Search results for "kappa"

showing 10 items of 419 documents

In Vitro Phenotypic, Genomic and Proteomic Characterization of a Cytokine-Resistant Murine β-TC3 Cell Line

2012

Type 1 diabetes mellitus (T1DM) is caused by the selective destruction of insulin-producing β-cells. This process is mediated by cells of the immune system through release of nitric oxide, free radicals and pro-inflammatory cytokines, which induce a complex network of intracellular signalling cascades, eventually affecting the expression of genes involved in β-cell survival. The aim of our study was to investigate possible mechanisms of resistance to cytokine-induced β-cell death. To this purpose, we created a cytokine-resistant β-cell line (β-TC3R) by chronically treating the β-TC3 murine insulinoma cell line with IL-1β + IFN-γ. β-TC3R cells exhibited higher proliferation rate and resistan…

ProteomicsAnatomy and Physiologymedicine.medical_treatmentCell Culture Techniqueslcsh:MedicineApoptosisSettore MED/13 - EndocrinologiaMiceEndocrinologyImmune PhysiologyInsulin-Secreting CellsMolecular Cell BiologySOCS3lcsh:ScienceMultidisciplinaryCell DeathDiabetes mellitus cytokines. apoptosis SUMO4 NF-kBCell CycleNF-kappa BGenomicsCell cycleImmunohistochemistryCell biologyPhenotypeCytokineMedicineCytokinesResearch ArticleProgrammed cell deathCell SurvivalImmunologyDown-RegulationBiologyAutoimmune DiseasesCell LineDownregulation and upregulationmedicineAnimalsGene SilencingBiologyCell ProliferationDiabetic EndocrinologyEndocrine PhysiologyCell growthlcsh:RCell cultureApoptosisImmune SystemClinical ImmunologyInsulinomalcsh:QPLoS ONE
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Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.

2012

Reactive oxygen species (ROS) are involved in the pathogenesis of many inflammatory diseases such as chronic obstructive pulmonary disease (COPD). They can alter the expression of genes involved in cellular damage by activating transcription factors, including the NF-κB and the activator protein 1 (AP-1). Phosphodiesterase type 4 (PDE4) inhibitors have anti-inflammatory and antioxidant effects, as described in in vivo and in vitro COPD models. This study analysed the effects of piclamilast, a selective PDE4 inhibitor, on modulating the global gene expression profile in A549 cells exposed to H(2)O(2).Changes in gene expression were analysed using high-density Affymetrix microarrays and valid…

Proto-Oncogene Proteins c-junPyridinesActivating transcription factorApoptosisBiologymedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundPulmonary Disease Chronic ObstructiveIn vivoAnnexinCell Line TumorGene expressionmedicineHumansRNA MessengerPhosphorylationCell ProliferationOligonucleotide Array Sequence AnalysisA549 cellGene Expression ProfilingNF-kappa BGeneral MedicineCell Cycle CheckpointsHydrogen PeroxideMolecular biologyTranscription Factor AP-1chemistryGene Expression RegulationAlveolar Epithelial CellsBenzamidesPhosphodiesterase 4 InhibitorsSignal transductionReactive Oxygen SpeciesPiclamilastOxidative stressSignal TransductionFree radical research
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Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mR…

1999

Alveolar macrophages (AM) play a decisive role in the immunologic defense system of the lung and in inflammatory pulmonary pathomechanisms. AM and blood monocytes (BM) were exposed to chrysotile B, soot FR 101, and Printex 90 (P 90). We evaluated the reactive oxygen intermediate (ROI) release of AM and BM after particle exposure. ROI release was measured by chemiluminescence. Thirty-minute exposure caused a significant (up to 2.5-fold) increase in ROI release of AM (100 micrograms/10(6) cells) compared with control experiments (p0.01). Identical exposure conditions for BM resulted in a similar reaction pattern (maximum 2.2-fold increase in ROI release; p0.05). After a 90-min particle exposu…

Pulmonary and Respiratory MedicineAdultMaleP50Asbestos Serpentinemedicine.medical_treatmentMonocytesProinflammatory cytokineSuperoxide dismutaseGene expressionMacrophages AlveolarmedicineHumansRNA MessengerReceptorCells CulturedAgedLungbiologyDose-Response Relationship DrugChemistryReverse Transcriptase Polymerase Chain ReactionNF-kappa BMiddle AgedNFKB1Molecular biologyCarbonCytokinemedicine.anatomical_structureGene Expression RegulationImmunologyLuminescent Measurementsbiology.proteinFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidLung
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Endurance training damages small airway epithelium in mice.

2007

RATIONALE: In athletes, airway inflammatory cells were found to be increased in induced sputum or bronchial biopsies. Most data were obtained after exposure to cold and dry air at rest or during exercise. Whether training affects epithelial and inflammatory cells in small airways is unknown. OBJECTIVES: To test whether endurance training under standard environmental conditions causes epithelial damage and inflammation in the small airways of mice. METHODS AND MEASUREMENTS: Formalin-fixed, paraffin-embedded lung sections were obtained in sedentary (n = 14) and endurance-trained (n = 16) Swiss mice at baseline and after 15, 30, and 45 days of training. The following variables were assessed (m…

Pulmonary and Respiratory MedicineMalePathologymedicine.medical_specialtyInflammationApoptosisCritical Care and Intensive Care MedicineSettore BIO/09 - FisiologiaEpitheliumEpithelial DamageLeukocyte CountMiceEndurance trainingIntensive carePhysical Conditioning AnimalProliferating Cell Nuclear AntigenmedicineLeukocytesAnimalsBronchitisCell ProliferationBasement membraneLungAerobic exercise bronchial responsivenes methacholine deep inspiration leukotrienesbusiness.industryNF-kappa Brespiratory systemImmunohistochemistryEpitheliumrespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureRespiratory epitheliummedicine.symptombusinessAmerican journal of respiratory and critical care medicine
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Pulsed Electric Fields Alter Expression of NF-κB Promoter-Controlled Gene

2021

The possibility to artificially adjust and fine‐tune gene expression is one of the key mile-stones in bioengineering, synthetic biology, and advanced medicine. Since the effects of proteins or other transgene products depend on the dosage, controlled gene expression is required for any ap-plications, where even slight fluctuations of the transgene product impact its function or other critical cell parameters. In this context, physical techniques demonstrate optimistic perspectives, and pulsed electric field technology is a potential candidate for a noninvasive, biophysical gene regulator, exploiting an easily adjustable pulse generating device. We exposed mammalian cells, transfected with a…

QH301-705.5Microsecond pulsed electric fieldSecreted alkaline phosphataseReporter assaymicrosecond pulsed electric field; inducible gene transcription control; reporter assay; secreted alkaline phosphatase; mammalian cells; cell line; NF-κBTransfectionCatalysisArticleNF-κBInorganic Chemistry03 medical and health sciencesMice0302 clinical medicineElectricityinducible gene transcription controlAnimalsHumansmammalian cellsBiology (General)Physical and Theoretical ChemistryInducible gene transcription controlQD1-999Molecular BiologySpectroscopy030304 developmental biology0303 health sciencessecreted alkaline phosphataseOrganic ChemistryNF‐κBreporter assayNF-kappa BMammalian cells:NATURAL SCIENCES::Physics [Research Subject Categories]General Medicinecell linemicrosecond pulsed electric field3. Good healthComputer Science ApplicationsChemistryGene Expression Regulation030220 oncology & carcinogenesismicrosecond pulsed electric field ; inducible gene transcription control ; reporter assay ; secreted alkaline phosphatase ; mammalian cells ; cell line ; NF-κBCell lineInternational Journal of Molecular Sciences
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Molecular Mechanisms Leading from Periodontal Disease to Cancer

2022

Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axi…

QH301-705.5periodontal diseaseReviewOdontologi<i>Porphyromonas gingivalis</i>Catalysisimmune responseInorganic ChemistrycancerHumansBiology (General)Physical and Theoretical ChemistryImmune responseQD1-999Molecular BiologySpectroscopyPeriodontal DiseasesCancerCancer och onkologiRANK ligandFusobacterium nucleatumReceptor Activator of Nuclear Factor-kappa B<i>Fusobacterium nucleatum</i>Organic ChemistryGeneral MedicineComputer Science ApplicationsChemistrytumorigenesisGene Expression RegulationDentistryCancer and OncologyTumorigenesisDisease ProgressionCytokinesMouth NeoplasmsPeriodontal diseasePorphyromonas gingivalisSignal Transduction
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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Indirect evaluation of pit and fissure sealants: a 3D-based method validation

2019

Background The aim of the present study was to compare indirect methods to assess the clinical performance of pit and fissure sealants and validate the use of 3D scanners. Material and Methods Sample consisted of 58 plaster models of upper and lower first permanent molars, sealed with resin sealants, as well as photographs obtained during the 18-month follow-up. Pre-established criteria were applied to categorize the sealant presence/absence and marginal integrity. Two calibrated examiners performed the evaluations, independently, using Scanning Electron Microscopy (SEM; gold-standard), Photography, 3D (CEREC In Lab) and Stereomicroscope analysis. Results The intra-examiner Spearman correla…

Receiver operating characteristicFissurebusiness.industrySealantResearchDentistryGold standard (test):CIENCIAS MÉDICAS [UNESCO]Spearman's rank correlation coefficientCommunity and Preventive DentistryFOTOGRAFIA EM ODONTOLOGIAmedicine.anatomical_structureCERECStereo microscopeUNESCO::CIENCIAS MÉDICASmedicinebusinessGeneral DentistryKappaMathematics
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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