Search results for "CASP"

showing 10 items of 470 documents

Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Differential regulation of apoptosis-associated genes by estrogen receptor alpha in human neuroblastoma cells

2012

Purpose: The neuroendocrinology of female sex hormones is of great interest for a variety of neuropsychiatric disorders. In fact, estrogens and estrogen receptors (ERs) exert neuromodulatory and neuroprotective functions. Here we investigated potential targets of the ER subtype alpha that may mediate neuroprotection and focused on direct modulators and downstream executors of apoptosis. Methods: We employed subclones of human neuroblastoma cells (SK-N-MC) stably transfected with one of the ER subtypes, ERalpha or ERbeta. Differences between the cell lines regarding the mRNA expression levels were examined by qPCR, changes on protein levels were examined by Western Blot and immunocytochemist…

Cell SurvivalEstrogen receptorApoptosisCaspase 3BiologyNeuroprotectionRats Sprague-DawleyNeuroblastomaDevelopmental NeuroscienceCell Line TumorAnimalsEstrogen Receptor betaHumansGene silencingAdaptor Proteins Signal TransducingNeuronsCaspase 3Estrogen Receptor alphaTransfectionMolecular biologyRatsUp-RegulationDNA-Binding ProteinsProto-Oncogene Proteins c-bcl-2NeurologyCell cultureApoptosisCancer researchNeurology (clinical)Apoptosis Regulatory ProteinsEstrogen receptor alphahormones hormone substitutes and hormone antagonistsTranscription FactorsRestorative Neurology and Neuroscience
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In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries.

2020

Abstract BackgroundInhalation is the main route of exposure to airborne pollutants. To evaluate the safety and assess the risks of occupational hazards different testing approaches are used. 3D airway epithelial tissues allow to mimic exposure conditions in vitro, generates human-relevant toxicology data, allows to elucidate mode of action of pollutants. ResultsGilian 3500 pumps equipped with Standard Midget Impingers were used to collect the airborne particulate from woodworking and metalworking environments. EpiAirway™ tissues were used to model half working day (4 h), full working day (8 h), and 3 working day exposures to occupational pollutants. Tissue viability was assessed using MTT a…

Cell biologyScienceArticleAndrologyOccupational ExposuremedicinebiochemistryHumansMTT assayParticle SizeLungGelsolinCell ProliferationA549 cellPollutantTissue SurvivalInhalation ExposureMultidisciplinaryInhalationChemistryCaspase 3Interleukin-6Gene Expression ProfilingQRWoodworkingIn vitro exposureParticulatesWoodEpitheliumIn vitromedicine.anatomical_structureGene Expression RegulationRisk factorsA549 CellsEnvironmental chemistryMetalworkingMetallurgyEnvironmental scienceMedicineParticulate MatterGelsolinHealth occupationsEnvironmental MonitoringScientific reports
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Cell cycle arrest and induction of apoptosis by cajanin stilbene acid from Cajanus cajan in breast cancer cells

2015

Abstract Background: The low abundant cajanin stilbene acid (CSA) from Pigeon Pea ( Cajanus cajan ) has been shown to kill estrogen receptor α positive cancer cells in vitro and in vivo . Downstream effects such as cell cycle and apoptosis-related mechanisms have not been analyzed yet. Material and methods: We analyzed the activity of CSA by means of flow cytometry (cell cycle distribution, mitochondrial membrane potential, MMP), confocal laser scanning microscopy (MMP), DNA fragmentation assay (apoptosis), Western blotting (Bax and Bcl-2 expression, caspase-3 activation) as well as mRNA microarray hybridization and Ingenuity pathway analysis. Results: CSA induced G2/M arrest and apoptosis …

Cell cycle checkpointDNA damageCellPharmaceutical ScienceApoptosisBiologyFlow cytometryCajanusStilbenesDrug DiscoverymedicineHumansbcl-2-Associated X ProteinMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testCaspase 3Cell Cycle CheckpointsCell cycleMolecular biologySalicylatesGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Complementary and alternative medicineApoptosisCancer cellMCF-7 CellsMolecular MedicineDNA fragmentationDNA DamageSignal TransductionPhytomedicine
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Corrigendum to "poly (ADP-ribose) polymerase inhibition synergizes with the NF-κB inhibitor DHMEQ to kill hepatocellular carcinoma cells" [Biochim. B…

2018

Fig. 1. The effects of the DHMEQ–Olaparib combination on HCC cells. (A) Cells were treated for 72 hwith the indicated concentrations of DHMEQ–Olaparib and cell viability was assessed by MTS assays. The DHMEQ–Olaparib combination showed synergistic inhibition of cell viability in Hep3B cells and additive inhibition in Huh7 cells. Combination index (CI) values are indicated above the bar. Data are expressed as percent cell growth and are the mean ± SD of three separate experiments (each of which was performed in triplicate). *p b 0.05 and **p b 0.01 versus each agent alone. (B) Cells were treated for 24 h with DHMEQ (μg/ml) or Olaparib (μM) alone or in combination, allowed to grow for 14 days…

Cell growthPoly ADP ribose polymeraseCellCaspase 3Cell BiologyTransfectionBiologyMolecular biologyOlaparibchemistry.chemical_compoundmedicine.anatomical_structurechemistryApoptosismedicineViability assayMolecular BiologyBiochimica et biophysica acta. Molecular cell research
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Studying the Neurovascular Unit: An Improved Blood–Brain Barrier Model

2009

The blood–brain barrier (BBB) closely interacts with the neuronal parenchyma in vivo. To replicate this interdependence in vitro, we established a murine coculture model composed of brain endothelial cell (BEC) monolayers with cortical organotypic slice cultures. The morphology of cell types, expression of tight junctions, formation of reactive oxygen species, caspase-3 activity in BECs, and alterations of electrical resistance under physiologic and pathophysiological conditions were investigated. This new BBB model allows the application of techniques such as laser scanning confocal microscopy, immunohistochemistry, fluorescent live cell imaging, and electrical cell substrate impedance se…

Cell typeBlood–brain barrierCell LineTight JunctionsBrain ischemiaMiceIn vivoLive cell imagingParenchymaElectric ImpedancemedicineAnimalsTight junctionCaspase 3ChemistryBrainEndothelial CellsMembrane Proteinsmedicine.diseaseImmunohistochemistryCoculture TechniquesEndothelial stem cellmedicine.anatomical_structureNeurologyBlood-Brain BarrierBiophysicsNeurology (clinical)Reactive Oxygen SpeciesCardiology and Cardiovascular MedicineNeuroscienceJournal of Cerebral Blood Flow & Metabolism
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U937 variant cells as a model of apoptosis without cell disintegration

2012

AbstractThe variant cell line U937V was originally identified by a higher sensitivity to the cytocidal action of tumor necrosis factor alpha (TNFα) than that of its reference cell line, U937. We noticed that a typical morphological feature of dying U937V cells was the lack of cellular disintegration, which contrasts to the formation of apoptotic bodies seen with dying U937 cells. We found that both TNFα, which induces the extrinsic apoptotic pathway, and etoposide (VP-16), which induces the intrinsic apoptotic pathway, stimulated U937V cell death without cell disintegration. In spite of the distinct morphological differences between the U937 and U937V cells, the basic molecular events of ap…

Cell typeProgrammed cell deathBlotting WesternCellApoptosisU937 cellsDNA FragmentationBiologyModels BiologicalBiochemistrymedicineHumansCell ShapeMolecular BiologyU937 cellCytochrome cCytochromes chemic and immune systemsCell BiologyApoptotic bodyCaspase 9MitochondriaCell biologyEnzyme Activationmedicine.anatomical_structureApoptosisCell culturebiology.proteinApoptotic bodiesLymphoma Large B-Cell DiffuseCell disintegrationSignal TransductionResearch ArticleCellular and Molecular Biology Letters
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Powerful tumor cell growth-inhibiting activity of a synthetic derivative of atractyligenin: Involvement of PI3K/Akt pathway and thioredoxin system

2014

The semi-synthetic ent-kaurane 15-ketoatractyligenin methyl ester (SC2017) has been previously reported to possess high antiproliferative activity against several solid tumor-derived cell lines. Our study was aimed at investigating SC2017 tumor growth-inhibiting activity and the underlying mechanisms in Jurkat cells (T-cell leukemia) and xenograft tumor models. METHODS: Cell viability was evaluated by MTT assay. Cell cycle progression, reactive oxygen species (ROS) elevation and apoptotic hallmarks were monitored by flow cytometry. Inhibition of thioredoxin reductase (TrxR) by biochemical assays. Levels and/or activation status of signaling proteins were assessed by western blotting. Xenogr…

CellBiophysicsAntineoplastic AgentsApoptosisAtractylosideBiologyCell cycleBiochemistryJurkat cellsMicePhosphatidylinositol 3-KinasesThioredoxinsTumor Cells CulturedmedicineAnimalsHumansMTT assayViability assaySettore BIO/15 - Biologia FarmaceuticaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationPI3K/AktHCT 116 xenograftCytochromes cApoptosiThioredoxin systemSettore CHIM/06 - Chimica OrganicaCell cycleXenograft Model Antitumor AssaysCell biologymedicine.anatomical_structureCaspasesCancer researchThioredoxinDiterpenes KauraneProto-Oncogene Proteins c-aktEnt-kaurane
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Possible Pathomechanisms Responsible for Injury to the Central Nervous System in the Settings of Chronic Cerebrospinal Venous Insufficiency

2012

The discovery of stenoses in the azygous and internal jugular veins, the so-called chronic cerebrospinal venous insufficiency that accompanies multiple sclerosis, has enabled the reinterpretation of knowledge about this neurologic dis- ease. Pathologic venous outflow from the central nervous system appears to lead to two main problems. Firstly, it disas- sembles the blood-brain barrier and may allow the penetration of nervous parenchyma by glutamate and leukocytes. Sec- ondly, it may result in significant hypoperfusion of the brain and spinal cord. These two overlapping pathologies are likely to trigger plaques through caspase-1-driven pyroptosis of oligodendrocytes and to evoke neurodegene…

Central Nervous SystemPathologymedicine.medical_specialtyCentral nervous systemExcitotoxicityglutamatemultiple sclerosismedicine.disease_causeAxonal injuryCentral Nervous System Diseasescaspase 1venous insufficiencymedicineHumansBrachiocephalic Veinsjugular veinsPharmacologybusiness.industryMultiple sclerosisazygous veinNeurodegenerationPyroptosisGlutamate receptorGeneral Medicineblood-brain barriermedicine.diseaseSpinal cordChronic cerebrospinal venous insufficiencymedicine.anatomical_structureSpinal CordbusinessReviews on Recent Clinical Trials
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Mechanisms of ceramide-induced COX-2-dependent apoptosis in human ovarian cancer OVCAR-3 cells partially overlapped with resveratrol.

2013

Ceramide is a member of the sphingolipid family of bioactive molecules demonstrated to have profound, diverse biological activities. Ceramide is a potential chemotherapeutic agent via the induction of apoptosis. Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation. Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide. Induct…

CeramideMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesApoptosisBiologyResveratrolCeramidesBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation Enzymologicchemistry.chemical_compoundCell Line TumorStilbenesHumansPhosphorylationRNA Small InterferingMolecular BiologyNitrobenzenesCaspase 7Membrane Potential MitochondrialOvarian NeoplasmsSulfonamidesKinaseCaspase 3Anti-Inflammatory Agents Non-SteroidalCell BiologyLipid signalingSphingolipidCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCyclooxygenase 2ResveratrolFemaleSignal transductionTumor Suppressor Protein p53Journal of cellular biochemistry
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