Search results for "APOPTOSI"

showing 10 items of 1846 documents

β-Amyloid-induced activation of Caspase-3 in primary cultures of rat neurons

2000

It is known that beta-amyloid peptide (Abeta) contributes to the neurodegeneration in Alzheimer's disease (AD) and operates through activation of an apoptotic pathway. Apoptotic signal is driven by a family of cysteine proteases called caspases. The beta-amyloid precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated beta-amyloid peptide formation. Cerebellar neurons from rat pups were treated with the aged Abeta(25-35) at 1 and 5 microM and fluorescence assays of caspase activity performed over 4 days. We observed an increase in caspase activity after 48 h treatment in both 1 and 5 microM treated cells, then (72-96 h) caspase activity…

AgingTime FactorsAmyloidProteolysisApoptosisCaspase 3medicineAnimalsCells CulturedCaspaseNeuronsAmyloid beta-Peptidesbiologymedicine.diagnostic_testCaspase 3NeurodegenerationIntrinsic apoptosismedicine.diseaseMolecular biologyPeptide FragmentsRatsEnzyme Activationmedicine.anatomical_structureApoptosisCaspasesImmunologybiology.proteinNeuronDevelopmental BiologyMechanisms of Ageing and Development
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Pharmacological intervention in age-associated brain disorders by Flupirtine: Alzheimer’s and Prion diseases

1998

Alzheimer's disease, a major form of dementia in the elderly has become an increasingly important health problem in developed countries. In vitro studies on primary neurons demonstrate that Flupirtine (Katadolon) at a concentration of 1 microg/ml, significantly reduces the neurotoxic (apoptotic) effect displayed by A beta25-35, a segment of the amyloid beta-protein precursor the etiologic agent of Alzheimer's disease. Flupirtine, which has been in clinical use since 10 years ago, prevents the toxic effect of PrP, the presumed etiologic agent of the Creutzfeldt-Jakob disease as well as the excitatory amino acid glutamate on cortical neurons. Flupirtine displays a bimodal activity. Its strong…

AgingTime FactorsCell SurvivalPrionsMolecular Sequence DataAminopyridinesApoptosisPharmacologyBiologyNeuroprotectionPrion Diseaseschemistry.chemical_compoundGlutamatesAlzheimer DiseasemedicineAnimalsAmino Acid SequenceRats WistarCells CulturedNeuronsAmyloid beta-PeptidesGlutamate receptorNeurotoxicityBiological activityGlutathionemedicine.diseasePeptide FragmentsRatsNeuroprotective Agentsmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2BiochemistrychemistryCalciumNeuronAlzheimer's diseaseFlupirtineDevelopmental Biologymedicine.drugMechanisms of Ageing and Development
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Induction of apoptosis in cardiac myocytes by an A3 adenosine receptor agonist.

1998

The effects of the selective adenosine (ADO) A3 receptor agonist IB-MECA (N6-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide) on cultured newborn rat cardiomyocytes were examined in comparison with ADO, the ADO A1 receptor-selective agonist R-PIA (N6-R-phenylisopropyladenosine), or the ADO A3 selective antagonist MRS 1191 (3-ethyl-5-benzyl-2-methyl-6-phenyl-4-phenylethynyl-1, 4-(+/-)-dihydropyridine-3,5 dicarboxylate), using digital image analysis of Feulgen-stained nuclei. At high concentration, IB-MECA (/=10 microM ) and ADO (200 microM) induced apoptosis; however, R-PIA or MRS 1191 did not have any detectable effects on cardiac cells. In addition, DNA breaks in cardiomyocytes undergoing a…

AgonistContraction (grammar)TUNEL assayAdenosinemedicine.drug_classMyocardiumReceptor Adenosine A3ApoptosisHeartCell BiologyDNA FragmentationBiologyAdenosine receptorMolecular biologyAdenosineRatsApoptosismedicinePurinergic P1 Receptor AgonistsMyocyteAnimalsCalciumReceptorCells Culturedmedicine.drugExperimental cell research
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Cancer relapse under chemotherapy: why TLR2/4 receptor agonists can help.

2007

Liver or lung metastases usually relapse under chemotherapy. Such life-threatening condition urgently needs new, systemic anticancer compounds, with original and efficient mechanisms of action. In B16 melanoma mice treated with cyclophosphamide, D'Agostini et al. [D'Agostini, C., Pica, F., Febbraro, G., Grelli, S., Chiavaroli, C., Garaci, E., 2005. Antitumour effect of OM-174 and Cyclophosphamide on murine B16 melanoma in different experimental conditions. Int. Immunopharmacol. 5, 1205-1212.] recently found that OM-174, a chemically defined Toll-like receptor(TLR)2/4 agonist, reduces tumor progression and prolongs survival. Here we review 149 articles concerning molecular mechanisms of TLR2…

AgonistLipopolysaccharidesCyclophosphamidemedicine.drug_classmedicine.medical_treatmentNitric Oxide Synthase Type IIAntineoplastic AgentsApoptosisNitric oxidechemistry.chemical_compoundRecurrenceNeoplasmsMedicineAnimalsHumansPharmacologyChemotherapybusiness.industryTumor Necrosis Factor-alphaCancerDendritic Cellsmedicine.diseaseNeoadjuvant TherapyToll-Like Receptor 2Interleukin-10Toll-Like Receptor 4TLR2Lipid ATreatment OutcomechemistryTumor progressionChemotherapy AdjuvantDrug Resistance NeoplasmEnzyme InductionImmunologyCancer researchBCG VaccineTumor necrosis factor alphaImmunotherapybusinessmedicine.drugSignal TransductionT-Lymphocytes CytotoxicEuropean journal of pharmacology
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Induction of apoptosis by the adenosine derivative IB-MECA in parental or multidrug-resistant HL-60 leukemia cells: possible relationship to the effe…

2004

<i>Background:</i> The effects of the A<sub>3</sub> adenosine receptor (A<sub>3</sub>AR) agonist IB-MECA were examined in HL-60 leukemia and in its multidrug-resistant variant HL-60R cells. <i>Methods:</i> Cytotoxicity was evaluated by MTS assays and apoptosis by flow cytometry analyses of DNA fragmentation and phosphatidylserine exposure. The mRNAs of A<sub>3</sub>AR and inhibitor of apoptosis proteins (IAPs) were determined by RT-PCR. <i>Results:</i> A<sub>3</sub>AR expression was similar in HL-60 and HL-60R cells. At ≧100 µ<i>M</i>, IB-MECA exhibited strong cytotoxic and apoptotic effects in H…

AgonistProgrammed cell deathAdenosinemedicine.drug_classApoptosisHL-60 CellsBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsDrug DiscoverymedicineNeoplasmHumansPharmacology (medical)PharmacologyGeneral Medicinemedicine.diseaseAdenosine A3 receptorFlow CytometryAdenosineDrug Resistance MultipleLeukemiaInfectious DiseasesOncologyBiochemistryApoptosisDrug Resistance NeoplasmA 3 adenosine receptor IB-MECA Apoptosis Multidrug resistance Inhibitor of apoptosis proteinsCancer researchmedicine.drugChemotherapy
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Selection and characterization of a novel agonistic human recombinant anti-Trail-R2 minibody with anti-leukemic activity

2009

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising natural anticancer therapeutic agent because through its “death receptors”, TRAIL-R1 and TRAIL-R2, it induces apoptosis in many transformed tumor cells, but not in the majority of normal cells. Hence, agonistic compounds directed against TRAIL death receptors have the potential of being excellent cancer therapeutic agents, with minimal cytotoxicity in normal tissues. Here, we report the selection and characterization of a new single-chain fragment variable (scFv) to TRAIL-R2 receptor isolated from a human phage-display library, produced as minibody (MB), and characterized for the in vitro anti-leukemic tumoricid…

Agonistmedicine.drug_classTRAIL; TRAIL-R2; minibody; anticancer therapyImmunologylymphoma; therapy; recombinant antibodyTRAILApoptosislymphomaCHO CellsCricetulusPeptide LibraryTRAIL-R2CricetinaeImmunoglobulin FragmentmedicineAnimalsHumansImmunology and Allergyrecombinant antibodyanticancer therapyReceptorCytotoxicityImmunoglobulin FragmentsPharmacologytherapyLeukemiaChemistryAnimalChinese hamster ovary cellAntibody-Dependent Cell CytotoxicityminibodyApoptosiIn vitroRecombinant ProteinsReceptors TNF-Related Apoptosis-Inducing LigandCHO CellCell cultureApoptosisImmunologyCancer researchTumor necrosis factor alphaCricetuluHuman
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Induction of Apoptosis in Rat Cardiocytes by A3 Adenosine Receptor Activation and Its Suppression by Isoproterenol

2000

The purpose of the present study was to investigate the mechanisms involved in the induction of apoptosis in newborn cultured cardiomyocytes by activation of adenosine (ADO) A3 receptors and to examine the protective effects of beta-adrenoceptors. The selective agonist for A3 ADO receptors Cl-IB-MECA (2-chloro-N6-iodobenzyl-5-N-methylcarboxamidoadenosine) and the antagonist MRS1523 (5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpy rid ine-5-carboxylate) were used. High concentrations of the Cl-IB-MECA (or = 10 microM) agonist induced morphological modifications of myogenic cells, such as rounding and retraction of cell body and dissolution of contractile filaments, followed by…

Agonistmedicine.medical_specialtyProgrammed cell deathAdenosineCardiotonic Agentsmedicine.drug_classApoptosisStimulationBiologyInternal medicinePurinergic P1 Receptor AgonistsmedicineAnimalsProtein kinase AReceptorCells CulturedMyocardiumReceptor Adenosine A3IsoproterenolReceptors Purinergic P1HeartCell BiologyAdenosineAdenosine receptorRatsCell biologyEndocrinologyApoptosisSignal Transductionmedicine.drugExperimental Cell Research
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Induction of Transglutaminase 2 by a Liver X Receptor/Retinoic Acid Receptor α Pathway Increases the Clearance of Apoptotic Cells by Human Macrophages

2009

Rationale: Liver X receptors (LXRs) are oxysterol-activated nuclear receptors that are involved in the control of cholesterol homeostasis and inflammatory response. Human monocytes and macrophages express high levels of these receptors and are appropriate cells to study the response to LXR agonists. Objective: The purpose of this study was to identify new LXR targets in human primary monocytes and macrophages and the consequences of their activation. Methods and Results: We show that LXR agonists significantly increase the mRNA and protein levels of the retinoic acid receptor (RAR)α in primary monocytes and macrophages. LXR agonists promote RARα gene transcription through binding to a spec…

Agonistmedicine.medical_specialtyReceptors Retinoic AcidPhysiologymedicine.drug_classResponse elementReceptors Cytoplasmic and NuclearApoptosisBiologyCell LinePhagocytosisGTP-Binding ProteinsInternal medicinemedicineHumansMacrophageProtein Glutamine gamma Glutamyltransferase 2ReceptorLiver X receptorLiver X ReceptorsTransglutaminasesMacrophagesRetinoic Acid Receptor alphaMacrophage ActivationAtherosclerosisOrphan Nuclear ReceptorsCell biologyDNA-Binding ProteinsRetinoic acid receptorEndocrinologyNuclear receptorRetinoic acid receptor alphaEnzyme InductionCardiology and Cardiovascular MedicineCirculation Research
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Mitochondrial function in liver disease.

2006

Oxidative stress is involved in the pathogenesis and progression of different liver diseases, such as alcoholic liver disease and biliary cirrhosis. The increased mitochondrial production of O2(-) at complexes I and III, and consequently of H2O2 and other reactive oxygen species (ROS), triggered by NADH overproduction seems the major cause of mitochondrial and cellular oxidative stress and damage in chronic alcoholism. The mitochondrial oxidative stress renders hepatocytes susceptible to ethanol- or acetaldehyde-induced mitochondrial membrane permeability transition (MMPT) and apoptosis. Nitrosative stress contributes to cell death by peroxynitrite formation. The expression of the death rec…

Alcoholic liver diseaseProgrammed cell deathBiliary cirrhosisPopulationApoptosisMitochondria LiverMitochondrionmedicine.disease_causechemistry.chemical_compoundmedicineCardiolipinAnimalsHumanseducationLiver Diseases Alcoholicchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesLiver Cirrhosis BiliaryLiver Diseasesmedicine.diseaseNADCell biologyRatsOxidative StresschemistryHepatocytesOxidative stressFrontiers in bioscience : a journal and virtual library
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Change in expression of MGMT during maturation of human monocytes into dendritic cells.

2005

Dendritic cells (DCs) maturated from monocytes play an important role in the immune system, not only in defense against conventional infections but also in cancer rejection. Because of the central role of DCs in tumor host defense it is highly important that DCs as well as the progenitor cell population are protected during cancer therapy. Since most anticancer drugs target DNA, the DNA repair capacity is most importance for the response of DCs and their precursor cells. Here, we studied the expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) in monocytes obtained from peripheral blood of healthy donors and DCs maturated from monocytes (moDCs). We show that MG…

Alkylating AgentsDNA RepairDNA repairPopulationAntigens CD34ApoptosisBiologyBiochemistryMonocytesO(6)-Methylguanine-DNA MethyltransferaseImmune systemmedicineGene silencingHumansLymphocytesProgenitor celleducationPromoter Regions GeneticneoplasmsMolecular BiologyCells CulturedRegulation of gene expressioneducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionMonocyteCell DifferentiationCell BiologyDendritic CellsDNA MethylationFlow Cytometrydigestive system diseasesmedicine.anatomical_structureImmunologyCytokinesStem cellDNA repair
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