Search results for "Apoptosis."

showing 10 items of 1794 documents

Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination.

2010

Abstract Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADDODC-KO). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADDODC-KO mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADDODC-KO mice followed an ameliorated clinical di…

Encephalomyelitis Autoimmune ExperimentalMultiple Sclerosisgenetic structuresEncephalomyelitisFas-Associated Death Domain ProteinImmunologyApoptosisurologic and male genital diseasesMiceConditional gene knockoutDemyelinating diseasemedicineImmunology and AllergyAnimalsFADDLymphocytesMyelin SheathDeath domainInflammationMice KnockoutbiologyMultiple sclerosisMacrophagesfungiExperimental autoimmune encephalomyelitismedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureGene Expression RegulationSpinal CordCancer researchbiology.proteinbiological phenomena cell phenomena and immunityGene DeletionJournal of immunology (Baltimore, Md. : 1950)
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High levels of the molecular chaperone Mdg1/ERdj4 reflect the activation state of endothelial cells

2003

Mdg1/ERdj4, a mammalian chaperone that belongs to the HSP40 protein family, has been reported to be located in the endoplasmic reticulum (ER), is induced by ER stress, and protects ER stressed cells from apoptosis. Here we show that under normal physiological conditions, Mdg1/ERdj4 is expressed at various levels in the vasculature due to different activation states of the endothelium. To elucidate the stimuli that induce ER stress and thus upregulate Mdg1/ERdj4, we investigated the effect of several endothelium specific stressors on its expression. Mdg1/ERdj4 mRNA is induced by activated macrophages, by nitric oxide (NO) and heat shock, and during terminal cell differentiation, whereas shea…

EndotheliumCell SurvivalCellular differentiationApoptosisCell CommunicationEndoplasmic ReticulumNitric OxideMiceStress PhysiologicalmedicineAnimalsHumansRNA MessengerHeat shockEndoplasmic Reticulum Chaperone BiPbiologyMacrophagesEndoplasmic reticulumMembrane ProteinsProteinsCell BiologyHSP40 Heat-Shock ProteinsCoculture TechniquesUp-RegulationHsp70Cell biologyProtein Transportmedicine.anatomical_structureApoptosisChaperone (protein)biology.proteinUnfolded protein responseEndothelium VascularStress MechanicalCarrier ProteinsCell NucleolusHeat-Shock ResponseHeLa CellsMolecular ChaperonesExperimental Cell Research
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Oxysterol mixture in hypercholesterolemia-relevant proportion causes oxidative stress-dependent eryptosis.

2014

Background/Aims: Oxysterol activity on the erythrocyte (RBC) programmed cell death (eryptosis) had not been studied yet. Effects of an oxysterol mixture in hyper-cholesterolemic-relevant proportion, and of individual compounds, were investigated on RBCs from healthy humans. Methods: Membrane phosphatidylserine (PS) externalization, calcium entry, ROS production, amino-phospholipid translocase (APLT) activity were evaluated by cytofluorimetric assays, cell volume from forward scatter. Prostaglandin PGE2 was measured by ELISA; GSH-adducts and lipoperoxides by spectrophotometry. Involvement of protein kinase C and caspase was investigated by inhibitors staurosporin, calphostin C, and Z-DEVD-FM…

ErythrocytesPhysiologyEryptosisApoptosisPharmacologylcsh:PhysiologyAntioxidantschemistry.chemical_compoundPhospholipid scramblingSettore BIO/10 - Biochimicapolycyclic compoundslcsh:QD415-436PhosphatidylserineKetocholesterolsProtein Kinase Clcsh:QP1-981OxysterolsPhosphatidylserineErythrocyteCalphostin CBiochemistryCaspaseslipids (amino acids peptides and proteins)AntioxidantReactive Oxygen SpecieHumanProgrammed cell deathOxysterolHypercholesterolemiachemistry.chemical_elementPhosphatidylserinesCalciumCalcium ChannelDinoprostonelcsh:BiochemistryOxysterolLipid oxidationHumansCalphostinHypercholesterolemia Human red blood cell Oxysterols Eryptosis Oxidative stressKetocholesterolApoptosiOxidative StreCaspaseOxidative StresschemistryCalciumCalcium ChannelsReactive Oxygen SpeciesEryptosiHuman red blood cellCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
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A role for caspases in the differentiation of erythroid cells and macrophages

2007

Several cysteine proteases of the caspase family play a central role in many forms of cell death by apoptosis. Other enzymes of the family are involved in cytokine maturation along inflammatory response. In recent years, several caspases involved in cell death were shown to play a role in other cellular processes such as proliferation and differentiation. In the present review, we summarize the current knowledge of the role of caspases in the differentiation of erythroid cells and macrophages. Based on these two examples, we show that the nature of involved enzymes, the pathways leading to their activation in response to specific growth factors, and the specificity of the target proteins th…

Erythroid Precursor CellsProteasesCell typeProgrammed cell deathErythrocytesbiologyMacrophagesmedicine.medical_treatmentIntrinsic apoptosisCell DifferentiationGeneral MedicineBiochemistryMonocytesHematopoiesisCell biologyCytokineApoptosisCaspasesmedicinebiology.proteinAnimalsHumansMacrophageMyeloid Progenitor CellsCaspaseBiochimie
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Sugammadex, a Neuromuscular Blockade Reversal Agent, Causes Neuronal Apoptosis in Primary Cultures

2013

Sugammadex, a γ-cyclodextrin that encapsulates selectively steroidal neuromuscular blocking agents, such as rocuronium or vecuronium, has changed the face of clinical neuromuscular pharmacology. Sugammadex allows a rapid reversal of muscle paralysis. Sugammadex appears to be safe and well tolerated. Its blood-brain barrier penetration is poor (< 3% in rats), and thus no relevant central nervous toxicity is expected. However the blood brain barrier permeability can be altered under different conditions (i.e. neurodegenerative diseases, trauma, ischemia, infections, or immature nervous system). Using MTT, confocal microscopy, caspase-3 activity, cholesterol quantification and Western-blot we …

Estrès oxidatiuSmac/Diablo and CASP-3.BiologyPharmacologymedicine.disease_causeSugammadexSugammadexAIFmedicineAnimalsRocuroniumCytCCells CulturedFisiologia cel·lularNeuronsNeuromuscular BlockadeapoptosisGeneral MedicineNeuromuscular Blocking AgentsRatsOxidative StressApoptosisAnesthesiaToxicityNeuromuscular BlockadeNeuron deathOxidative stressmedicine.drugResearch Papergamma-CyclodextrinsInternational Journal of Medical Sciences
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Cross-talk between phosphatidic acid and ceramide during ethanol-induced apoptosis in astrocytes

2005

Background Ethanol inhibits proliferation in astrocytes, an effect that was recently linked to the suppression of phosphatidic acid (PA) formation by phospholipase D (PLD). The present study investigates ethanol's effect on the induction of apoptosis in astrocytes and the formation of ceramide, an apoptotic signal. Evidence is presented that the formation of PA and ceramide may be reciprocally linked during ethanol exposure. Results In cultured rat cortical astrocytes, ethanol (0.3–1 %, v/v) induced nuclear fragmentation and DNA laddering indicative of apoptosis. Concomitantly, in cells prelabeled with [3H]-serine, ethanol caused a dose-dependent, biphasic increase of the [3H]-ceramide/ [3H…

EthanolAstrocytesHydrolysisPhospholipase DAnimalsPhosphatidic AcidsApoptosisCeramidesCells CulturedResearch ArticleRatsSphingomyelinsBMC Pharmacology
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Novel mechanism for the radiation-induced bystander effect: nitric oxide and ethylene determine the response in sponge cells.

2006

Until now the bystander effect had only been described in vertebrates. In the present study the existence of this effect has been demonstrated for the phylogenetically oldest metazoan phylum, the Porifera. We used the demosponge Suberites domuncula for the experiments in the two-chamber-system. The lower dish contained irradiated "donor" cells (single cells) and the upper dish the primmorphs ("recipient" primmorphs). The "donor" cells were treated with UV-B light (40 mJ/cm2) and 100 microM hydrogen peroxide (H2O2), factors that exist also in the natural marine aquatic environment of sponges; these factors caused a high level of DNA strand breaks followed by a reduced viability of the cells.…

EthyleneDNA ComplementaryDNA damageCell SurvivalUltraviolet RaysHealth Toxicology and MutagenesisMolecular Sequence DataGene ExpressionApoptosisBiologyNitric OxideModels BiologicalNitric oxideAmidohydrolaseschemistry.chemical_compoundGene expressionGeneticsBystander effectAnimalsAmino Acid SequenceCloning MolecularMolecular BiologyNitriteschemistry.chemical_classificationBase SequenceSequence Homology Amino AcidEthylenesbiology.organism_classificationCell biologyAmino acidPoriferaSuberites domunculachemistryBiochemistryApoptosisDNA DamageMutation research
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Defective apoptosis as potential mechanism in the tumorogenesis of myelolipoma

1999

Apoptosis is considered an important mechanism of selective deletion that occurs during hematopoiesis. Myelolipoma is a rare benign tumor composed of adipose tissue and hematopoietic cells. The pathogenesis of this benign tumor is still unclear. Analysing the structural levels and apoptosis of normal human bone marrow (NHBM) and human myelolipoma (HM), the apoptotic events resulted abundantly present in NHBM compared to HM, which showed a small number of apoptotic cells. By contrast, Fas expression was strongly present both in NHBM and HM. These findings suggest that an altered function of Fas in myelolipoma is not able to trigger the apoptotic machinery. In conclusion, we hypothesize that …

FaAdrenal Gland NeoplasmsAntigens Differentiation MyelomonocyticApoptosiApoptosisBone Marrow CellsCell BiologyChoristomaImmunohistochemistryApoptosis; Bone marrow; Choristoma; Fas; Myelolipoma; Cell Biology; Anatomy; Animal Science and Zoology; Developmental BiologyMyelolipomaAntigens CDIn Situ Nick-End LabelingHumansBone marrowAnimal Science and Zoologyfas ReceptorAnatomyDevelopmental Biology
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The CD95/CD95 ligand system is not the major effector in anticancer drug-mediated apoptosis.

1998

Many anticancer drugs are able to induce apoptosis in tumor cells but the mechanisms underlying this phenomenon are poorly understood. Some authors reported that the p53 tumor suppressor gene may be responsible for drug-induced apoptosis; however, chemotherapy-induced apoptosis can also be observed in p53 negative cells. Recently, doxorubicin (DXR) was reported to induce CD95L expression to mediate apoptosis through the CD95/CD95L system. Thus, an impairment of such a system may be involved in drug resistance. We evaluated the in vitro antitumor activity of several cytotoxic drugs on two human p53-negative T-cell lymphoma cell lines, the HUT78-B1 CD95L-resistant cell line and the HUT78 pare…

Fas Ligand ProteinCaspase 3Antineoplastic AgentsApoptosismedicineTumor Cells CulturedCytotoxic T cellHumansfas ReceptorCytotoxicityMolecular BiologyEtoposideEtoposideMembrane GlycoproteinsChemistryCaspase 3Cell BiologyFas receptorCaspase InhibitorsProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicinCaspasesCancer researchTumor Suppressor Protein p53Camptothecinmedicine.drugCell death and differentiation
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Defective apoptosis and tumorigenesis: role of p53 mutation and Fas/FasL system dysregulation

2010

The transcription factor p53 and the cytokine receptor FasL are two of the most famous regulators of cell life, and their alterations can cause a large number of pathologies, including cancer. In this review, we focused on how they can determine defective apoptosis, one of the causes of tumorigenesis and tumor progression. The importance of this knowledge lies in the new perspectives that gene therapy can offer to cure cancer.

Fas Ligand ProteinHistologyFree RadicalsCellBiophysicsApoptosisBiologymedicine.disease_causeFas ligandNeoplasmsmedicineAnimalsHumansfas ReceptorTranscription factorlcsh:QH301-705.5Membrane GlycoproteinsfungiCancerfood and beveragesGenetic TherapyCell BiologyGenes p53medicine.diseaseGenes bcl-2medicine.anatomical_structurelcsh:Biology (General)ApoptosisTumor progressionImmunologyCarcinogenesisCytokine receptorEuropean Journal of Histochemistry
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