Search results for "Apoptosis Inducing Factor"

showing 4 items of 4 documents

Activation of a caspase-3-independent mode of cell death associated with lysosomal destabilization in cultured human retinal pigment epithelial cells…

2008

International audience; Purpose: To characterize the possible cytotoxic effects of oxysterols (7-hydroxycholesterol (7-OH), 25-hydroxycholesterol (25-OH)) in human retinal pigment epithelial cells (ARPE-19) and to detail the relationships between some of these effects. Methods: ARPE-19 cells were treated with 7-OH and 25-OH. Cell viability was measured with the MTT assay. Membrane permeability, mitochondrial potential, and lysosomal integrity were measured by flow cytometry with propidium iodide, DiOC6(3), and acridine orange, respectively. Cell death was characterized by staining with Hoechst 33342, transmission electron microscopy, and analysis of the DNA fragmentation pattern. Caspase ac…

HUMAN BRUCHS MEMBRANECell Membrane PermeabilityMembrane PotentialsAGE-RELATED MACULOPATHYchemistry.chemical_compound0302 clinical medicineFluorescent Antibody Technique IndirectPigment Epithelium of EyeCaspaseCells CulturedElectrophoresis Agar Gel0303 health sciencesbiologyCell DeathCaspase 3CHOLESTEROLAcridine orangeApoptosis Inducing FactorCytochromes cDipeptidesKetonesFlow CytometrySensory SystemsCell biologyMitochondrial MembranesDNA fragmentationCOLORIMETRIC ASSAYMembrane permeabilityCell SurvivalBlotting WesternLOW-DENSITY-LIPOPROTEINCaspase 3DNA FragmentationCysteine Proteinase Inhibitors03 medical and health sciencesCellular and Molecular NeuroscienceBASAL DEPOSITSAPOPTOSIS-INDUCING FACTORHumansRPE CELLSViability assayPropidium iodide[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory Organs030304 developmental biologyMACULAR DEGENERATIONMolecular biologyHydroxycholesterolsEnzyme ActivationOphthalmologychemistryApoptosis030221 ophthalmology & optometrybiology.proteinLysosomes7-KETOCHOLESTEROL-INDUCED APOPTOSIS[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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Neuronal effects of Sugammadex in combination with Rocuronium or Vecuronium.

2017

Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these…

vecuroniumNecrosisEstrès oxidatiuPrimary Cell CulturerocuroniumCaspase 3NeuronesPharmacologySugammadexSugammadex03 medical and health sciences0302 clinical medicine030202 anesthesiologymedicineAnimalsHumansAndrostanolsRocuroniumCell damageNeuronsVecuronium BromideDose-Response Relationship DrugCaspase 3business.industryapoptosis.Apoptosis Inducing FactorCytochromes c030208 emergency & critical care medicineGeneral Medicinemedicine.diseaseneuronRatsDrug Combinationsmedicine.anatomical_structureGene Expression RegulationApoptosisToxicityNeuronNeuromuscular Blocking Agentsmedicine.symptombusinessResearch Papergamma-Cyclodextrinsmedicine.drug
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