0000000000524098

AUTHOR

Marco De Curtis

showing 4 related works from this author

Caspase-3 contributes to ZO-1 and Cl-5 tight-junction disruption in rapid anoxic neurovascular unit damage.

2011

BACKGROUND: Tight-junction (TJ) protein degradation is a decisive step in hypoxic blood-brain barrier (BBB) breakdown in stroke. In this study we elucidated the impact of acute cerebral ischemia on TJ protein arrangement and the role of the apoptotic effector protease caspase-3 in this context. METHODOLOGY/PRINCIPAL FINDINGS: We used an in vitro model of the neurovascular unit and the guinea pig whole brain preparation to analyze with immunohistochemical methods the BBB properties and neurovascular integrity. In both methodological approaches we observed rapid TJ protein disruptions after 30 min of oxygen and glucose deprivation or middle cerebral artery occlusion, which were accompanied by…

Time FactorsAnatomy and Physiologylcsh:MedicineMiceMolecular Cell BiologyPathologySignaling in Cellular ProcessesHypoxia Brainlcsh:ScienceCells CulturedNeuropathologyApoptotic SignalingMultidisciplinaryTight junctionCaspase 3ChemistryAnimal ModelsCell biologyTransport proteinProtein Transportmedicine.anatomical_structureNeurologyBlood-Brain BarrierMedicineResearch ArticleSignal TransductionClinical Research DesignCerebrovascular DiseasesGuinea PigsIschemiaContext (language use)Caspase 3Protein degradationBlood–brain barrierNeurological SystemTight JunctionsCapillary PermeabilityModel OrganismsDiagnostic MedicinemedicineAnimalsTransient Ischemic AttacksAnimal Models of DiseaseClaudinBiologyIschemic Strokelcsh:REndothelial CellsMembrane ProteinsPhosphoproteinsmedicine.diseaseAnatomical PathologyClaudinsImmunologyZonula Occludens-1 ProteinNervous System Componentslcsh:QPLoS ONE
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Molecular chaperones and mirnas in epilepsy: Pathogenic implications and therapeutic prospects

2021

Epilepsy is a pathologic condition with high prevalence and devastating consequences for the patient and its entourage. Means for accurate diagnosis of type, patient monitoring for predicting seizures and follow up, and efficacious treatment are desperately needed. To improve this adverse outcome, miRNAs and the chaperone system (CS) are promising targets to understand pathogenic mechanisms and for developing theranostics applications. miRNAs implicated in conditions known or suspected to favor seizures such as neuroinflammation, to promote epileptic tolerance and neuronal survival, to regulate seizures, and others showing variations in expression levels related to seizures are promising ca…

QH301-705.5Adverse outcomesReviewDiseaseBioinformaticsCatalysisInorganic ChemistryEpilepsychaperone systemmicroRNAmedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologyHeat-Shock ProteinsSpectroscopyNeuroinflammationmiRNAHigh prevalencebiologybusiness.industryOrganic Chemistrymolecular chaperonesGeneral Medicinetemporal lobe epilepsymedicine.diseaseComputer Science ApplicationsMicroRNAsChemistryChaperone (protein)Molecular targetsbiology.proteinepilepsyAnticonvulsantsbusiness
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Mechanisms of C-reactive protein-induced blood-brain barrier disruption.

2009

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…

medicine.medical_specialtyMyosin light-chain kinaseMyosin Light ChainsGuinea PigsBrain Edemamedicine.disease_causeBlood–brain barrierp38 Mitogen-Activated Protein KinasesMyosin light chain kinase activityTight JunctionsInternal medicineMyosinmedicineAnimalsPhosphorylationReceptorCells CulturedAdvanced and Specialized Nursingbusiness.industryReceptors IgGCoculture TechniquesCell biologyRatsStrokeEndocrinologymedicine.anatomical_structureC-Reactive ProteinBlood-Brain BarrierPhosphorylationNeurology (clinical)Endothelium VascularSignal transductionCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressSignal TransductionStroke
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26th Annual Computational Neuroscience Meeting (CNS*2017): Part 2

2017

International audience; No abstract available

0301 basic medicineCerebellumComputer science[SDV]Life Sciences [q-bio]General Neurosciencelcsh:QP351-495Meeting Abstractslcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencelcsh:Neurophysiology and neuropsychology030104 developmental biologymedicine.anatomical_structuremedicineNeuronlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroscienceComputingMilieux_MISCELLANEOUScomputational neuroscienceBMC Neuroscience
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