Search results for "Caspase 9"

showing 10 items of 30 documents

Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus

2017

Dysregulation of NO production is implicated in pregnancy-related diseases, including gestational diabetes mellitus (GDM). The role of NO and its placental targets in GDM pregnancies has yet to be determined. S-Nitrosylation is the NO-derived posttranslational protein modification that can modulate biological functions by forming NO-derived complexes with longer half-life, termed S-nitrosothiol (SNO). Our aim was to examine the presence of endogenous S-nitrosylated proteins in cysteine residues in relation to antioxidant defense, apoptosis, and cellular signal transduction in placental tissue from control (n=8) and GDM (n=8) pregnancies. S-Nitrosylation was measured using the biotin-switch …

0301 basic medicineAgingendocrine system diseasesPlacentaNitric Oxide Synthase Type IIExpressionApoptosisBiochemistryBody Mass Index0302 clinical medicineNitric-oxidePregnancyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyCaspase 3lcsh:CytologyNitrosylationP38General MedicineCatalaseCaspase 9TrophoblastsGestational diabetesmedicine.anatomical_structureCatalase030220 oncology & carcinogenesisFemaleResearch ArticleAdultmedicine.medical_specialtyArticle SubjectNitrosationNitric OxidePathophysiology03 medical and health sciencesErk1/2Internal medicinePlacentamedicineHumanslcsh:QH573-671Protein kinase BPregnancyFetusNitratesS-NitrosothiolsCesarean SectionCell BiologyPeroxiredoxinsmedicine.diseaseProtein s-nitrosylationDiabetes Gestational030104 developmental biologyEndocrinologyOxidative stressCase-Control Studiesbiology.proteinPeroxiredoxinProto-Oncogene Proteins c-aktOxidative Medicine and Cellular Longevity
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Rapid generation of hydrogen peroxide contributes to the complex cell death induction by the angucycline antibiotic landomycin E

2017

Landomycin E (LE) is an angucycline antibiotic produced by Streptomyces globisporus. Previously, we have shown a broad anticancer activity of LE which is, in contrast to the structurally related and clinically used anthracycline doxorubicin (Dx), only mildly affected by multidrug resistance-mediated drug efflux. In the present study, cellular and molecular mechanisms underlying the anticancer activity of landomycin E towards Jurkat T-cell leukemia cells were dissected focusing on the involvement of radical oxygen species (ROS). LE-induced apoptosis distinctly differed in several aspects from the one induced by Dx. Rapid generation of both extracellular and cell-derived hydrogen peroxide alr…

0301 basic medicinePoly (ADP-Ribose) Polymerase-1ApoptosisBiochemistryLandomycin EJurkat Cellschemistry.chemical_compoundSuperoxidesCaspaseCaspase-9chemistry.chemical_classificationCaspase 7Antibiotics AntineoplasticLeukemiabiologySuperoxideStreptomycesCaspase 9Respiratory burstMitochondriaBiochemistrySettore CHIM/03 - Chimica Generale E InorganicaReactive oxygen specieHumanJurkat CellCaspase 7Article03 medical and health sciencesPhysiology (medical)HumansReactive oxygen speciesAminoglycosideIntrinsic apoptosisApoptosiOxidative StreAnticancer drugHydrogen PeroxideMolecular biologyN-acetylcysteineSuperoxide radicalAcetylcysteineMulti-drug resistanceOxidative StressAminoglycosides030104 developmental biologychemistryStreptomyceApoptosisDoxorubicinbiology.proteinReactive Oxygen Species
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How Can Interleukin-1 Receptor Antagonist Modulate Distinct Cell Death Pathways?

2018

Multiple mechanisms of cell death exist (apoptosis, necroptosis, pyroptosis) and the subtle balance of several distinct proteins and inhibitors tightly regulates the cell fate toward one or the other pathway. Here, by combining coimmunoprecipitation, enzyme assays, and molecular simulations, we ascribe a new role, within this entangled regulatory network, to the interleukin-1 receptor antagonist (IL-1Ra). Our study enlightens that IL-1Ra, which usually inhibits the inflammatory effects of IL-1α/β by binding to IL-1 receptor, under advanced pathological states prevents apoptosis and/or necroptosis by noncompetitively inhibiting the activity of caspase-8 and -9. Consensus docking, followed by…

0301 basic medicineProgrammed cell deathProtein ConformationGeneral Chemical EngineeringNecroptosis-Library and Information SciencesMolecular Dynamics SimulationInhibitor of apoptosis01 natural sciencesArticle03 medical and health sciences0103 physical sciencesReceptorsmedicineCaspaseCaspase 8010304 chemical physicsbiologyCell DeathChemistryNeurodegenerationPyroptosisComputational BiologyReceptors Interleukin-1General Chemistrymedicine.diseaseCaspase 9Computer Science ApplicationsCell biologyXIAPEnzyme ActivationInterleukin 1 Receptor Antagonist Protein030104 developmental biologyApoptosisbiology.proteinThermodynamicsInterleukin-1
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The role of intrinsic pathway in apoptosis activation and progression in Peyronie's Disease.

2014

Peyronie’s disease (PD) is characterized with formation of fibrous plaques which result in penile deformity, pain, and erectile dysfunction. The aim of this study was to investigate the activation of the intrinsic apoptotic pathway in plaques from PD patients. Tunica albuginea from either PD or control patients was assessed for the expression of bax, bcl-2 and caspases 9 and 3 using immunohistochemistry and by measurement of apoptotic cells using TUNEL assay. Bax overexpression was observed in metaplastic bone tissue, in fibroblasts, and in myofibroblast of plaques from PD patients. Little or no bcl-2 immunostaining was detected in samples from either patients or controls. Caspase 3 immunos…

AdultMalePathologymedicine.medical_specialtyArticle SubjectPenile Indurationlcsh:MedicineCaspase 3Apoptosisapoptosis peironie's disease urethraBone tissueGeneral Biochemistry Genetics and Molecular BiologySettore MED/24 - UrologiaYoung AdultBcl-2-associated X proteinPeyronie’s diseasemedicineIn Situ Nick-End LabelingHumansCaspaseAgedbcl-2-Associated X ProteinGeneral Immunology and MicrobiologybiologyStaining and LabelingOssificationCaspase 3Settore BIO/16 - Anatomia Umanalcsh:RGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistryCaspase 9medicine.anatomical_structurePeyronie’s disease. ; Apoptosis; Immunohistochemistrybiology.proteinDisease Progressionmedicine.symptomPeyronie's diseaseMyofibroblastImmunostainingSignal TransductionResearch Article
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Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion.

2003

The aim of the study was to investigate mitochondrial electron transfer during rat liver reperfusion after cold storage and hypothermic machine perfusion. Livers from male Brown Norway rats were preserved (UW) for 10h either by cold storage (CS) or by hypothermic oxygenated perfusion extracorporal (HOPE). Transhepatic photometric analysis allowed determination of the redox status of mitochondrial cytochromes during preservation, rewarming and reperfusion. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and cyanide in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of …

AnionsMaleTime FactorsCytochromeLightCold storageCaspase 3ElectronsDNA FragmentationMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundSuperoxidesAnimalsCaspase-9CryopreservationCyanidesbiologySuperoxideCaspase 3Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesTemperatureNADH DehydrogenaseGeneral MedicineRotenoneDNAOrgan PreservationLipid MetabolismCaspase 9MitochondriaRatsCold TemperatureOxygenLight intensitychemistryBiochemistryElectron Transport Chain Complex ProteinsLiverCaspasesReperfusionbiology.proteinCytochromesLipid PeroxidationMitogen-Activated Protein KinasesGeneral Agricultural and Biological SciencesReactive Oxygen SpeciesOxidation-ReductionCryobiology
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Ionizing radiation but not anticancer drugs causes cell cycle arrest and failure to activate the mitochondrial death pathway in MCF-7 breast carcinom…

2001

There is considerable evidence that ionizing radiation (IR) and chemotherapeutic drugs mediate apoptosis through the intrinsic death pathway via the release of mitochondrial cytochrome c and activation of caspases -9 and -3. Here we show that MCF-7 cells that lack caspase-3 undergo a caspase-dependent apoptotic cell death in the absence of DNA fragmentation and alpha-fodrin cleavage following treatment with etoposide or doxorubicin, but not after exposure to IR. Re-expression of caspase-3 restored DNA fragmentation and alpha-fodrin cleavage following drug treatment, but it did not alter the radiation-resistant phenotype of these cells. In contrast to the anticancer drugs, IR failed to induc…

Cancer ResearchCell cycle checkpointAntineoplastic AgentsApoptosisBreast NeoplasmsDNA FragmentationMitochondrionHeLaTransformation GeneticRadiation IonizingGeneticsTumor Cells CulturedHumansMolecular BiologyCaspaseEtoposidebiologyCaspase 3CarcinomaCell CycleMicrofilament ProteinsDNA NeoplasmCell cyclebiology.organism_classificationCaspase 9MitochondriaApoptosisCell cultureDoxorubicinCaspasesImmunologyCancer researchbiology.proteinDNA fragmentationFemaleCarrier ProteinsDNA DamageHeLa CellsOncogene
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Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.

2001

Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. Th…

Cancer ResearchDNA RepairDNA repairDNA damageUltraviolet RaysPoly ADP ribose polymeraseFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsCaspase 8TransfectionFas ligandMembrane PotentialsCricetinaeGeneticsUltraviolet lightAnimalsRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingCaspase 8Caspase 3Fas receptorMolecular biologyCaspase InhibitorsCaspase 9MitochondriaEnzyme ActivationProto-Oncogene Proteins c-bcl-2CaspasesPoly(ADP-ribose) PolymerasesCarrier ProteinsNucleotide excision repairDNA DamageOncogene
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Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation.

2002

Although ganciclovir (GCV) is most often used in suicide anticancer gene therapy, the mechanism of GCV-induced cell killing and apoptosis is not fully understood. We analysed the mechanism of apoptosis triggered by GCV using a model system of CHO cells stably transfected with HSV-1 thymidine kinase (HSVtk). GCV-induced apoptosis is due to incorporation of the drug into DNA resulting in replication-dependent formation of DNA double-strand breaks and, at later stages, S and G2/M arrest. GCV-provoked DNA instability was likely to be responsible for the observed initial decline in Bcl-2 level and caspase-9/-3 activation. Further decline in the Bcl-2 level was due to cleavage of the protein by c…

Cancer ResearchTime FactorsvirusesPoly ADP ribose polymeraseApoptosisCytochrome c GroupCHO CellsHerpesvirus 1 HumanTransfectionThymidine KinaseCricetinaeGeneticsAnimalsfas ReceptorMolecular BiologyGanciclovirbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cCell CycleTransfectionSuicide geneFas receptorMolecular biologyCaspase 9Enzyme ActivationGene Expression Regulation NeoplasticCell killingProto-Oncogene Proteins c-bcl-2ApoptosisThymidine kinaseCaspasesbiology.proteinPoly(ADP-ribose) PolymerasesDNA DamageOncogene
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Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon

2007

Colorectal cancer is an increasingly important cause of death in Western countries. Endocannabinoids inhibit colorectal carcinoma cell proliferation in vitro. In this paper, we investigated the involvement of endocannabinoids on the formation of aberrant crypt foci (ACF, earliest preneoplastic lesions) in the colon mouse in vivo. ACF were induced by azoxymethane (AOM); fatty acid amide hydrolase (FAAH) and cannabinoid receptor messenger ribonucleic acid (mRNA) levels were analyzed by the quantitative reverse transcription polymerase chain reaction (RT-PCR); endocannabinoid levels were measured by liquid chromatography-mass spectrometry; caspase-3 and caspase-9 expressions were measured by W…

Cannabinoid receptormedicine.medical_treatment2-Arachidonoylglycerolpreneoplastic lesionsMass Spectrometrychemistry.chemical_compoundMice0302 clinical medicineFatty acid amide hydrolaseDrug DiscoveryFatty acid amide hydrolase (FAAH)Aberrant crypt fociGenetics(clinical)ReceptorReceptors CannabinoidGenetics (clinical)Medicine(all)0303 health sciencesCaspase 3Reverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemCaspase 93. Good health2-arachidonoylglycerolColon cancer030220 oncology & carcinogenesisColonic NeoplasmsMolecular Medicinelipids (amino acids peptides and proteins)psychological phenomena and processesRapid CommunicationAberrant crypt focimedicine.medical_specialtyColonAzoxymethaneBiologydigestive systemAmidohydrolases03 medical and health sciencesInternal medicineCannabinoid Receptor ModulatorsmedicineAnimalsRNA MessengerCannabinoid receptors030304 developmental biologyAzoxymethaneendocannabinoiddigestive system diseasesEndocrinologychemistrynervous systemCancer researchCannabinoidcancer pharmacologyPrecancerous ConditionsEndocannabinoids
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