Search results for "caspase"

showing 10 items of 390 documents

Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

2005

Rhinoviruses are the major trigger of acute asthma exacerbations and asthmatic subjects are more susceptible to these infections. To investigate the underlying mechanisms of this increased susceptibility, we examined virus replication and innate responses to rhinovirus (RV)-16 infection of primary bronchial epithelial cells from asthmatic and healthy control subjects.Viral RNA expression and late virus release into supernatant was increased 50- and 7-fold, respectively in asthmatic cells compared with healthy controls. Virus infection induced late cell lysis in asthmatic cells but not in normal cells. Examination of the early cellular response to infection revealed impairment of virus induc…

MaleRhinovirusvirusesCHILDRENApoptosisResearch & Experimental MedicineINHALED CORTICOSTEROIDSmedicine.disease_causeVirus ReplicationImmunology and AllergyTRANSCRIPTIONCells CulturedCaspase 7Caspase 311 Medical And Health SciencesMiddle AgedMedicine Research & ExperimentalCaspasesRNA ViralFemalemedicine.symptomRhinovirusLife Sciences & BiomedicineEXPRESSIONAdultVIRUSESImmunologyInflammationBronchiBiologyAntiviral AgentsVirusArticleImmune systemINFLAMMATIONImmunitymedicineKINASELOWER AIRWAYSHumansInnate immune systemScience & TechnologyPicornaviridae InfectionsRECEPTOREpithelial CellsInterferon-betaAsthmaImmunity InnateEXACERBATIONSViral replicationGene Expression RegulationApoptosisImmunology
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Pneumocyte Apoptosis Induction during Cardiopulmonary Bypass: Effective Prevention by Radical Scavenging UsingN-Acetylcysteine

2007

Cardiopulmonary bypass (CPB) and cardioplegic arrest are associated with pulmonary dysfunction. We sought to investigate whether pulmonary ischemia/reperfusion during standard CPB and cardioplegic arrest is associated with reactive oxygen species (ROS)-mediated pulmonary tissue injury and pneumocyte apoptosis induction, and whether ROS scavenging using N-acetylcysteine (NAC) attenuates these alterations. Twelve pigs (41 +/- 8 kg) were randomized to receive either NAC (100 mg/kg prior to CPB; n = 7) or placebo (n = 5) and subjected to CPB and 60 min of cold (4 degrees C) crystalloid cardioplegic arrest. We collected lung biopsies prior to CPB, at 60 min CPB, as well as at 30, 60, and 120 min…

MaleSwineApoptosismedicine.disease_causePlacebolaw.inventionAcetylcysteinechemistry.chemical_compoundlawCardiopulmonary bypassAnimalsMedicineLungchemistry.chemical_classificationReactive oxygen speciesCardiopulmonary BypassLungCaspase 3business.industryNitrotyrosineFree Radical ScavengersAcetylcysteinesurgical procedures operativemedicine.anatomical_structurechemistryApoptosisAnesthesiaTyrosineFemaleSurgeryReactive Oxygen SpeciesbusinessOxidative stresscirculatory and respiratory physiologymedicine.drugJournal of Investigative Surgery
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Increase in Bcl-2 phosphorylation and reduced levels of BH3-only Bcl-2 family proteins in kainic acid-mediated neuronal death in the rat brain.

2003

Kainic acid induces excitotoxicity and nerve cell degeneration in vulnerable regions of rat brain, most markedly in hippocampus and amygdala. Part of the cell death following kainic acid is apoptotic as shown by caspase 3 activation and chromatin condensation. Here we have studied the regulation of pro- and anti-apoptotic proteins belonging to the Bcl-2 family in rat hippocampus and amygdala by kainic acid in relationship to ensuing neuronal death. The pro-apoptotic protein Bax was up-regulated in hippocampus 6 h after kainic acid administration. The increase in Bax was followed by the appearance of TdT-mediated dUTP nick end labelling-positive cells which were prominent at 24 h. Immunohist…

MaleTime FactorsExcitotoxicityCell Countmedicine.disease_causeSettore BIO/09 - Fisiologiachemistry.chemical_compoundPrecipitin TestExcitatory Amino Acid AgonistsSerinePhosphorylationCells CulturedNuclear Proteinbcl-2-Associated X ProteinNeuronsProto-Oncogene ProteinKainic AcidbiologyCell DeathImmunochemistryGeneral NeuroscienceBrainNuclear ProteinsImmunohistochemistryProto-Oncogene Proteins c-bcl-2Programmed cell deathKainic acidTime FactorNeuronal deathExcitatory Amino Acid AgonistBlotting WesternCaspase 3HippocampuBcl-2-associated X proteinProto-Oncogene ProteinsGlial Fibrillary Acidic ProteinmedicineIn Situ Nick-End LabelingAnimalsRats WistarProtein kinase AStaining and LabelingAnimalBcl-2 familyNeuronButylated HydroxytolueneEmbryo MammalianMolecular biologyPrecipitin Testsnervous system diseasesRatsnervous systemchemistrybiology.proteinRatNeuNBcl-2 proteinThe European journal of neuroscience
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Effects of small interfering RNAs targeting fascin on human esophageal squamous cell carcinoma cell lines

2010

Abstract Background Fascin induces membrane protrusions and cell motility. Fascin overexpression was associated with poor prognosis, and its downregulation reduces cell motility and invasiveness in esophageal squamous cell carcinoma (ESCC). Using a stable knockdown cell line, we revealed the effect of fascin on cell growth, cell adhesion and tumor formation. Methods We examined whether fascin is a potential target in ESCC using in vitro and in vivo studies utilizing a specific siRNA. We established a stable transfectant with downregulated fascin from KYSE170 cell line. Results The fascin downregulated cell lines showed a slower growth pattern by 40.3% (p In vivo, the tumor size was signific…

MaleTime FactorsHistologyEsophageal NeoplasmsMice NudeApoptosismacromolecular substancesCysteine Proteinase InhibitorsBiologyTransfectionAmino Acid Chloromethyl KetonesPathology and Forensic MedicineExtracellular matrixMiceDownregulation and upregulationCell Line TumorCell Adhesionlcsh:PathologyAnimalsHumansRNA Small InterferingCell adhesionCell ProliferationFascinMice Inbred BALB CCell growthResearchMicrofilament ProteinsGeneral MedicineTransfectionCaspase InhibitorsXenograft Model Antitumor AssaysTumor BurdenCell biologyCell cultureApoptosisCaspasesCarcinoma Squamous Cellbiology.proteinRNA InterferenceCollagenCarrier Proteinslcsh:RB1-214Diagnostic Pathology
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TLR7 and TLR8 ligands and antiphospholipid antibodies show synergistic effects on the induction of IL-1beta and caspase-1 in monocytes and dendritic …

2009

TLRs represent the first line of defense against invading pathogens in the innate immune system. Certain cytokines are important mediators and essentially necessary to assure an appropriately regulated immune response. Recent data gave initial evidence that IL-1beta is one of the most relevant members of these regulating cytokines. We investigated the induction of IL-1beta production in monocytes and pDCs stimulated with ligands for TLR7 and TLR8 and with antiphospholipid antibodies (aPL). Using human monocytes and pDCs for stimulation with specific TLR7 and TLR8 ligands such as resiquimod (R848) and single stranded RNA (RNA42) as well as with a human monoclonal aPL HL5B resulted in a speci…

Malemedicine.drug_classImmunologyInterleukin-1betaCaspase 1Enzyme-Linked Immunosorbent AssayCell SeparationBiologyRegulatory Sequences Nucleic AcidMonoclonal antibodyLigandsMonocytesProinflammatory cytokinechemistry.chemical_compoundImmune systemmedicineImmunology and AllergyHumansInnate immune systemCaspase 1ImidazolesHematologyTLR7Dendritic CellsTLR8Oligonucleotides AntisenseAntiphospholipid SyndromeFlow CytometrychemistryToll-Like Receptor 7Toll-Like Receptor 8Enzyme InductionImmunologyAntibodies AntiphospholipidRNAFemaleResiquimodImmunobiology
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BCL-2 UPREGULATION AFTER 3-NITROPROPIONIC ACID PRECONDITIONING IN WARM RAT LIVER ISCHEMIA

2008

We aimed to determine whether 3-nitropropionic acid (3-NPA) preconditioning protects rat livers against warm ischemia/reperfusion injury. We hypothesized that 3-NPA mediates its protective effects by Bcl-2 upregulation. Brown-Norway rats (200 g) were injected with 3-NPA (10 mg/kg intraperitoneally) 24 h before 90 min of selective warm in situ ischemia. In additional experiments, 30-day survival was studied after 90 min of warm liver ischemia and resection of nonischemic liver tissue. We demonstrate increased mRNA and protein levels of Bcl-2 by real-time polymerase chain reaction, immunohistochemistry, and Western blot analysis in 3-NPA-pretreated rats. All treated animals survived, whereas …

Malemedicine.medical_specialtyBlotting WesternIschemiaCritical Care and Intensive Care MedicineLipid peroxidationchemistry.chemical_compoundstomatognathic systemWestern blotDownregulation and upregulationInternal medicinemedicineAnimalsWarm IschemiaIschemic PreconditioningCaspasechemistry.chemical_classificationReactive oxygen speciesmedicine.diagnostic_testbiologyCaspase 3Reverse Transcriptase Polymerase Chain ReactionNitro Compoundsmedicine.diseaseImmunohistochemistryCaspase 9RatsEndocrinologyLiverProto-Oncogene Proteins c-bcl-2chemistryApoptosisReperfusion InjuryEmergency Medicinebiology.proteinPropionatesReperfusion injuryShock
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Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhib…

2006

Benfotiamine, a vitamin B1 analogue, reportedly prevents diabetic microangiopathy. The aim of this study was to evaluate whether benfotiamine is of benefit in reparative neovascularisation using a type I diabetes model of hindlimb ischaemia. We also investigated the involvement of protein kinase B (PKB)/Akt in the therapeutic effects of benfotiamine. Streptozotocin-induced diabetic mice, given oral benfotiamine or vehicle, were subjected to unilateral limb ischaemia. Reparative neovascularisation was analysed by histology. The expression of Nos3 and Casp3 was evaluated by real-time PCR, and the activation state of PKB/Akt was assessed by western blot analysis and immunohistochemistry. The f…

Malemedicine.medical_specialtyProgrammed cell deathAngiogenesisEndocrinology Diabetes and MetabolismBlotting WesternNeovascularization PhysiologicApoptosisMice Inbred StrainsBiologyDiabetes Mellitus ExperimentalNeovascularizationMiceRandom AllocationIschemiaInternal medicineInternal MedicinemedicineAnimalsThiamineMuscle SkeletalProtein kinase BCell ProliferationCaspase 3Stem Cellsprotein kinase PKB/AktBody WeightHemodynamicsEndothelial CellsCaspase InhibitorsImmunohistochemistryEndothelial stem cellEnzyme ActivationOxidative StressEndocrinologyBenfotiamineApoptosisCaspasesDietary SupplementsTransketolase activitymedicine.symptomProto-Oncogene Proteins c-aktDiabetic Angiopathiesmedicine.drugDiabetologia
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Monocytes from patients with rheumatoid arthritis and type 2 diabetes mellitus display an increased production of interleukin (IL)-1β via the nucleot…

2015

Summary A better understanding about the mechanisms involved in the pathogenesis of type 2 diabetes mellitus (T2D) showed that inflammatory cytokines such as tumour necrosis factor (TNF) and interleukin (IL)-1β play a pivotal role, mirroring data largely reported in rheumatoid arthritis (RA). IL-1β is produced mainly by monocytes (MO), and hyperglycaemia may be able to modulate, in the cytoplasm of these cells, the assembly of a nucleotide-binding domain and leucine-rich repeat containing family pyrin (NLRP3)-inflammosome, a cytosolic multi-protein platform where the inactive pro-IL-1β is cleaved into active form, via caspase-1 activity. In this paper, we evaluated the production of IL-1 β …

Maletype 2 diabetes mellituInflammasomesMessengerIL-1β; NLRP3-inflammasome; rheumatoid arthritis; type 2 diabetes mellitus; Adult; Arthritis Rheumatoid; Carrier Proteins; Caspase 1; Cells Cultured; Diabetes Mellitus Type 2; Enzyme Activation; Female; Glucose; Humans; Hyperglycemia; Inflammasomes; Inflammation; Interleukin-1beta; Leukocytes Mononuclear; Male; Middle Aged; RNA Messenger; Tumor Necrosis Factor-alphaInterleukin-1betaArthritisPyrin domainInflammasomeArthritis RheumatoidRheumatoidImmunology and AllergyCells CulturedCulturedCaspase 1InterleukinDiabetes MellituMiddle AgedIL-1βTumor necrosis factor alphaNLRP3-inflammasomeFemalemedicine.symptomType 2ArthritiHumanAdultmedicine.medical_specialtyMononuclearImmunologyCaspase 1InflammationProinflammatory cytokineInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansRNA MessengerInflammationbusiness.industryTumor Necrosis Factor-alphaType 2 Diabetes MellitusOriginal Articlesrheumatoid arthritiLeukocytemedicine.diseaseEnzyme ActivationEndocrinologyGlucoseDiabetes Mellitus Type 2HyperglycemiaImmunologyLeukocytes MononuclearRNACellbusinessCarrier ProteinsCarrier Protein
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Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine

2006

Methylating drugs such as temozolomide (TMZ) are widely used in the treatment of brain tumours (malignant gliomas). The mechanism of TMZ-induced glioma cell death is unknown. Here, we show that malignant glioma cells undergo apoptosis following treatment with the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and TMZ. Cell death determined by colony formation and apoptosis following methylation is greatly stimulated by p53. Transfection experiments with O(6)-methylguanine-DNA methyltransferase (MGMT) and depletion of MGMT by O(6)-benzylguanine showed that, in gliomas, the apoptotic signal originates from O(6)-methylguanine (O(6)MeG) and that repair of O(6)MeG by MGMT prevent…

MethylnitronitrosoguanidineCancer ResearchProgrammed cell deathFas Ligand ProteinGuanineDNA repairFas-Associated Death Domain ProteinBlotting WesternApoptosisBiologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseGliomaTemozolomideTumor Cells CulturedGeneticsmedicineHumansDNA Breaks Double-StrandedRNA Small InterferingAntineoplastic Agents AlkylatingneoplasmsMolecular BiologyTumor Stem Cell AssayCell ProliferationTemozolomideBrain NeoplasmsCell CycleGliomaCell cycleFlow CytometryFas receptormedicine.diseaseDacarbazineProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesCancer researchTumor Suppressor Protein p53CarcinogenesisDNA Damagemedicine.drugOncogene
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Correlation of renal tubular epithelial cell-derived interleukin-18 up-regulation with disease activity in MRL-Faslpr mice with autoimmune lupus neph…

2002

Objective MRL-Faslpr mice spontaneously develop an autoimmune disease that mimics systemic lupus erythematosus in humans. Infiltrating T cells expressing interferon-γ (IFNγ) are responsible for the autoimmune kidney destruction in MRL-Faslpr mice, and interleukin-18 (IL-18) released by mononuclear phagocytes stimulates T cells to produce the IFNγ. Since MRL-Faslpr T cells are characterized by an overexpression of the IL-18 receptor accessory chain, we sought to determine the impact of IL-18 on the progression of lupus nephritis in MRL-Faslpr mice. Methods IL-18 expression in sera and kidney tissues from MRL-Faslpr mice was determined by enzyme-linked immunosorbent assay (ELISA), reverse tra…

Mice Inbred MRL lprmedicine.medical_treatmentImmunologyBlotting WesternLupus nephritisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeAutoimmunityAutoimmune DiseasesMiceRheumatologyimmune system diseasesInterferonmedicineImmunology and AllergyMacrophageAnimalsPharmacology (medical)Interferon gammaskin and connective tissue diseasesLupus erythematosusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-18Epithelial Cellsmedicine.diseaseMolecular biologyImmunohistochemistryLupus NephritisUp-RegulationCytokineKidney TubulesImmunologymedicine.drugArthritis and rheumatism
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