOR have also been suggested to play a role in the behavioral dysfunction of binge ethanol drinking in adolescence. Therefore, by considering the critical ro…

MaleautophagyDendritic spineSynaptic pruningPeriod (gene)synaptic pruningBiologyPathology and Forensic MedicineBinge Drinkingbinge ethanol treatmentMyelinMicemedicineAnimalsPI3K/AKT/mTOR pathwayNeuroinflammationResearch Articlescognitive functionMemory DisordersNeuronal PlasticityGeneral NeuroscienceTOR Serine-Threonine KinasesAutophagyBraindendritic spinesMice Inbred C57BLmedicine.anatomical_structureSynaptic plasticitymTORFemaleadolescenceNeurology (clinical)NeuroscienceResearch ArticleBrain pathology (Zurich, Switzerland)
researchProduct

Circulating MicroRNAs in Extracellular Vesicles as Potential Biomarkers of Alcohol-Induced Neuroinflammation in Adolescence: Gender Differences

2020

Current studies evidence the role of miRNAs in extracellular vesicles (EVs) as key regulators of pathological processes, including neuroinflammation and neurodegeneration. As EVs can cross the blood&ndash

Maleadolescent micelcsh:ChemistryMiceAlcohol intoxicationCAMK2Alcsh:QH301-705.5SpectroscopyBrain DiseasesSex CharacteristicsNeurodegenerationfood and beveragesBrainGeneral MedicineComputer Science Applicationsgender differencesmiRNAsFemalemedicine.symptomextracellular vesiclesadolescent humansmedicine.medical_specialtyAdolescentInflammationBrain damageArticleCatalysisInorganic ChemistryExtracellular VesiclesInternal medicinemicroRNAmedicineAnimalsHumansCirculating MicroRNAPhysical and Theoretical ChemistryMolecular BiologyNeuroinflammationInflammationEthanolbusiness.industryOrganic Chemistrybiomarkersmedicine.diseaseMice Inbred C57BLCirculating MicroRNAEndocrinologylcsh:Biology (General)lcsh:QD1-999inflammationethanolbusinessInternational Journal of Molecular Sciences
researchProduct

Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects

2017

Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate the pathophysiological mechanisms underpinning axonal injury through hitherto unknown factors present in cerebrospinal fluid (CSF) that may regulate axonal damage, remyelinate the axon and make functional recovery possible. We employed primary cultures of rat unmyelinated cerebellar granule neurons and treated them with CSF obtained from MS and Neuromyelitis optica (NMO) patients. We performed microarray …

0301 basic medicinePathologymedicine.medical_specialtyglucose metabolismneuromyelitis opticaBiologymultiple sclerosisArticlecerebrospinal fluidlcsh:RC321-57103 medical and health sciencesMyelin0302 clinical medicineCerebrospinal fluidDownregulation and upregulationGene expressionmedicineRemyelinationAxonlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymultiple sclerosis; glucose metabolism; neuromyelitis optica; cerebrospinal fluid; gene expressionNeuromyelitis opticaGeneral NeuroscienceMultiple sclerosismedicine.disease030104 developmental biologymedicine.anatomical_structurenervous systemgene expression030217 neurology & neurosurgery
researchProduct