Search results for "caspase 7"

showing 10 items of 13 documents

Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.

2016

The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens. Using the human leukemia cell line THP-1 and/or primary monocyte-derived macrophages, skepinone-L inhibited eLDL-induced ac…

0301 basic medicineAdultMaleChemokineMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesCD36CCL4Dibenzocycloheptenes030204 cardiovascular system & hematologyBiochemistryGene Expression Regulation EnzymologicMonocytesMitogen-Activated Protein Kinase 1403 medical and health sciences0302 clinical medicineCell Line TumorGeneticsHumansInterleukin 8Molecular BiologyFoam cellMAPK14AgedAged 80 and overCaspase 7biologyChemistryCaspase 3Cholesterol LDLAtherosclerosisMolecular biology030104 developmental biologyBiochemistryMitogen-activated protein kinasebiology.proteinFemaleBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Beauvericin and enniatin B effects on a human lymphoblastoid Jurkat T-cell model

2018

Abstract Several mycotoxins exert their effect on the immunological system; some are classified as immunotoxic. Jurkat T-cells were used to study toxic effects of beauvericin (BEA) and enniatin B (ENN B). Both are not legislated mycotoxins with increasing presence in feed and food. Concentrations studied were from 1 to 15 μM at 24, 48 and 72 h. Cell death by increasing the percentage of apoptotic/necrotic cells was: BEA > ENN B. IC50 values ranged from 3 to 7.5 μM for BEA. ENN B 15 μM decreased viability (21-29%). The percentage of apoptotic/necrotic cells was BEA > ENN B at 24 h but not at 48 h. Caspase-3&7 activation profile varied, although both mycotoxins increased this activation. No d…

0301 basic medicineCell SurvivalT-LymphocytesT cellApoptosisToxicologyJurkat cells03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyDepsipeptidesmedicineHumansMycotoxinCytotoxicityCaspase 7Caspase 3LymphoblastCell Cycle04 agricultural and veterinary sciencesGeneral MedicineMycotoxins040401 food scienceMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisToxicityFood ScienceFood and Chemical Toxicology
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Tetrandrine, an Activator of Autophagy, Induces Autophagic Cell Death via PKC-α Inhibition and mTOR-Dependent Mechanisms

2017

Emerging evidence suggests the therapeutic role of autophagic modulators in cancer therapy. This study aims to identify novel traditional Chinese medicinal herbs as potential anti-tumor agents through autophagic induction, which finally lead to autophagy mediated-cell death in apoptosis-resistant cancer cells. Using bioactivity-guided purification, we identified tetrandrine (Tet) from herbal plant, Radix stephaniae tetrandrae, as an inducer of autophagy. Across a number of cancer cell lines, we found that breast cancer cells treated with tetrandrine show an increase autophagic flux and formation of autophagosomes. In addition, tetrandrine induces cell death in a panel of apoptosis-resistant…

0301 basic medicinePharmacologyProgrammed cell deathautophagylcsh:RM1-950AutophagyCaspase 3BiologytetrandrineCaspase 7Cell biologyTetrandrine03 medical and health scienceschemistry.chemical_compoundlcsh:Therapeutics. Pharmacology030104 developmental biologychemistryCancer cellmTORPharmacology (medical)apoptosis-resistantPKC-αProtein kinase API3K/AKT/mTOR pathwayOriginal ResearchFrontiers in Pharmacology
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Rapid generation of hydrogen peroxide contributes to the complex cell death induction by the angucycline antibiotic landomycin E

2017

Landomycin E (LE) is an angucycline antibiotic produced by Streptomyces globisporus. Previously, we have shown a broad anticancer activity of LE which is, in contrast to the structurally related and clinically used anthracycline doxorubicin (Dx), only mildly affected by multidrug resistance-mediated drug efflux. In the present study, cellular and molecular mechanisms underlying the anticancer activity of landomycin E towards Jurkat T-cell leukemia cells were dissected focusing on the involvement of radical oxygen species (ROS). LE-induced apoptosis distinctly differed in several aspects from the one induced by Dx. Rapid generation of both extracellular and cell-derived hydrogen peroxide alr…

0301 basic medicinePoly (ADP-Ribose) Polymerase-1ApoptosisBiochemistryLandomycin EJurkat Cellschemistry.chemical_compoundSuperoxidesCaspaseCaspase-9chemistry.chemical_classificationCaspase 7Antibiotics AntineoplasticLeukemiabiologySuperoxideStreptomycesCaspase 9Respiratory burstMitochondriaBiochemistrySettore CHIM/03 - Chimica Generale E InorganicaReactive oxygen specieHumanJurkat CellCaspase 7Article03 medical and health sciencesPhysiology (medical)HumansReactive oxygen speciesAminoglycosideIntrinsic apoptosisApoptosiOxidative StreAnticancer drugHydrogen PeroxideMolecular biologyN-acetylcysteineSuperoxide radicalAcetylcysteineMulti-drug resistanceOxidative StressAminoglycosides030104 developmental biologychemistryStreptomyceApoptosisDoxorubicinbiology.proteinReactive Oxygen Species
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Human neutrophil elastase induces endothelial cell apoptosis by activating the PERK‐CHOP branch of the unfolded protein response

2017

Human neutrophil elastase impacts on atherosclerotic plaque stability by inducing apoptosis in endothelial cells. Our aim was to investigate the proapoptotic mechanism of elastase on endothelial cells and to evaluate the presence of elastase in human plaque material. Human endothelial cells were treated with purified human neutrophil elastase. Apoptosis was assayed by capsase-3/7 activation, TUNEL, and sub-G1 assay. Activation of unfolded protein response (UPR) effector molecules binding Ig protein, soluble X-binding protein-1, protein kinase RNA-like ER kinase (PERK), and C/EBP-homologous protein (CHOP) was analyzed by RT-PCR, immunocytochemistry, and Western blot. Genetic silencing of CHO…

0301 basic medicineSmall interfering RNACell SurvivalApoptosisCHOPBiochemistryGene Expression Regulation EnzymologicCell LineeIF-2 Kinase03 medical and health sciencesGeneticsHumansReceptor PAR-2Receptor PAR-1Protein kinase AMolecular BiologyCaspase 7Caspase 3KinaseChemistryElastaseEndothelial CellsAtherosclerosisMolecular biologyEndothelial stem cellCarotid Arteries030104 developmental biologyApoptosisUnfolded Protein ResponseUnfolded protein responseLeukocyte ElastaseTranscription Factor CHOPBiotechnologyThe FASEB Journal
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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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Topoisomerase II{alpha}-dependent and -independent apoptotic effects of dexrazoxane and doxorubicin.

2009

Abstract Coadministration of the iron chelator dexrazoxane reduces by 80% the incidence of heart failure in cancer patients treated with anthracyclines. The clinical application of dexrazoxane is limited, however, because its ability to inhibit topoisomerase IIα (TOP2A) is feared to adversely affect anthracycline chemotherapy, which involves TOP2A-mediated generation of DNA double-strand breaks (DSB). Here, we investigated the apoptotic effects of dexrazoxane and the anthracycline doxorubicin, alone and in combination, in a tumor cell line with conditionally regulated expression of TOP2A. Each drug caused apoptosis that was only partly dependent on TOP2A. Unexpectedly, dexrazoxane was found…

DrugCancer ResearchAnthracyclinemedicine.medical_treatmentmedia_common.quotation_subjectAntineoplastic AgentsApoptosisPharmacologyHistonesAntigens NeoplasmCell Line TumormedicineHumansDoxorubicinAdverse effectPoly-ADP-Ribose Binding Proteinsmedia_commonCaspase 7ChemotherapyChemistryCaspase 3Gene Expression ProfilingCancermedicine.diseaseGlutathioneDNA-Binding ProteinsGene Expression Regulation NeoplasticDNA Topoisomerases Type IIOncologyApoptosisDoxorubicinCancer researchDexrazoxaneTumor Suppressor Protein p53Razoxanemedicine.drugMolecular cancer therapeutics
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Mild Heat Stress Enhances Angiogenesis in a Co-culture System Consisting of Primary Human Osteoblasts and Outgrowth Endothelial Cells

2013

The repair and regeneration of large bone defects, including the formation of functional vasculature, represents a highly challenging task for tissue engineering and regenerative medicine. Recent studies have shown that vascularization and ossification can be stimulated by mild heat stress (MHS), which would offer the option to enhance the bone regeneration process by relatively simple means. However, the mechanisms of MHS-enhanced angiogenesis and osteogenesis, as well as potential risks for the treated cells are unclear. We have investigated the direct effect of MHS on angiogenesis and osteogenesis in a co-culture system of human outgrowth endothelial cells (OECs) and primary osteoblasts …

Hot TemperatureCell SurvivalAngiogenesisCellular differentiationBiomedical EngineeringNeovascularization PhysiologicMedicine (miscellaneous)ApoptosisBioengineeringBiologyRegenerative medicineArticleTissue engineeringOsteogenesisHeat shock proteinHumansRNA MessengerHeat shockBone regenerationCells CulturedCaspase 7OsteoblastsCaspase 3Regeneration (biology)Endothelial CellsCell DifferentiationCoculture TechniquesCapillariesUp-RegulationCell biologyImmunologyHeat-Shock ResponseTissue Engineering Part C: Methods
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Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

2005

Rhinoviruses are the major trigger of acute asthma exacerbations and asthmatic subjects are more susceptible to these infections. To investigate the underlying mechanisms of this increased susceptibility, we examined virus replication and innate responses to rhinovirus (RV)-16 infection of primary bronchial epithelial cells from asthmatic and healthy control subjects.Viral RNA expression and late virus release into supernatant was increased 50- and 7-fold, respectively in asthmatic cells compared with healthy controls. Virus infection induced late cell lysis in asthmatic cells but not in normal cells. Examination of the early cellular response to infection revealed impairment of virus induc…

MaleRhinovirusvirusesCHILDRENApoptosisResearch & Experimental MedicineINHALED CORTICOSTEROIDSmedicine.disease_causeVirus ReplicationImmunology and AllergyTRANSCRIPTIONCells CulturedCaspase 7Caspase 311 Medical And Health SciencesMiddle AgedMedicine Research & ExperimentalCaspasesRNA ViralFemalemedicine.symptomRhinovirusLife Sciences & BiomedicineEXPRESSIONAdultVIRUSESImmunologyInflammationBronchiBiologyAntiviral AgentsVirusArticleImmune systemINFLAMMATIONImmunitymedicineKINASELOWER AIRWAYSHumansInnate immune systemScience & TechnologyPicornaviridae InfectionsRECEPTOREpithelial CellsInterferon-betaAsthmaImmunity InnateEXACERBATIONSViral replicationGene Expression RegulationApoptosisImmunology
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Anticancer activities of six selected natural compounds of some Cameroonian medicinal plants.

2011

BACKGROUND: Natural products are well recognized as sources of drugs in several human ailments. In the present work, we carried out a preliminary screening of six natural compounds, xanthone V(1) (1); 2-acetylfuro-1,4-naphthoquinone (2); physcion (3); bisvismiaquinone (4); vismiaquinone (5); 1,8-dihydroxy-3-geranyloxy-6-methylanthraquinone (6) against MiaPaCa-2 pancreatic and CCRF-CEM leukemia cells and their multidrug-resistant subline, CEM/ADR5000. Compounds 1 and 2 were then tested in several other cancer cells and their possible mode of action were investigated. METHODOLOGY/FINDINGS: The tested compounds were previously isolated from the Cameroonian medicinal plants Vismia laurentii (1,…

PhytochemistryPhytopharmacologyPhytochemicalslcsh:MedicinePharmacologyToxicologyBiochemistryHeLachemistry.chemical_compoundDrug DiscoveryMolecular Cell BiologyBasic Cancer ResearchXanthoneCameroonCytotoxicitylcsh:ScienceCellular Stress ResponsesCaspase 7MultidisciplinaryCell DeathCaspase 3Cell CycleCell cycleChemistryOncologyMedicineResearch ArticleDrugs and DevicesToxic AgentsAntineoplastic AgentsBiologyQuailCaspase 7Cell GrowthComplementary and Alternative MedicineCell Line TumorChemical BiologyAnimalsHumansBiologyCell ProliferationBiological ProductsPlants MedicinalCell growthlcsh:Rbiology.organism_classificationCapillarieschemistryDoxorubicinApoptosisCancer celllcsh:QMedicinal ChemistryCytometryPLoS ONE
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