Search results for "Apoptosi"

showing 10 items of 1846 documents

Biological effects of inorganic arsenic on primary cultures of rat astrocytes

2010

It is well established that inorganic arsenic induces neurotoxic effects and neurological defects in humans and laboratory animals. The cellular and molecular mechanisms of its actions, however, remain elusive. Herein we report the effects of arsenite (NaAsO2) on primary cultures of rat astrocytes. Cells underwent induction of heat shock protein 70 only at the highest doses of inorganic arsenic (30 and 60 microM), suggesting a high threshold to respond to stress. We also investigated arsenic genotoxicity with the comet assay. Interestingly, although cells treated with 10 microM arsenite for 24 h maintained >70% viability, with respect to untreated cells, high DNA damage was already observed…

ArsenitesCell SurvivalDNA damagechemistry.chemical_elementBiologymedicine.disease_causeRats Sprague-Dawleychemistry.chemical_compoundSuperoxide Dismutase-1Settore BIO/10 - BiochimicaGeneticsmedicineAnimalsCell damageCells CulturedArsenicArseniteSuperoxide DismutaseGeneral Medicinemedicine.diseaseMolecular biologyCarcinogens EnvironmentalRatsHsp70Comet assaySettore BIO/18 - GeneticachemistryBiochemistryApoptosisAstrocytesComet Assayinorganic arsenic astrocytes cell damage DNA damage PIPPin.Reactive Oxygen SpeciesGenotoxicityDNA DamageInternational Journal of Molecular Medicine
researchProduct

Early induction of genetic instability and apoptosis by arsenic in cultured Chinese hamster cells

2002

In order to assess at what time from the beginning of exposure inorganic arsenic can give rise to genetic instability and trigger apoptosis, V79-C13 Chinese hamster cells were treated with 10 microM sodium arsenite for 24 h. Under these conditions, cell survival was >70% and cells showed neither an increase in chromosome aberration frequency nor a delay in cell cycle progression. Investigations, which were carried out every 6 h during the treatment, revealed an early appearance of genetically unstable cells, namely micronucleated, multinucleated and mononucleated 'giant' cells, as well as apoptotic cells. Indirect immunostaining using anti-beta-tubulin antibody showed severe alterations in …

ArsenitesCell SurvivalHealth Toxicology and MutagenesisPopulationMitosisHamsterApoptosisToxicologyChromosome aberrationChromosomesChinese hamsterCricetulusMultinucleateCricetinaeGeneticsAnimalseducationMitosisGenetics (clinical)Chromosome Aberrationseducation.field_of_studybiologyAneuploidybiology.organism_classificationSodium CompoundsMolecular biologyCell biologySettore BIO/18 - GeneticaCell cultureApoptosisCytogenetic AnalysisMutationarsenic genomic instability apoptosisFluorescein-5-isothiocyanate
researchProduct

Atherogenic properties of enzymatically degraded LDL: selective induction of MCP-1 and cytotoxic effects on human macrophages.

1998

Abstract —The mechanisms underlying the selective accumulation of macrophages in early atherosclerotic lesions are poorly understood but are likely to be related to specific properties of altered low density lipoprotein (LDL) deposited in the subendothelium. Enzymatic, nonoxidative degradation of LDL converts the lipoprotein to a potentially atherogenic moiety, enzymatically altered LDL (E-LDL), which activates complement and is rapidly taken up by human macrophages via a scavenger receptor–dependent pathway. Immunohistological evidence indicates that E-LDL is present in an extracellular location in the early lesion. We report that E-LDL causes massive release of monocyte chemotactic prote…

ArteriosclerosisHydrolasesGene ExpressionNeuraminidaseBiologyCCL2Polymerase Chain Reactionchemistry.chemical_compoundExtracellularmedicineMacrophageHumansTrypsinInterleukin 8RNA MessengerCells CulturedChemokine CCL2Cell DeathMonocyteMacrophagesRNA-Directed DNA PolymeraseSterol EsteraseMolecular biologyLipoproteins LDLKineticsmedicine.anatomical_structureBiochemistrychemistryApoptosisLow-density lipoproteinlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
researchProduct

Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothal…

2015

Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamine…

AstrocitosNeurobiologia del desenvolupamentAmidohidrolasasCannabinoid receptorCarbamatos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Apoptosis Regulatory Proteins::Caspases [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings]medicine.medical_treatment:Chemicals and Drugs::Carbohydrates::Monosaccharides::Hexoses::Glucose [Medical Subject Headings]Apoptosis:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings]chemistry.chemical_compound:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Membrane Proteins::Receptors Cell Surface::Receptors G-Protein-Coupled::Receptors Cannabinoid::Receptor Cannabinoid CB1 [Medical Subject Headings]0302 clinical medicine:Chemicals and Drugs::Organic Chemicals::Carboxylic Acids::Acids Acyclic::Carbamates [Medical Subject Headings]Fatty acid amide hydrolaseReceptor cannabinoide CB1:Organisms::Eukaryota::Animals [Medical Subject Headings]FAAHGliosishealth care economics and organizations:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleosides::Deoxyribonucleosides::Deoxyuridine::Bromodeoxyuridine [Medical Subject Headings]:Chemicals and Drugs::Lipids::Glycerides::Triglycerides [Medical Subject Headings]Original Research0303 health sciencesNeurogenesisBenzamidas:Chemicals and Drugs::Polycyclic Compounds::Steroids::Cholestanes::Cholestenes::Cholesterol [Medical Subject Headings]Endocannabinoid systemEtanolaminas3. Good healthEndocannabinoides:Chemicals and Drugs::Lipids::Fatty Acids::Fatty Acids Unsaturated::Fatty Acids Monounsaturated::Oleic Acids [Medical Subject Headings]CannabinoidesMicroglíalipids (amino acids peptides and proteins)medicine.symptomColesterol:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Terpenes::Cannabinoids [Medical Subject Headings]:Chemicals and Drugs::Lipids::Fatty Acids::Palmitic Acids [Medical Subject Headings]psychological phenomena and processesProliferación celularmedicine.medical_specialtyCerebroNeurogenesiseducationBiologyBromodesoxiuridina:Anatomy::Nervous System::Neuroglia::Microglia [Medical Subject Headings]Triglicéridoslcsh:RC321-571Ácidos oléicosRatas03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineHipocampomedicineCaspasa 3:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologyPalmitoylethanolamide:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoids [Medical Subject Headings]:Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases [Medical Subject Headings]Cannabinoids:Anatomy::Cells::Neuroglia::Astrocytes [Medical Subject Headings]Peso corporalEnergy metabolism:Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings]:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hypothalamus [Medical Subject Headings]URB597:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Gliosis [Medical Subject Headings]:Chemicals and Drugs::Organic Chemicals::Amines::Amino Alcohols::Ethanolamines [Medical Subject Headings]Muerte celular:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings]EndocrinologyURB597chemistryGliosisnervous systemGlucosaCannabinoidEnergy Metabolism:Chemicals and Drugs::Organic Chemicals::Amides::Benzamides [Medical Subject Headings]HipotálamoÁcidos palmíticos030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
researchProduct

Caractérisation des figures myéliniques associées à l'accumulation de lipides polaires induites par différents oxystérols cytotoxiques identifiés dan…

2006

Atherosclerosis is a complex and chronic arterial process which is characterized by a remodeling of the vascular wall, associated with inflammatory reactions, proliferation and cell death process, and with accumulation of oxidized lipids among which oxysterols (cholesterol oxidation products) which might play key roles in the initiation and development of atheromatous lesions. Our work performed on U937 and THP1 promonocytic cells, rat aorta embryonic A7R5 cells, and breast carcinoma MCF7 cells (caspase-3 deficient). Different oxysterols, present in large quantity in atheromatous lesions, were used: 7-cétocholestérol (7KC), 7Β-hydroxycholestérol, 25-hydroxycholestérol, cholestérol-5Α, 6Α-ep…

AthéroscléroseCell DeathApoptose[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyLipidesApoptosisOxystérolsAtherosclerosisLipidsPhospholipidosisPhospholipidose<br />Vitamine-ECaspase-2[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Mort cellulaireVitamin E[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM][SDV.BC] Life Sciences [q-bio]/Cellular Biology
researchProduct

Thyrocytes--not innocent bystanders in autoimmune disease.

2001

Autoimmune diseasebusiness.industryT-LymphocytesImmunologyThyroid GlandThyroiditis AutoimmuneApoptosismedicine.diseaseGraves DiseaseImmunologyImmunology and AllergyMedicineHumansfas ReceptorbusinessNature immunology
researchProduct

Artesunate Activates Mitochondrial Apoptosis in Breast Cancer Cells via Iron-catalyzed Lysosomal Reactive Oxygen Species Production

2011

The antimalarial agent artesunate (ART) activates programmed cell death (PCD) in cancer cells in a manner dependent on the presence of iron and the generation of reactive oxygen species. In malaria parasites, ART cytotoxicity originates from interactions with heme-derived iron within the food vacuole. The analogous digestive compartment of mammalian cells, the lysosome, similarly contains high levels of redox-active iron and in response to specific stimuli can initiate mitochondrial apoptosis. We thus investigated the role of lysosomes in ART-induced PCD and determined that in MCF-7 breast cancer cells ART activates lysosome-dependent mitochondrial outer membrane permeabilization. ART impac…

AutophagosomeProgrammed cell deathEndosomeIronArtesunateApoptosisBreast NeoplasmsMitochondrionBiologyBiochemistryPermeabilityAntimalarialsCell Line TumorLysosomemedicineHumansEnzyme InhibitorsMolecular BiologyAutophagyChloroquineCell BiologyArtemisininsMitochondriaCell biologymedicine.anatomical_structureApoptosisMitochondrial MembranesCancer cellFemaleMacrolidesLysosomesReactive Oxygen SpeciesJournal of Biological Chemistry
researchProduct

p62: Friend or Foe? Evidences for OncoJanus and NeuroJanus Roles

2020

p62 is a versatile protein involved in the delicate balance between cell death and survival, which is fundamental for cell fate decision in the context of both cancer and neurodegenerative diseases. As an autophagy adaptor, p62 recognizes polyubiquitin chains and interacts with LC3, thereby targeting the selected cargo to the autophagosome with consequent autophagic degradation. Beside this function, p62 behaves as an interactive hub in multiple signalling including those mediated by Nrf2, NF-κB, caspase-8, and mTORC1. The protein is thus crucial for the control of oxidative stress, inflammation and cell survival, apoptosis, and metabolic reprogramming, respectively. As a multifunctional pr…

AutophagosomeProgrammed cell deathP62ApoptosisContext (language use)mTORC1Cell fate determinationBiologyCatalysislcsh:ChemistryInorganic ChemistryStress granuleAutophagymedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCancerNeurodegenerative diseasesOrganic ChemistryNeurodegenerationAutophagyGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologylcsh:Biology (General)lcsh:QD1-999International Journal of Molecular Sciences
researchProduct

Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
researchProduct

Autophagy is related to apoptosis in Paracentrotus lividus embryos cadmium exposed

2012

P. lividus embryo offers an excellent opportunity to investigate the adaptive response of cells exposed to different stress. We previously demonstrated that cadmium treatment triggers the accumulation of metal in embryonic cells and the activation of defense system depending on concentration and exposure time, through the synthesis of HSPs and/or the initiation of apoptosis. Analysing autophagy, by neutral red, acridine orange and LC3-detection, we demonstrated that Cd-exposed embryos adopt this process as an additional stratagem to safeguard the developmental program. We observed that embryos treated at subletal Cd concentration activate a massive autophagic response after 18h, which decre…

Autophagy apoptosis cadmium stress sea urchin embryosSettore BIO/06 - Anatomia Comparata E Citologia
researchProduct