Search results for "caspase"

showing 10 items of 390 documents

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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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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Triclosan induces Fas receptor-dependent apoptosis in mouse neocortical neurons in vitro

2014

Triclosan (TCS) is a commonly used antimicrobial agent in personal care and sanitizing products, as well as in household items. Numerous studies have demonstrated the presence of TCS in various human tissues. Several studies have reported the accumulation of TCS in fish and human brain tissue. The aim of the present study was to investigate the effect of TCS on apoptosis in mouse neocortical neurons after 7 days of culture in vitro following 3, 6 and 24 h of exposure. To explore the mechanism underlying the effects of TCS in neurons, we studied the activation and protein expression of the Fas receptor (FasR) and caspase- 8, caspase-9 and caspase-3, as well as DNA fragmentation in TCS-treate…

Time FactorsExtrinsic apoptotic signaling pathwayApoptosisNeocortexDNA fragmentation.DNA FragmentationCaspase 8caspase-8FasRMicePregnancyAnimalsfas ReceptorFADDEnzyme InhibitorsCells CulturedNeuronsDose-Response Relationship DrugL-Lactate DehydrogenasebiologyGeneral NeurosciencefungiEmbryo MammalianStaurosporineFas receptorApoptotic bodyTriclosanIn vitroCell biologyBiochemistryApoptosisCaspasesbiology.proteinFatty Acid Synthesis InhibitorsDNA fragmentationFemaleNeuroscience
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Induction of apoptosis in human osteosarcoma Saos-2 cells by the proteasome inhibitor MG132 and the protective effect of pRb

2003

Induction of apoptosis in human osteosarcoma Saos-2 cells by the proteasome inhibitor MG132 and the protective effect of pRb

Time FactorsLeupeptinsApoptosisRetinoblastoma ProteinAntioxidantsAmino Acid Chloromethyl KetonesMembrane Potentialschemistry.chemical_compoundSettore BIO/10 - BiochimicaMG132Caspase 8OsteosarcomaChemistryCaspase 3Cytochromes cFlow CytometryMitochondriaCysteine EndopeptidasesProto-Oncogene Proteins c-bcl-2CaspasesOsteosarcomamedicine.drugmusculoskeletal diseasesProteasome Endopeptidase ComplexCell SurvivalBlotting Westernbcl-X Proteinmacromolecular substancesTransfectionMultienzyme ComplexesCell Line Tumorparasitic diseasesmedicineHumansProtease InhibitorsneoplasmsMolecular BiologySaos-2 cellsDose-Response Relationship DrugCell Biologymedicine.diseaseAcetylcysteineApoptosis osteosarcoma proteasome inhibitorsMicroscopy FluorescenceApoptosisCancer researchProteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen Specieshuman activities
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In human endothelial cells rapamycin causes mTORC2 inhibition and impairs cell viability and function.

2008

Aim Drug-eluting stents are widely used to prevent restenosis but are associated with late endothelial damage. To understand the basis for this effect, we have studied the consequences of a prolonged incubation with rapamycin on the viability and functions of endothelial cells. Methods and results Human umbilical vein or aorta endothelial cells were exposed to rapamycin in the absence or in the presence of tumour necrosis factor α (TNFα). After a 24 h-incubation, rapamycin (100 nM) caused a significant cell loss associated with the increase of both apoptosis and necrosis, as quantified by propidium iodide staining, caspase 3 activity, and lactate dehydrogenase release. Rapamycin also impair…

Time FactorsPhysiologyApoptosismTORC1Polymerase Chain Reactionchemistry.chemical_compoundCell MovementStress FibersMicroscopy ConfocalCaspase 3TOR Serine-Threonine KinasesNitric Oxide Synthase Type IIIRibosomal Protein S6 Kinases 70-kDaUp-RegulationEndothelial stem cellmedicine.anatomical_structureBiochemistryCardiology and Cardiovascular MedicineE-SelectinEndotheliumNitric Oxide Synthase Type IIICell SurvivalBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyMechanistic Target of Rapamycin Complex 1Nitric OxideTacrolimusNecrosisTheophyllinePhysiology (medical)medicineHumansImmunoprecipitationViability assayPropidium iodideProtein kinase BAdaptor Proteins Signal TransducingSirolimusDose-Response Relationship DrugL-Lactate DehydrogenaseTumor Necrosis Factor-alphaEndothelial CellsProteinsCardiovascular AgentsRegulatory-Associated Protein of mTORMolecular biologyRapamycin-Insensitive Companion of mTOR ProteinchemistryMultiprotein ComplexesTOR Serine-Threonine KinasesCarrier ProteinsProtein KinasesTranscription FactorsCardiovascular research
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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Inhibitors of apoptosis confer resistance to tumour suppression by adoptively transplanted cytotoxic T-lymphocytes in vitro and in vivo

2005

Deregulation of apoptosis signalling is commonly found in cancer and results in resistance to cytotoxic therapies. Immunotherapy is a promising strategy to eliminate resistant cancer cells. The transfer of T-lymphocytes during allogeneic stem cell transplantation is clinically explored to induce a 'graft-versus-tumor' effect (GvT). Cytotoxic T-lymphocytes (CTL), which are major effectors of GvT, eliminate cancer cells by inducing apoptosis via multiple parallel pathways. Here, we study in vitro and in vivo the susceptibility of murine cancer cells engineered to express single antiapoptotic genes to CTL-mediated cytotoxicity. Interestingly, we find that single inhibitors of caspase activatio…

Time Factorsmedicine.medical_treatmentbcl-X ProteinApoptosisMice TransgenicMiceHLA-A2 AntigenTumor Cells CulturedmedicineAnimalsCytotoxic T cellFADDMolecular BiologybiologyCancerCell BiologyImmunotherapymedicine.diseaseAdoptive TransferMitochondriaEnzyme ActivationTransplantationCTL*Proto-Oncogene Proteins c-bcl-2CaspasesCancer cellImmunologybiology.proteinCancer researchTumor Suppressor Protein p53Stem cellT-Lymphocytes CytotoxicCell Death & Differentiation
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Bleomycin induced pulmonary toxicity and its subpleural onset

2016

Idiopathic Pulmonary Fibrosis (PF) is a rare and devastating disease without efficient treatment at this time. Idiopathic FP is characterized by accumulation of myofibroblasts and has a typical sub-pleural onset suggesting a role of the pleura in the disease. Transforming Growth Factor (TGF)-ß1 induces transformation of pleural mesothelial cells (PMC) into active cells exhibiting myofibroblast phenotype. Heat shock proteins can act as regulator of the TGF-ß1 signaling. A role for caspase-1/IL-1ß axis has already been described in animal models of PF.The heat shock protein AlphaB-crystallin has been studied in PF at the PMC level and the importance of caspase-1/IL-1ß axis has been investigat…

Transforming Growth Factor-β1Cellules mésothéliales pleuralesTransition épithélio-mésenchymateuseBléomycineCaspase-1AlphaB-crystallin[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyFibrose pulmonaire idiopatique[SDV.BC] Life Sciences [q-bio]/Cellular Biology
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dsRNA induces apoptosis through an atypical death complex associating TLR3 to caspase-8

2012

Toll-like receptor 3 (TLR3) is a pattern-recognition receptor known to initiate an innate immune response when stimulated by double-stranded RNA (dsRNA). Components of TLR3 signaling, including TIR domain-containing adapter inducing IFN-α (TRIF), have been demonstrated to contribute to dsRNA-induced cell death through caspase-8 and receptor interacting protein (RIP)1 in various human cancer cells. We provide here a detailed analysis of the caspase-8 activating machinery triggered in response to Poly(I:C) dsRNA. Engagement of TLR3 by dsRNA in both type I and type II lung cancer cells induces the formation of an atypical caspase-8-containing complex that is devoid of classical death receptors…

Ubiquitin-Protein LigasesvirusesApoptosischemical and pharmacologic phenomenaInhibitor of Apoptosis ProteinsCell Line TumorHumansFADDMolecular BiologyRNA Double-StrandedDeath domainCaspase 8Original PaperbiologyUbiquitinationRNA-Binding Proteinshemic and immune systemsMDA5Cell BiologyTNF Receptor-Associated Factor 2Fas receptorTRADDBaculoviral IAP Repeat-Containing 3 ProteinTNF Receptor-Associated Death Domain ProteinToll-Like Receptor 3Cell biologyNuclear Pore Complex ProteinsUbiquitin ligase complexDeath-inducing signaling complexTLR3biology.proteinSignal TransductionCell Death & Differentiation
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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