Search results for "Apoptosi"

showing 10 items of 1846 documents

The cyclopentenone-type prostaglandin 15-deoxy-delta12,14-prostaglandin J2 inhibits CD95 ligand gene expression in T lymphocytes: interference with p…

2003

Abstract 15-Deoxy-Δ12,14-PGJ2 (15d-PGJ2) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. 15d-PGJ2 is a natural ligand of the peroxisome proliferator-activated receptor (PPAR)-γ nuclear receptor, but relevant PPARγ-independent actions mediated by this prostanoid have been described. Fas (APO-1/CD95) and its ligand (Fas-L) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death and has been implicated in diseases in which lymphocyte homeostasis is compromised. Moreover, several studies have desc…

Fas Ligand ProteinNerve growth factor IBT-LymphocytesImmunologyPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearApoptosisCyclopentanesBiologyLigandsLymphocyte ActivationJurkat cellsImmediate-Early ProteinsTransactivationchemistry.chemical_compoundJurkat CellsMiceHeat Shock Transcription FactorsPeroxisomesImmunology and AllergyAnimalsHumansHSP70 Heat-Shock ProteinsGene Silencingfas ReceptorReceptorPromoter Regions GeneticCell Line TransformedEarly Growth Response Protein 1chemistry.chemical_classificationHybridomasMembrane GlycoproteinsProstaglandin D2Fas receptorMolecular biologyDNA-Binding ProteinschemistryNuclear receptorlipids (amino acids peptides and proteins)Prostaglandin D2Transcription Factors
researchProduct

In vitro generated human memory-like T cells are CD95 type II cells and resistant towards CD95-mediated apoptosis

2006

An adaptive immune response implies expansion of activated T cells and subsequent elimination to maintain homeostasis in a process called activation-induced cell death. Some cells, however, differentiate into memory cells and ensure a strong secondary immune response. To analyze the apoptosis phenotype of memory T cells on a cellular and molecular level, we have established an in vitro model of T cell activation and generation of cells phenotypically and functionally similar to memory cells. These long-term cultured T cells show a CD95-resistant phenotype, although they are still sensitive towards TCR/CD3-mediated apoptosis. Biochemical analysis revealed that these cells shift from CD95 typ…

Fas Ligand ProteinT-LymphocytesT cellImmunologyCell Culture Techniquesbcl-X ProteinApoptosisLymphocyte ActivationmedicineHumansImmunology and AllergyCytotoxic T cellfas ReceptorIL-2 receptorAntigen-presenting cellCells CulturedCD40biologyZAP70Acquired immune systemNatural killer T cellMitochondriaUp-RegulationCell biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2biology.proteinImmunologic MemoryEuropean Journal of Immunology
researchProduct

p53 triggers apoptosis in oncogene-expressing fibroblasts by the induction of Noxa and mitochondrial Bax translocation.

2003

The mechanism of p53-dependent apoptosis is still only partly defined. Using early-passage embryonic fibroblasts (MEF) from wild-type (wt), p53(-/-) and bax(-/-) mice, we observe a p53-dependent translocation of Bax to the mitochondria and a release of mitochondrial Cytochrome c during stress-induced apoptosis. These events proceed independent of zVAD-inhibitable caspase activation, are not prevented by dominant negative FADD (DN-FADD), but are negatively regulated by Mdm-2. Bcl-x(L) expression prevents the release of mitochondrial Cytochrome c and apoptosis, but not Bax translocation. At a single-cell level, enforced expression of p53 is sufficient to induce Bax translocation and Cytochrom…

Fas-Associated Death Domain ProteinDown-RegulationChromosomal translocationApoptosisCytochrome c GroupMitochondrionMiceBcl-2-associated X proteinFetusDownregulation and upregulationProto-Oncogene ProteinsAnimalsFADDEnzyme InhibitorsMolecular BiologyCells CulturedAdaptor Proteins Signal Transducingbcl-2-Associated X ProteinMice KnockoutbiologyOncogeneChemistryCytochrome cCell BiologyFibroblastsMolecular biologyCell biologyMitochondriaProtein TransportGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinTumor Suppressor Protein p53Carrier ProteinsCell death and differentiation
researchProduct

Enniatin A1, enniatin B1 and beauvericin on HepG2: Evaluation of toxic effects

2015

Hepatotoxicity of three Fusarium mycotoxins, beauvericin (BEA) and two enniatins (ENNs) ENN A1 and ENN B1, in hepatocarcinoma cells (HepG2) were evaluated and compared. Concentrations used were 1.5 and 3 μM at 24, 48 and 72 h for each mycotoxin. Flow cytometry was used to examine enniatins effects on cell proliferation, to characterize the cell cycle phase where the cells blocked and to study the mitochondria role in ENNs-induced apoptosis. ENN B1 treated cells showed a time dependent G1 blockade at both concentrations used. ENN A1 and BEA decreased the apoptotic-necrotic percentage of cells comparing to control and disrupted the MMP as observed by TMRM and ToPro-3 fluorochromes signal. It …

FusariumStereochemistryApoptosisToxicologyFlow cytometryNecrosischemistry.chemical_compoundFusariumDepsipeptidesmedicineHumansMycotoxinCell ProliferationMembrane Potential Mitochondrialbiologymedicine.diagnostic_testCell growthCell CycleStereoisomerismHep G2 CellsGeneral MedicineMycotoxinsCell cyclebiology.organism_classificationMolecular biologyBeauvericinKineticschemistryApoptosisHepatocytesEnniatinFood ScienceFood and Chemical Toxicology
researchProduct

Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-…

2002

This report is focused on the apoptotic effect induced by MG132, an inhibitor of 26S proteasome, in human hepatoma HepG2 cells. The results were compared with those obtained with non-transformed human Chang liver cells. MG132 reduced the viability of HepG2 cells in a time- and dose-dependent manner. The effect was in tight connection with the induction of apoptosis, as indicated by fluorescence microscopy and cytometric analysis, and was accompanied by a remarkable increase in the production of H2O2 and a reduction in mitochondrial transmembrane potential (Deltapsim). In addition cell death was prevented by antioxidants such as GSH, N-acetylcysteine or catalase. Western blot analysis showed…

G2 PhaseHepatoblastomaCancer ResearchProgrammed cell deathProteasome Endopeptidase ComplexMG132Time FactorsCell SurvivalLeupeptinsPoly ADP ribose polymeraseBlotting Westernbcl-X ProteinMitosisCaspase 3Antineoplastic AgentsApoptosismacromolecular substancesMembrane Potentialschemistry.chemical_compoundCytosolMultienzyme ComplexesMG132medicineTumor Cells CulturedHumansCaspasebiologyCaspase 3Cytochrome cCell CycleLiver NeoplasmsHydrogen PeroxideFlow CytometryMolecular biologyMitochondriaEnzyme ActivationCysteine EndopeptidasesOxidative StressOncologyBiochemistrychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinProteasome inhibitormedicine.drug
researchProduct

Beauvericin-induced cytotoxicity via ROS production and mitochondrial damage in Caco-2 cells.

2013

The cytotoxicity of beauvericin (BEA) on human colon adenocarcinoma (Caco-2) cells was studied as a function of time. Moreover, the oxidative damage and cell death endpoints were monitored after 24, 48 and 72 h. After BEA exposure, the IC₅₀ values ranged from 1.9 ± 0.7 to 20.6 ± 6.9 μM. A decrease in reduced glutathione (GSH; 31%) levels, as well as an increase in oxidized glutathione (GSSG, 20%) was observed. In the presence of BEA, reactive oxygen species (ROS) level was highly increased at an early stage with the highest production of 2.0-fold higher than the control that was observed at 120 min. BEA induced cell death by mitochondria-dependent apoptotic process with loss of the mitochon…

G2 PhaseProgrammed cell deathDNA damageCell SurvivalApoptosisBiologyToxicologymedicine.disease_causechemistry.chemical_compoundInhibitory Concentration 50NecrosisDepsipeptidesmedicineHumansIntestinal Mucosachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesIonophoresCell growthGeneral MedicineGlutathioneMycotoxinsMolecular biologyGlutathioneBeauvericinCell biologyMitochondriaKineticsOxidative StresschemistryApoptosisLipid PeroxidationCaco-2 CellsReactive Oxygen SpeciesOxidation-ReductionOxidative stressDNA DamageToxicology letters
researchProduct

TTAS a New Stilbene Derivative that Induces Apoptosis in Leishmania Infantum

2012

Leishmania parasites are able to undergo apoptosis (programmed cell death), similarly to mammalian cells. Recently it was demonstrated in vitro the anti-leishmanial effect of some natural and synthetic stilbenoids including resveratrol and piceatannol. In this study we evaluated the Leishmanicidal activity of a pool of stilbene derivatives which had previously shown high apoptotic efficacy against neoplastic cells. All the compounds tested were capable to decrease the parasite viability in a dose-dependent manner. Trans-stilbenes proved to be markedly more effective than cis-isomers. This was different from that observed in tumor cells in which cis-stilbenes were more potent cytotoxic agent…

G2 PhaseProgrammed cell deathLeishmaniasiSettore MED/17 - Malattie InfettiveImmunologyAntiprotozoal AgentsTUBULINApoptosisResveratrolChromatography AffinityLethal Dose 50chemistry.chemical_compoundGranulocyte-Macrophage Progenitor CellsAnnexin A5Leishmania infantumCytotoxicityCells CulturedMembrane Potential MitochondrialPiceatannolDose-Response Relationship DrugbiologyGeneral MedicineFlow CytometryHematopoietic Stem Cellsbiology.organism_classificationLeishmaniaPROGRAMMED CELL DEATHIn vitroInfectious DiseaseschemistryBiochemistrySTILBENESAntimony Sodium GluconateApoptosisStilbeneElectrophoresis Polyacrylamide GelParasitologyLeishmania infantumCell DivisionLEISHMANIASIS
researchProduct

Staurosporine-induced apoptosis in Chang liver cells is associated with down-regulation of Bcl-2 and Bcl-XL.

2004

A potent inhibitor of serine/threonine kinases, staurosporine exerts antiproliferative and apoptotic effects in many cancer cells, although the exact mechanism of its action is still unclear. This study examines the effects of staurosporine on Chang liver cells, an immortalized non-tumor cell line, in comparison with those caused in HuH-6 and HepG2 cells, two human hepatoma cell lines. Our results provide evidence that staurosporine promotes apoptosis in Chang liver cells as observed by flow cytometric analysis and acridine orange/ethidium bromide staining. The effect appeared already after 8 h of treatment and increased with treatment time and dose. After 48 h of exposure to 200 nM stauros…

G2 PhaseProgrammed cell deathTime FactorsCell SurvivalLiver cytologyBlotting Westernbcl-X ProteinDown-RegulationMitosisApoptosisBcl-xLAmino Acid Chloromethyl KetonesCell LineMembrane PotentialsEthidiumSettore BIO/10 - BiochimicaGeneticsmedicineHumansStaurosporineEnzyme InhibitorsBcl-2 family factors.CaspaseApoptosis staurosporineDose-Response Relationship DrugbiologyCaspase 3Cell CycleGeneral MedicineFlow CytometryStaurosporineMolecular biologyAcridine OrangeMitochondriaEnzyme ActivationLiverProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCaspasesCancer cellbiology.proteinCell Divisionmedicine.drug
researchProduct

Synthesis and antiproliferative activity of thiazolyl-bis-pyrrolo[2,3-b]pyridines and indolyl-thiazolyl-pyrrolo[2,3-c]pyridines, nortopsentin analogu…

2015

Two new series of nortopsentin analogues, in which the imidazole ring of the natural product was replaced by thiazole and indole units were both substituted by 7-azaindole moieties or one indole unit was replaced by a 6-azaindole portion, were efficiently synthesized. Compounds belonging to both series inhibited the growth of HCT-116 colorectal cancer cells at low micromolar concentrations, whereas they did not affect the viability of normal-like intestinal cells. A compound of the former series induced apoptosis, evident as externalization of plasma membrane phosphatidylserine (PS), and changes of mitochondrial trans-membrane potential, while blocking the cell cycle in G2/M phase. In contr…

G2 Phaseantiproliferative activitybis-indolyl alkaloidsStereochemistryPyridinesPharmaceutical ScienceNortopsentin analoguesthiazolyl-bis-pyrrolo [23-b]pyridinesVacuoleArticlechemistry.chemical_compoundDrug DiscoveryImidazoleHumansPyrrolesautophagic deathThiazolelcsh:QH301-705.5Pharmacology Toxicology and Pharmaceutics (miscellaneous)Cell ProliferationIndole testMembrane Potential MitochondrialnortopsentinsDose-Response Relationship DrugMolecular Structureindolyl-thiazolyl-pyrrolo[23-c]pyridinesthiazolyl-bis-pyrrolo[23-b]pyridinesapoptosisPhosphatidylserineCell cycleHCT116 CellsSettore CHIM/08 - Chimica Farmaceuticaindolyl-thiazolyl-pyrrolo[23-<i>c</i>]pyridinesThiazoleslcsh:Biology (General)chemistryCytoplasmApoptosismarine alkaloidsthiazolyl-bis-pyrrolo [23-<i>b</i>]pyridinesMarine drugs
researchProduct

G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids

2022

The nuclear export factor CRM1-mediated pathway is known to be important for the nuclear egress of progeny parvovirus capsids in the host cells with virus-mediated cell cycle arrest at G2/M. However, it is still unclear whether this is the only pathway by which capsids exit the nucleus. Our studies show that the nuclear egress of DNA-containing full canine parvovirus. capsids was reduced but not fully inhibited when CRM1-mediated nuclear export was prevented by leptomycin B. This suggests that canine parvovirus capsids might use additional routes for nuclear escape. This hypothesis was further supported by our findings that nuclear envelope (NE) permeability was increased at the late stages…

G2/M checkpointnuclear egress of capsidsgeenitisäntäsolutcyclin B1canine parvovirusapoptosisApoptosisCRM1Crm1bakteeritsolut1182 Biochemistry cell and molecular biology3111 BiomedicineCanine parvovirusparvoviruksetNuclear egress of capsidssolukiertosolubiologia
researchProduct