Search results for "cell survival"

showing 10 items of 870 documents

In situ crosslinkable hyaluronan hydrogels for tissue engineering

2003

We describe the development of an injectable, cell-containing hydrogel that supports cell proliferation and growth to permit in vivo engineering of new tissues. Two thiolated hyaluronan (HA) derivatives were coupled to four alpha,beta-unsaturated ester and amide derivatives of poly(ethylene glycol) (PEG) 3400. The relative chemical reactivity with cysteine decreased in the order PEG-diacrylate (PEGDA)>>PEG-dimethacrylate>PEG-diacrylamide>PEG-dimethacrylamide. The 3-thiopropanoyl hydrazide derivative (HA-DTPH) was more reactive than the 4-thiobutanoyl hydrazide, HA-DTBH. The crosslinking of HA-DTPH with PEGDA in a molar ratio of 2:1 occurred in approximately 9 min, suitable for an in situ cr…

MaleMaterials sciencePolyethylene glycolCell SurvivalBiophysicsMice NudeBioengineeringBiocompatible Materialsmacromolecular substancesPolyethylene glycolBiomaterialschemistry.chemical_compoundMiceTissue engineeringIn vivoPEG ratioHyaluronic acidMaterials TestingmedicineAnimalsHumansHyaluronic AcidCell encapsulationFibroblastCells CulturedTissue EngineeringForeign-Body Reactiontechnology industry and agricultureHydrogelsCell encapsulationFibroblastsmedicine.anatomical_structureCross-Linking ReagentsBiochemistrychemistryGlycosaminoglycanDiacrylateCell-compatible crosslinkingMechanics of MaterialsSelf-healing hydrogelsCeramics and CompositesBiophysicsIn vivo biocompatibilityCell Division
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Low Density Lipoprotein Receptor-related Protein 1 (LRP1) Modulates N-Methyl-d-aspartate (NMDA) Receptor-dependent Intracellular Signaling and NMDA-i…

2013

The lipoprotein receptor LRP1 is essential in neurons of the central nervous system, as was revealed by the analysis of conditional Lrp1-deficient mouse models. The molecular basis of its neuronal functions, however, is still incompletely understood. Here we show by immunocytochemistry, electron microscopy, and postsynaptic density preparation that LRP1 is located postsynaptically. Basal and NMDA-induced phosphorylation of the transcription factor cAMP-response element-binding protein (CREB) as well as NMDA target gene transcription are reduced in LRP1-deficient neurons. In control neurons, NMDA promotes γ-secretase-dependent release of the LRP1 intracellular domain (LRP1-ICD). However, pul…

MaleN-MethylaspartateCell SurvivalBlotting WesternGene ExpressionMice Transgenicmacromolecular substancesAMPA receptorBiologyCREBReceptors N-Methyl-D-AspartateBiochemistryMiceNeurobiologyPostsynaptic potentialAnimalsMolecular BiologyCells CulturedMice KnockoutNeuronsReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyTumor Suppressor ProteinsMembrane ProteinsCell BiologyEmbryo MammalianLRP1Cell biologyProtein SubunitsReceptors LDLnervous systemSynapsesLDL receptorbiology.proteinNMDA receptorFemaleAmyloid Precursor Protein SecretasesSignal transductionDisks Large Homolog 4 ProteinGuanylate KinasesPostsynaptic densityLow Density Lipoprotein Receptor-Related Protein-1Protein BindingSignal TransductionSynaptosomesJournal of Biological Chemistry
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Glutathione and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor in vivo.

1997

Low rates of cellular proliferation are associated with low GSH content and enhanced sensitivity of Ehrlich ascites-tumour (EAT) cells to the cytotoxic effects of recombinant human tumour necrosis factor (rhTNF-alpha). Buthionine sulphoximine, a selective inhibitor of GSH synthesis, inhibited tumour growth and increased rhTNF-alpha cytoxicity in vitro. Administration of sublethal doses (10(6)units/kg per day) of rhTNF-alpha to EAT-bearing mice promoted oxidative stress (as measured by increases in intracellular peroxide levels, O2(-); generation and mitochondrial GSSG) and resulted in a slight reduction (19%) in tumour cell number when controls showed the highest rate of cellular proliferat…

MaleNecrosisCell SurvivalMice Inbred StrainsBiologyPharmacologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceIn vivomedicineTumor Cells CulturedCytotoxic T cellAnimalsHumansCytotoxicityCarcinoma Ehrlich TumorMolecular BiologyButhionine SulfoximineTumor Necrosis Factor-alphaDrug SynergismCell BiologyGlutathioneGlutathioneRecombinant ProteinsKineticschemistryBiochemistryCancer cellmedicine.symptomOxidative stressIntracellularCell DivisionResearch ArticleThe Biochemical journal
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Identification of Patulin from

2019

The identification and characterization of fungal commensals of the human gut (the mycobiota) is ongoing, and the effects of their various secondary metabolites on the health and disease of the host is a matter of current research. While the neurons of the central nervous system might be affected indirectly by compounds from gut microorganisms, the largest peripheral neuronal network (the enteric nervous system) is located within the gut and is exposed directly to such metabolites. We analyzed 320 fungal extracts and their effect on the viability of a human neuronal cell line (SH-SY5Y), as well as their effects on the viability and functionality of the most effective compound on primary ent…

MaleNeuronsCell SurvivalPrimary Cell CulturePenicilliummicrobiomeComplex MixturesMycotoxinsEnteric Nervous SystemArticleMice Inbred C57BLMicePatulinCell Line TumorAnimalsHumansgastrointestinal systemFemaleCalcium SignalingfungiReactive Oxygen SpeciesfusariumMolecules (Basel, Switzerland)
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PSA-NCAM expression in the rat medial prefrontal cortex

2005

The rat medial prefrontal cortex, an area considered homologous to the human prefrontal cortex, is a region in which neuronal structural plasticity has been described during adulthood. Some plastic processes such as neurite outgrowth and synaptogenesis are known to be regulated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Since PSA-NCAM is present in regions of the adult CNS which are undergoing structural remodeling, such as the hypothalamus or the hippocampus, we have analyzed the expression of this molecule in the medial prefrontal cortex of adult rats using immunohistochemistry. PSA-NCAM immunoreactivity was found both in cell bodies and in the neuropil of…

MaleNeuropilNeuriteInterneuronAntimetabolitesCell SurvivalSynaptophysinSynaptogenesisPrefrontal CortexHippocampusNeural Cell Adhesion Molecule L1BiologyRats Sprague-DawleyNeuroplasticityNeuropilmedicineAnimalsFluorescent Antibody Technique IndirectPrefrontal cortexNeuronsNeuronal PlasticityGlutamate DecarboxylasePyramidal CellsGeneral NeuroscienceImmunohistochemistryRatsPhenotypemedicine.anatomical_structureBromodeoxyuridinenervous systemSialic AcidsNeural cell adhesion moleculeNeuroscienceNeuroscience
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An old method for good new cells

2009

The aim of this work was to demonstrate a greater number of viable cells using a micro-surgical in-situ perfusion to collect rat pancreata compared with the pancreas after exsanguination. We used 3 groups of 20 rats. Perfusion was performed by selective cannulation of the left common iliac artery with administration of UW solution at 4 degrees C. Collected pancreata were digested and cells separated by Ficoll gradient were placed in culture to permit adhesion to dishes. Cells were characterized and tested for viability. We observed a gain of about 14% in the number of viable cells compared with those obtained after exsanguination (P < .001 by chi-square).

MalePathologymedicine.medical_specialtyAdenosineCell SurvivalAllopurinolAntigens CD19Organ Preservation Solutionsviable cellsmicro-surgical in-situ perfusionpancreasafter exsanguinationRaffinosemedicineAnimalsFicollInsulinViaspanAorta AbdominalRats WistarPancreasTransplantationbusiness.industryLeft Common Iliac ArteryGlutathionePerfusionTransplantationSettore MED/18 - Chirurgia Generalemedicine.anatomical_structureFicoll gradientFemaleSurgeryPancreasbusinessPerfusion
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Sodium metabisulfite as a cytotoxic food additive induces apoptosis in HFFF2 cells

2021

Sodium metabisulfite (SMB), an antioxidant agent, is extensively used as a preservative in food industry. The current study was aimed to clarify its potential toxic effects on human fetal foreskin fibroblasts (HFFF2) cells, in vitro. Subsequently, MTT results illustrated that exposure to SMB significantly (p  0.0001) decreased HFFF2 cell viability in a dose-dependent manner, and the concentration of 25 μM reduced cell survival rates to 50% as the half-maximal inhibitory concentration of SMB. It was further shown that SMB exerted this cytotoxic effect on HFFF2 cells through apoptosis induction. qRT-PCR and western blotting results showed that treatment of HFFF2 cells with this food additive …

MalePreservativeAntioxidantfood.ingredientCell Survivalmedicine.medical_treatmentForeskinApoptosisPharmacology01 natural sciencesAnalytical Chemistrychemistry.chemical_compound0404 agricultural biotechnologyfoodAutophagymedicineHumansSulfitesCytotoxic T cellCytotoxicityCells Culturedbcl-2-Associated X ProteinCaspase 8Dose-Response Relationship DrugCaspase 3Food additive010401 analytical chemistry04 agricultural and veterinary sciencesGeneral MedicineSodium metabisulfiteFibroblasts040401 food scienceCaspase 9In vitro0104 chemical sciencesGene Expression RegulationchemistryApoptosisFood AdditivesReactive Oxygen SpeciesFood ScienceFood Chemistry
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Cocaine hepatotoxicity: two different toxicity mechanisms for phenobarbital-induced and non-induced rat hepatocytes.

1993

Abstract Hepatocytes isolated from both phenobarbital-induced and control rats were short-term cultured and exposed to cocaine (8–2000 μM) for varying times. Intracellular lactate dehydrogenase activity, free calcium levels ([Ca 2+ ] i ), reduced glutathione (GSH) and lipid peroxidation were investigated to evaluate the toxic effect of cocaine on hepatocytes. Cytochrome P450 induction by phenobarbital potentiated the in vitro cytotoxicity of cocaine by a factor of 13 (IC 50 = 84 μ M induced cells vs 1100 μM in non-induced cells). This difference in the susceptibility of the two types of hepatocytes to cocaine correlated well with the activity of cytochrome P450 2 B 1 2 . Rapid depletion of …

MaleProgrammed cell deathCell SurvivalPharmacologyBiochemistryLipid peroxidationRats Sprague-Dawleychemistry.chemical_compoundCocaineCytochrome P-450 Enzyme SystemLactate dehydrogenasemedicineAnimalsCells CulturedPharmacologybiologyDose-Response Relationship DrugCytochrome P450GlutathioneGlutathioneRatschemistryLiverPhenobarbitalToxicityCytochrome P-450 CYP2B1biology.proteinPhenobarbitalCalciumLipid PeroxidationOxidoreductasesIntracellularmedicine.drugBiochemical pharmacology
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Glutamine potentiates TNF-α-induced tumor cytotoxicity

2001

L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…

MaleProgrammed cell deathFree RadicalsCell SurvivalGlutamineApoptosisCytochrome c GroupMitochondrionBiologyBiochemistryMembrane PotentialsMiceNecrosischemistry.chemical_compoundAdenosine TriphosphateSuperoxidesPhysiology (medical)Tumor Cells CulturedAnimalsButhionine sulfoximineCaspase 3Tumor Necrosis Factor-alphaDrug SynergismHydrogen PeroxideGlutathioneGlutathioneMolecular biologyDietMitochondriaCell biologyOxygenGlutamineOxidative StressCytosolProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesReactive Oxygen SpeciesOxidation-ReductionCell DivisionIntracellularFree Radical Biology and Medicine
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Intrinsically determined cell death of developing cortical interneurons.

2009

The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…

MaleProgrammed cell deathInterneurongenetic structuresCell SurvivalPopulationApoptosisCell CountNeocortexBiologyArticle03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsInterneuronsmedicineAnimalseducationCellular Senescence030304 developmental biologybcl-2-Associated X Protein0303 health scienceseducation.field_of_studyMultidisciplinaryNeocortexMembrane GlycoproteinsCaspase 3musculoskeletal neural and ocular physiologyPyramidal CellsfungiProtein-Tyrosine KinasesCell biologyTransplantationMice Inbred C57BLmedicine.anatomical_structurenervous systemAnimals NewbornInhibitory Postsynaptic PotentialsCerebral cortexbiology.proteinFemaleCell aging030217 neurology & neurosurgeryNeurotrophinNature
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