Search results for "Programmed cell death"

showing 10 items of 609 documents

Citrus limon-derived nanovesicles inhibit cancer cell proliferation and suppress CML xenograft growth by inducing TRAIL-mediated cell death

2015

// Stefania Raimondo 1 , Flores Naselli 1 , Simona Fontana 1 , Francesca Monteleone 1 , Alessia Lo Dico 1 , Laura Saieva 1 , Giovanni Zito 2 , Anna Flugy 1 , Mauro Manno 3 , Maria Antonietta Di Bella 1 , Giacomo De Leo 1 , Riccardo Alessandro 1 1 Dipartimento di Biopatologia e Biotecnologie Mediche, Universita degli Studi di Palermo, sezione di Biologia e Genetica, Palermo, Italy 2 Laboratorio di Ingegneria Tissutale – Piattaforme Innovative per l’Ingegneria Tissutale (PON01–00829), Istituto Ortopedico Rizzoli, Palermo, Italy 3 Istituto di Biofisica, Consiglio Nazionale delle Ricerche, Palermo, Italy Correspondence to: Riccardo Alessandro, e-mail: riccardo.alessandro@unipa.it Keywords: canc…

MaleProteomicsCitrusCell signalingProgrammed cell deathTime Factorsexosome-like nanovesiclesCell SurvivalCellApoptosisMice SCIDBiologyExosomesTNF-Related Apoptosis-Inducing LigandCitrus limon L.; TRAIL-mediated cell death; cancer; exosome-like nanovesiclesCitrus limon L.Mice Inbred NODCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveHuman Umbilical Vein Endothelial CellsmedicinecancerAnimalsHumansCell ProliferationPlant ProteinsPlants MedicinalPlant ExtractsCell growthCancermedicine.diseaseTRAIL-mediated cell deathAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysMicrovesiclesTumor BurdenFruit and Vegetable Juicesmedicine.anatomical_structureOncologyApoptosisImmunologyCancer researchNanoparticlesSignal transductionResearch PaperPhytotherapySignal Transduction
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Occurrence of Retinal Ganglion Cell Loss via Autophagy and Apoptotic Pathways in an Autoimmune Glaucoma Model

2020

In glaucoma, an apoptotic death of retinal ganglion cells (RGCs) has been shown. However, little is known about other cell death mechanisms, like autophagy or necrosis. Therefore, we investigated these mechanisms in addition to antibody deposits in an experimental autoimmune glaucoma model.Rats were immunized with a retinal ganglion cell-layer homogenate (RGA), while controls received sodium chloride. Untreated rats served as natїve group. After seven weeks, retinal cross-sections were stained with antibodies against RGCs (Brn-3a), apoptosis (cleaved caspase 2, cleaved caspase 3 as well as caspase 3, 8, and 9), autophagy (LC3BII and LAMP1), and necrosis (RIPK3) followed by cell counts. Auto…

MaleRetinal Ganglion CellsProgrammed cell deathNecrosisgenetic structuresGlaucomaApoptosisAutoantigensRetinal ganglionAutoimmune Diseases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMicroscopy Electron TransmissionAutophagymedicineAnimalsAutoantibodiesCaspase 8biologyCaspase 3business.industryAutophagyLysosome-Associated Membrane GlycoproteinsGlaucomamedicine.diseaseCaspase 9eye diseasesSensory SystemsRatsDisease Models AnimalOphthalmologymedicine.anatomical_structureMicroscopy FluorescenceRetinal ganglion cellRats Inbred LewApoptosisImmunoglobulin G030221 ophthalmology & optometryCancer researchbiology.proteinsense organsAntibodymedicine.symptombusinessMicrotubule-Associated Proteins030217 neurology & neurosurgeryCurrent Eye Research
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Increase in Bcl-2 phosphorylation and reduced levels of BH3-only Bcl-2 family proteins in kainic acid-mediated neuronal death in the rat brain.

2003

Kainic acid induces excitotoxicity and nerve cell degeneration in vulnerable regions of rat brain, most markedly in hippocampus and amygdala. Part of the cell death following kainic acid is apoptotic as shown by caspase 3 activation and chromatin condensation. Here we have studied the regulation of pro- and anti-apoptotic proteins belonging to the Bcl-2 family in rat hippocampus and amygdala by kainic acid in relationship to ensuing neuronal death. The pro-apoptotic protein Bax was up-regulated in hippocampus 6 h after kainic acid administration. The increase in Bax was followed by the appearance of TdT-mediated dUTP nick end labelling-positive cells which were prominent at 24 h. Immunohist…

MaleTime FactorsExcitotoxicityCell Countmedicine.disease_causeSettore BIO/09 - Fisiologiachemistry.chemical_compoundPrecipitin TestExcitatory Amino Acid AgonistsSerinePhosphorylationCells CulturedNuclear Proteinbcl-2-Associated X ProteinNeuronsProto-Oncogene ProteinKainic AcidbiologyCell DeathImmunochemistryGeneral NeuroscienceBrainNuclear ProteinsImmunohistochemistryProto-Oncogene Proteins c-bcl-2Programmed cell deathKainic acidTime FactorNeuronal deathExcitatory Amino Acid AgonistBlotting WesternCaspase 3HippocampuBcl-2-associated X proteinProto-Oncogene ProteinsGlial Fibrillary Acidic ProteinmedicineIn Situ Nick-End LabelingAnimalsRats WistarProtein kinase AStaining and LabelingAnimalBcl-2 familyNeuronButylated HydroxytolueneEmbryo MammalianMolecular biologyPrecipitin Testsnervous system diseasesRatsnervous systemchemistrybiology.proteinRatNeuNBcl-2 proteinThe European journal of neuroscience
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Incidence of Abcd1 level on the induction of cell death and organelle dysfunctions triggered by very long chain fatty acids and TNF-alpha on oligoden…

2012

X-linked adrenoleukodystrophy (X-ALD) is characterized by ABCD1 deficiency. This disease is associated with elevated concentrations of very long chain fatty acids (C24:0 and C26:0) in the plasma and tissues of patients. Under its severe form, brain demyelination and inflammation are observed. Therefore, we determined the effects of C24:0 and C26:0 on glial cells:oligodendrocytes, which synthesize myelin, and astrocytes, which participate in immune response. So, 158N murine oligodendrocytes, rat C6 glioma cells, rat primary cultures of neuronal-glial cells, and of oligodendrocytes were treated for various periods of time in the absence or presence of C24:0 and C26:0 used at plasmatic concent…

MaleTime FactorsVacuoleMitochondrionToxicologyATP Binding Cassette Transporter Subfamily D Member 1chemistry.chemical_compoundMice0302 clinical medicineRNA Small InterferingAdrenoleukodystrophyCells CulturedComputingMilieux_MISCELLANEOUSMembrane Potential MitochondrialNeurons0303 health sciencesGeneral NeuroscienceFatty AcidsBrainPeroxisomeCatalaseFlow Cytometry3. Good healthCell biologyMitochondriaOligodendrogliamedicine.anatomical_structureFemaleProgrammed cell deathChromatography GasBiologyGas Chromatography-Mass SpectrometryStatistics Nonparametric03 medical and health sciencesMicroscopy Electron TransmissionLysosomeOrganellemedicineAnimalsHumansPropidium iodideRNA MessengerRats Wistar030304 developmental biologyCell SizeChemokine CCL22OrganellesDose-Response Relationship DrugCell growthTumor Necrosis Factor-alphaRatschemistryAnimals NewbornAstrocytesATP-Binding Cassette Transporters[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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Metformin increases APP expression and processing via oxidative stress, mitochondrial dysfunction and NF-κB activation: Use of insulin to attenuate m…

2015

AbstractClinical and experimental biomedical studies have shown Type 2 diabetes mellitus (T2DM) to be a risk factor for the development of Alzheimer's disease (AD). This study demonstrates the effect of metformin, a therapeutic biguanide administered for T2DM therapy, on β-amyloid precursor protein (APP) metabolism in in vitro, ex vivo and in vivo models. Furthermore, the protective role of insulin against metformin is also demonstrated. In LAN5 neuroblastoma cells, metformin increases APP and presenilin levels, proteins involved in AD. Overexpression of APP and presenilin 1 (Pres 1) increases APP cleavage and intracellular accumulation of β-amyloid peptide (Aβ), which, in turn, promotes ag…

Maleendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causeAntioxidantsNF-κBAmyloid beta-Protein PrecursorAspartic Acid EndopeptidasesInsulinBiguanideNF-kappa BBrainAlzheimer's diseaseMetforminMetforminMitochondriaProtein TransportAntioxidantmedicine.drugmetformin T2DM Alzheimer's diseaseAdultmedicine.medical_specialtyProgrammed cell deathmedicine.drug_classOxidative phosphorylationBiologyAntidiabetic drugModels BiologicalPresenilinInternal medicineCell Line Tumormental disordersmedicinePresenilin-1AnimalsHumansMolecular BiologyCell NucleusSettore MED/04 - Patologia GeneraleAmyloid beta-PeptidesInsulinAdenylate KinaseOxidative Stress Pathwaynutritional and metabolic diseasesCell BiologyHydrogen PeroxideMice Inbred C57BLEndocrinologyGene Expression RegulationCytoprotectionOxidative stressLeukocytes MononuclearAmyloid Precursor Protein SecretasesOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhib…

2006

Benfotiamine, a vitamin B1 analogue, reportedly prevents diabetic microangiopathy. The aim of this study was to evaluate whether benfotiamine is of benefit in reparative neovascularisation using a type I diabetes model of hindlimb ischaemia. We also investigated the involvement of protein kinase B (PKB)/Akt in the therapeutic effects of benfotiamine. Streptozotocin-induced diabetic mice, given oral benfotiamine or vehicle, were subjected to unilateral limb ischaemia. Reparative neovascularisation was analysed by histology. The expression of Nos3 and Casp3 was evaluated by real-time PCR, and the activation state of PKB/Akt was assessed by western blot analysis and immunohistochemistry. The f…

Malemedicine.medical_specialtyProgrammed cell deathAngiogenesisEndocrinology Diabetes and MetabolismBlotting WesternNeovascularization PhysiologicApoptosisMice Inbred StrainsBiologyDiabetes Mellitus ExperimentalNeovascularizationMiceRandom AllocationIschemiaInternal medicineInternal MedicinemedicineAnimalsThiamineMuscle SkeletalProtein kinase BCell ProliferationCaspase 3Stem Cellsprotein kinase PKB/AktBody WeightHemodynamicsEndothelial CellsCaspase InhibitorsImmunohistochemistryEndothelial stem cellEnzyme ActivationOxidative StressEndocrinologyBenfotiamineApoptosisCaspasesDietary SupplementsTransketolase activitymedicine.symptomProto-Oncogene Proteins c-aktDiabetic Angiopathiesmedicine.drugDiabetologia
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The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis.

2005

G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong anti-apoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neurona…

Malemedicine.medical_specialtyProgrammed cell deathNeutrophilsCellular differentiationApoptosisBiologyLigandsBrain IschemiaBrain ischemiaInternal medicineGranulocyte Colony-Stimulating FactormedicineAnimalsHumansGranulocyte Precursor CellsNerve TissueRats WistarReceptorAutocrine signallingStem CellsNeurogenesisCell DifferentiationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseNeural stem cellCell biologyRatsStrokeDisease Models AnimalEndocrinologyBlood-Brain BarrierReceptors Granulocyte Colony-Stimulating FactorStem cellResearch ArticleThe Journal of clinical investigation
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Programmed death-1 (PD-1): A novel mechanism for understanding the acute immune deregulation in ST-segment elevation myocardial infarction

2014

Malemedicine.medical_specialtySwinemedicine.medical_treatmentProgrammed Cell Death 1 ReceptorMyocardial InfarctionPercutaneous Coronary InterventionImmune systemInternal medicinemedicineAnimalsHumansST segmentProspective StudiesMyocardial infarctionAgedMechanism (biology)business.industryPercutaneous coronary interventionMiddle Agedmedicine.diseaseProgrammed Cell Death 1 ReceptorCardiologyFemaleProgrammed death 1ComprehensionCardiology and Cardiovascular MedicinebusinessInternational Journal of Cardiology
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Glial expression of Swiss cheese (SWS), the Drosophila orthologue of neuropathy target esterase (NTE), is required for neuronal ensheathment and func…

2016

ABSTRACT Mutations in Drosophila Swiss cheese (SWS) or its vertebrate orthologue neuropathy target esterase (NTE), respectively, cause progressive neuronal degeneration in Drosophila and mice and a complex syndrome in humans that includes mental retardation, spastic paraplegia and blindness. SWS and NTE are widely expressed in neurons but can also be found in glia; however, their function in glia has, until now, remained unknown. We have used a knockdown approach to specifically address SWS function in glia and to probe for resulting neuronal dysfunctions. This revealed that loss of SWS in pseudocartridge glia causes the formation of multi-layered glial whorls in the lamina cortex, the firs…

Medicine (miscellaneous)lcsh:MedicineAxonal degenerationSynaptic Transmission0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsNeurons0303 health sciencesGene knockdownCell Deathmusculoskeletal neural and ocular physiologyPhototaxisAnatomyCell biologymedicine.anatomical_structureDrosophila melanogasterPhospholipasesGene Knockdown TechniquesNeurogliaNeurogliaDrosophila Proteinpsychological phenomena and processesResearch Articlelcsh:RB1-214Programmed cell deathNeuriteNeuroscience (miscellaneous)Nerve Tissue ProteinsNeuropathy target esteraseNeurotransmissionBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesPNPLA6mental disordersNeuropilmedicineNeuriteslcsh:PathologyAnimalsPhospholipaseCell Shape030304 developmental biologySequence Homology Amino AcidSpastic paraplegialcsh:R302Reproducibility of ResultsEnsheathing gliabody regionsnervous systemVacuolesbiology.proteinCarboxylic Ester Hydrolases030217 neurology & neurosurgeryDisease Models & Mechanisms
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Beauvericin exposure induces cell cycle arrest, cell death and mitochondrial membrane potential disruption in CHO-K1 Cells

2015

Membrane potentialchemistry.chemical_compoundProgrammed cell deathCell cycle checkpointchemistryGeneral MedicineToxicologyBeauvericinCell biologyToxicology Letters
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