Search results for "programmed cell death"

showing 10 items of 609 documents

cAMP-dependent phosphorylation of CYP2B1 as a functional switch for cyclophosphamide activation and its hormonal controlin vitro andin vivo

2001

An important feature of cytochrome P450 (CYP) 2B1 is its high ability to convert the prodrug cyclophosphamide (CPA) to therapeutically cytotoxic metabolites, resulting in interstrand DNA-cross-linking and cell death. We have examined whether and how the phosphorylation of CYP2B1 influences CPA metabolic activation in vitro and in vivo. We found first that only part of the total CYP2B1 pool undergoes phosphorylation. This part is fully inactivated. Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic…

MaleCancer ResearchProgrammed cell deathTime FactorsCellRats Sprague-DawleyStructure-Activity RelationshipSex FactorsIn vivoCyclic AMPPhosphoprotein PhosphatasesSerinemedicineAnimalsCytotoxic T cellheterocyclic compoundsPhosphorylationProtein kinase AAntineoplastic Agents AlkylatingCyclophosphamideBiotransformationbiologyCytochrome P450GlucagonCyclic AMP-Dependent Protein KinasesIn vitroRatsCell biologymedicine.anatomical_structureOncologyBiochemistryCytochrome P-450 CYP2B1Hepatocytescardiovascular systembiology.proteinPhosphorylationFemaleMutagensInternational Journal of Cancer
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Effects of phenylbutyrate on proliferation and apoptosis in human prostate cancer cells in vitro and in vivo.

1999

Phenylbutyrate (PB) is a potent differentiating agent and currently under investigation for the treatment of prostate cancer (CaP) and other malignancies. We have studied the impact of PB in vitro and in vivo on differentiation, proliferation and apoptosis in the LNCaP and LuCaP 23.1 prostate cancer xenograft models. In vitro we found that i) PB increased PSA secretion/cell, ii) inhibited cell proliferation in a time- and dose-dependent manner resulting in a cell cycle arrest in G1-phase and iii) induced apoptosis at concentrations of 2.5 mM after 3 days of treatment. In PB treated animals tumor growth stabilized or regressed. Combination of castration and PB treatment had a synergistic ant…

MaleCancer Researchmedicine.medical_specialtyProgrammed cell deathTransplantation HeterologousMice NudeAntineoplastic AgentsApoptosisBiologyPhenylbutyrateMiceProstate cancerIn vivoInternal medicineLNCaPTumor Cells CulturedmedicineAnimalsHumansMice Inbred BALB CCell growthCell CycleProstatic NeoplasmsCancerCell Differentiationmedicine.diseasePhenylbutyratesDisease Models AnimalEndocrinologyOncologyCancer cellAndrogensCancer researchCell DivisionNeoplasm TransplantationInternational Journal of Oncology
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Study of Proliferation and Apoptosis in Neuroblastoma. Their Relation with Other Prognostic Factors

2002

Abstract Background Our objective was to study the proliferation and apoptotic process in 111 cases of neuroblastoma (NB) and to seek their relationship with other prognostic factors and survival. Methods Immunohistochemistry following ABC peroxidase was carried out for PCNA, Ki-67, bcl-2, and p53 proteins. Apoptosis analysis was performed with in situ detection of chromosomal breakdown. Molecular detection of DNA ladders by electrophoresis and amplification of MYCN was studied with PCR and Southern blot. Statistical study was performed with Pearson χ 2 and Kruskal-Wallis tests and Cox regression. Results Our results indicate that proliferative factors PCNA and Ki-67 were correlated to each…

MaleIn situProgrammed cell deathTime FactorsMitosisApoptosisPolymerase Chain ReactionNeuroblastomachemistry.chemical_compoundProliferating Cell Nuclear AntigenNeuroblastomamedicineHumansChildSouthern blotbiologyInfant NewbornInfantCell DifferentiationDNAGeneral MedicinePrognosismedicine.diseaseImmunohistochemistryMolecular biologyProliferating cell nuclear antigenBlotting SouthernKi-67 AntigenProto-Oncogene Proteins c-bcl-2chemistryApoptosisChild PreschoolMultivariate Analysisbiology.proteinImmunohistochemistryFemaleTumor Suppressor Protein p53Cell DivisionDNAFollow-Up StudiesArchives of Medical Research
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Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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A novel form of ataxia oculomotor apraxia characterized by oxidative stress and apoptosis resistance

2007

Several different autosomal recessive genetic disorders characterized by ataxia with oculomotor apraxia (AOA) have been identified with the unifying feature of defective DNA damage recognition and/or repair. We describe here the characterization of a novel form of AOA showing increased sensitivity to agents that cause single-strand breaks (SSBs) in DNA but having no gross defect in the repair of these breaks. Evidence for the presence of residual SSBs in DNA was provided by dramatically increased levels of poly (ADP-ribose)polymerase (PARP-1) auto-poly (ADP-ribosyl)ation, the detection of increased levels of reactive oxygen/nitrogen species (ROS/RNS) and oxidative damage to DNA in the patie…

MaleMethylnitronitrosoguanidineProgrammed cell deathAtaxiaDNA RepairApraxiasDNA damageMitomycinBlotting WesternPoly (ADP-Ribose) Polymerase-1Apoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundRadiation IonizingmedicineHumansDNA Breaks Single-StrandedOculomotor apraxiaMolecular BiologyCells CulturedEtoposideMembrane Potential MitochondrialbiologyCytochrome cHydrogen PeroxideCell BiologyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicReactive Nitrogen SpeciesMolecular biologyOxidative StresschemistryApoptosisbiology.proteinAtaxiaCamptothecinFemalePoly(ADP-ribose) Polymerasesmedicine.symptomDNAOxidative stressDNA DamageCell Death & Differentiation
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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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A possible biomarker for methadone related deaths

2017

Abstract Methadone (MTH) concentrations in those dying of MTH toxicity totally overlap concentrations where the presence of MTH is only an incidental finding, making it very difficult to make distinctions in actual cases. A biomarker, be it anatomical or biochemical for MTH toxicity is badly needed, particularly if that markers were known to disrupt effective ventilation. Because the brainstem houses the regulatory centers for cardiorespiratory-control enters, it would seem to be the most likely anatomical site to seek abnormalities in cardiorespiratory control. Objective To locate and describe the cells of nucleus of the solitary tract (TS)(NTS) in human brainstem and determine if neuronal…

MalePathologyNecrosisApoptosisAutopsyCohort Studies0302 clinical medicineRetrospective StudieMedicineForensic PathologyNeuronsPoisoningSolitary tractGeneral MedicineRostral ventrolateral medullaNecrosiImmunohistochemistryCaspase 9Narcotic030220 oncology & carcinogenesisToxicityFemaleBrainstemmedicine.symptomBrainstemCaspase-9HumanNarcoticsAdultProgrammed cell deathmedicine.medical_specialty2734Pathology and Forensic MedicineNecrosisForensic ToxicologyYoung Adult03 medical and health sciencesSettore MED/43 - Medicina LegaleSolitary NucleuSolitary NucleusNeurotoxicityHumansRetrospective Studiesbusiness.industryfungiApoptosiBiomarkerNeuronApoptosisApoptosis; Biomarker; Brainstem; Caspase-9; Methadone; Neurotoxicity; Adult; Apoptosis; Brain Stem; Caspase 9; Cohort Studies; Female; Forensic Pathology; Forensic Toxicology; Humans; Immunohistochemistry; Male; Methadone; Narcotics; Necrosis; Neurons; Poisoning; Retrospective Studies; Solitary Nucleus; Young Adult; 2734; LawCohort StudiebusinessLawMethadone030217 neurology & neurosurgeryBrain Stem
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Neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury

2012

After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. Thus, it is shown that newborn cells, mostly corresponded with blood vessels …

MaleProgrammed cell deathAngiogenesisBlotting WesternNeovascularization PhysiologicPharmacologyBiologyNeuroprotectionAntioxidantsGlial scarNeovascularizationLesionCicatrixchemistry.chemical_compoundMicroscopy Electron TransmissionIn Situ Nick-End LabelingmedicineAnimalsRats WistarChromatography High Pressure LiquidGliogenesisThioctic AcidGeneral NeuroscienceImmunohistochemistryRatsLipoic acidNeuroprotective AgentschemistryBrain Injuriesmedicine.symptomNeurogliaNeuroscienceNeuroscience
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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