Search results for "CASP"

showing 10 items of 470 documents

Role of caspase-8 in hepatocyte response to infection and injury in mice.

2007

Caspase-8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase-8 gene specifically in the liver, we found that caspase-8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes, attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the…

Programmed cell deathInflammationCaspase 8MiceConditional gene knockoutmedicineAnimalsListeriosisCaspaseCell ProliferationInflammationMice KnockoutCaspase 8HepatologybiologyCell DeathCell growthLiver Regenerationmedicine.anatomical_structureHepatocyteImmunologyCancer researchChronic inflammatory responsebiology.proteinHepatocytesmedicine.symptomHepatology (Baltimore, Md.)
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Histamine and spontaneously released mast cell granules affect the cell growth of human hepatocellular carcinoma cells

2007

The role of mast cells in tumor growth is still controversial. In this study we analyzed the effects of both histamine and pre-formed mediators spontaneously released by mast cells on the growth of two human hepatocellular carcinoma cell lines, HA22T/VGH and HuH-6, with different characteristics of differentiation, biological behavior and genetic defects. We showed that total mast cell releasate, exocytosed granules (granule remnants) and histamine reduced cell viability and proliferation in HuH-6 cells. In contrast, in HA22T/VGH cells granule remnants and histamine induced a weak but significant increase in cell growth. We showed that both cell lines expressed histamine receptors H(1) and …

medicine.medical_specialtyCarcinoma HepatocellularCell SurvivalSurvivinClinical BiochemistryHistamine AntagonistsApoptosisHistamine H1 receptorBiologyRanitidineBiochemistryExocytosisInhibitor of Apoptosis ProteinsHistamine receptorchemistry.chemical_compoundInternal medicineCell Line TumormedicineAnimalsHumansHistamine H4 receptorMast CellsEnterochromaffin-like cellRats WistarMolecular BiologyCells Culturedbeta CateninCell ProliferationCell growthCaspase 3Liver NeoplasmsMast cellMolecular biologyNeoplasm ProteinsRatsEnzyme ActivationEndocrinologymedicine.anatomical_structurechemistryCell cultureCyclooxygenase 2Molecular MedicineReceptors HistamineFemaleTerfenadinePoly(ADP-ribose) PolymerasesMicrotubule-Associated ProteinsHistamineHistamine
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Optimal doses of caspofungin during continuous venovenous hemodiafiltration in critically ill patients

2017

0301 basic medicineContinuous renal replacement therapymedicine.medical_specialtyLetterCritical Illness030106 microbiologyHemodiafiltrationCritical Care and Intensive Care MedicineEchinocandinsLipopeptides03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCaspofunginHumansMedicineIntensive care medicinebusiness.industryCritically illlcsh:Medical emergencies. Critical care. Intensive care. First aid030208 emergency & critical care medicinelcsh:RC86-88.9Invasive candidiasisContinuous venovenous hemodiafiltrationAcute Kidney Injurymedicine.diseaseInvasive candidiasisRenal Replacement TherapychemistryAdsorptionCaspofunginbusinessCritical Care
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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Retinoic Acid Induces Apoptosis-Associated Neural Differentiation of a Murine Teratocarcinoma Cell Line

2002

Abstract: Incubation with all-trans retinoic acid (RA) induces PCC7-Mz1 embryonic carcinoma cells to cease proliferation and to develop into a tissue-like pattern of neuronal, astroglial, and fibroblast-like derivatives over a period of several days. Concomitant with the induction of differentiation by RA, a sizable fraction of the Mz1 stem cells detaches and dies, with the maximal level of cell death achieved after 10 h of RA treatment. This RA-induced cell death fulfills all criteria of apoptosis, including nuclear condensation, intranucleosomal DNA degradation, expression of cysteine aspases (caspases), and the formation of apoptotic bodies. Apoptosis could be suppressed by the pan-caspa…

TeratocarcinomaProgrammed cell deathCellular differentiationRetinoic acidApoptosisTretinoinBiochemistryMiceCellular and Molecular Neurosciencechemistry.chemical_compoundGAP-43 ProteinTumor Cells CulturedAnimalsProtein Kinase CProtein kinase CCaspaseNeuronsbiologyCell DifferentiationGenes bcl-2Cell biologyGene Expression RegulationchemistryBiochemistryCell cultureApoptosisPhorbolbiology.proteinJournal of Neurochemistry
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A caspase-3-dependent pathway is predominantly activated by the excitotoxin pregnenolone sulfate and requires early and late cytochrome c release and…

2002

This study investigates the implication of mitochondria- and caspase-dependent pathways in the death of retinal neurones exposed to the neurosteroid pregnenolone sulfate (PS) shown to evoke apoptosis and contribute to amplification and propagation of excitotoxicity. After a brief PS challenge of intact retinas, caspase-3 and caspase-2 activation and cytochrome c release occur early and independent of changes in the oxidative state measured by superoxide dismutase activity. The temporal and spatial relationship of these events suggests that a caspase-3-dependent pathway is activated in response to cytochrome c release and requires caspase-2 activation and a late cytochrome c release in speci…

medicine.medical_specialtyProgrammed cell deathbiologyCytochrome cCaspase 2Caspase 3BiochemistryCell biologyCellular and Molecular Neurosciencechemistry.chemical_compoundEndocrinologychemistryApoptosisInternal medicinePregnenolonemedicinebiology.proteinPregnenolone sulfateCaspasemedicine.drugJournal of Neurochemistry
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Oxidative stress, glutathione, and gene expression as key indicators in SH-SY5Y cells exposed to zearalenone metabolites and beauvericin.

2020

The co-presence of mycotoxins from fungi of the genus Fusarium is a common fact in raw food and food products, as trace levels of them or their metabolites can be detected, unless safety practices during manufacturing are carried out. Zearalenone (ZEA), its metabolites α-zearalenol (α-ZEL) and β-zearalenol (β-ZEL) and, beauvericin (BEA) are co/present in cereals, fruits or their products which is a mixture that consumer are exposed and never evaluated in neuronal cells. In this study the role of oxidative stress and intracellular defense systems was assessed by evaluating reactive oxygen species (ROS) generation and glutathione (GSH) ratio activity in a human neuroblastoma cell line, SH-SY5…

0301 basic medicineSH-SY5YAntioxidantmedicine.medical_treatmentCell Culture TechniquesGene ExpressionApoptosisToxicologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDepsipeptidesmedicineHumanschemistry.chemical_classificationReactive oxygen speciesCaspase 3General MedicineGlutathioneGlutathioneBeauvericinUp-RegulationOxidative Stress030104 developmental biologychemistryBiochemistryApoptosisZearalenoneZeranolReactive Oxygen SpeciesOxidation-Reduction030217 neurology & neurosurgeryIntracellularOxidative stressToxicology letters
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In toxic demyelination oligodendroglial cell death occurs early and is FAS independent

2010

Oligodendroglial cell death is a frequent phenomenon of many neurological diseases, e.g. in demyelinating diseases such as multiple sclerosis (MS). The underlying mechanisms are largely unknown. Here, we demonstrate that in the toxic demyelination cuprizone model, oligodendroglial cell death and downregulation of myelin genes start days after initiation of the cuprizone diet and weeks before demyelination is obvious. In early – but not in later – stages, dying oligodendrocytes express activated caspase 3, suggesting a switch from classical apoptotic pathways to caspase 3-independent mechanisms during the course of the cuprizone diet. The expression level of FAS in the corpus callosum, a cel…

MaleProgrammed cell deathDown-RegulationMice TransgenicCaspase 3ApoptosisNerve Fibers MyelinatedArticleCorpus Callosumlcsh:RC321-571Mice03 medical and health sciencesMyelinCuprizone0302 clinical medicineDownregulation and upregulationmedicineAnimalsRNA Messengerfas Receptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCaspase030304 developmental biology0303 health sciencesCell DeathbiologyCaspase 3CytotoxinsMultiple sclerosisExperimental autoimmune encephalomyelitisFASmedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalOligodendrogliamedicine.anatomical_structureGene Expression RegulationNeurologyApoptosisMyelinImmunologybiology.proteinFemaleMyelin Proteins030217 neurology & neurosurgeryDemyelinating DiseasesSignal TransductionNeurobiology of Disease
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Caspase 9 and Caspase 3 Immunohistochemical Pattern in Skeletal and Cardiac Muscles at Different Times after Death: An Experimental Study on PMI Esti…

2021

(1) Background: The estimation of the post mortem interval (PMI) is a challenge for forensic pathologists because data emerging from methods commonly applied are not always conclusive, since several conditions exist that may affect the reliability of these parameters. Thus, new approaches have been proposed to overcome such a limit. In recent years, several studies have been performed on proteins analyzing their expression/degradation patterns in relation to the progressing of the post mortem interval. (2) Methods: The immunoreactivity patterns of two apoptosis mediators—Caspase 9 and Caspase 3—have been tested in order to evaluate their potential role as markers of the post mortem interval…

Pathologymedicine.medical_specialtyMedicine (General)cardiac muscleforensic sciencesClinical BiochemistryCaspase 3Article03 medical and health sciences0302 clinical medicineR5-920caspase 3Medicine030216 legal & forensic medicineskeletal musclecaspase 9Caspase030304 developmental biologyPost-mortem intervalCaspase-90303 health sciencespost mortem intervalbiologybusiness.industryCardiac muscleSkeletal musclemedicine.anatomical_structureApoptosisbiology.proteinImmunohistochemistrybusinesstime after deathDiagnostics
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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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