Search results for "Transcription"

showing 10 items of 2278 documents

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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Theileria parasites secrete a prolyl isomerase to maintain host leukocyte transformation

2015

Infectious agents develop intricate mechanisms to interact with host cell pathways and hijack their genetic and epigenetic machinery to change host cell phenotypic states. Among the Apicomplexa phylum of obligate intracellular parasites, which cause veterinary and human diseases, Theileria is the only genus that transforms its mammalian host cells. Theileria infection of bovine leukocytes induces proliferative and invasive phenotypes associated with activated signalling pathways, notably JNK and AP-1 (ref. 2). The transformed phenotypes are reversed by treatment with the theilericidal drug buparvaquone. We used comparative genomics to identify a homologue of the peptidyl-prolyl isomerase PI…

Proto-Oncogene Proteins c-jun[SDV]Life Sciences [q-bio]Drug ResistanceparasitesBiologyArticleCell LineHost-Parasite InteractionsmiR-155TheileriaTheileriaLeukocytesProlyl isomeraseAnimalsHumanscancerSecretionNIMA-Interacting Peptidylprolyl IsomeraseZebrafishComputingMilieux_MISCELLANEOUSPeptidylprolyl isomeraseSKP Cullin F-Box Protein LigasesMultidisciplinaryProtein StabilityGeneral CommentaryIntracellular parasiteUbiquitinationPeptidylprolyl Isomerasebiology.organism_classificationXenograft Model Antitumor AssaysMolecular biology3. Good healthCell biologyUbiquitin ligaseNIMA-Interacting Peptidylprolyl IsomeraseTranscription Factor AP-1Cell Transformation NeoplasticSchistosoma haematobiumPIN1biology.proteinMedicineCattleNaphthoquinonesSignal Transduction
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TLR4 Up-regulation and Reduced Foxp3 Expression in Mechanically Ventilated Smokers with Obstructive Chronic Bronchitis

2013

Background: Chronic bronchitis (CB) is a risk factor in chronic obstructive pulmonary disease (COPD) for accelerated lung function decline and increased mortality. The lung and systemic inflammatory and immunological profile of COPD patients with CB which acutely experience respiratory failure upon a disease exacerbation is unknown. Methods: In this study, we explored the expression of Foxp3 by western blot analysis, TLR4 by immunocytochemistry and the concentrations of IP-10 and IL-8 by ELISA in the mini-bronchoalveolar lavages (mini-BAL) and in the peripheral blood of patients with respiratory failure requiring intubation and mechanical ventilation. The recruited subjects were separated i…

Pulmonary and Respiratory MedicineMaleChronic bronchitismedicine.medical_specialtyPathologyNeutrophilsmedicine.medical_treatmentSettore MED/41 - AnestesiologiaGastroenterologyStatistics NonparametricLeukocyte CountPulmonary Disease Chronic ObstructiveAcute Lung InjuryToll-like receptors Foxp3 Chemokines Smokers Respiratory failureInternal medicineMedicineHumansRisk factorAgedMechanical ventilationAged 80 and overCOPDLungbusiness.industryInterleukin-8SmokingFOXP3Forkhead Transcription Factorsmedicine.diseaseRespiration Artificialrespiratory tract diseasesUp-RegulationBronchitis ChronicChemokine CXCL10Toll-Like Receptor 4medicine.anatomical_structureRespiratory failureBronchitisFemalebusinessBronchoalveolar Lavage Fluid
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CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death.

2006

KEYWORDS CLASSIFICATION: 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide;Antigens,CD40;Apoptosis;Bronchi;cytology;Caspases;Cell Cycle;Cell Death;Cell Line,Transformed;Cell Survival;Cell Transformation,Viral;Cytoprotection;drug effects;Epithelial Cells;Humans;Italy;mechanisms of carcinogenesis;metabolism;Oxidants;pharmacology;physiology;Research;Simian virus 40;toxicity;Transcription Factor AP-1. CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major t…

Pulmonary and Respiratory MedicineNF-BProgrammed cell deathCell SurvivalClinical Biochemistry78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideApoptosisBronchiSimian virus 40Inhibitor of apoptosisAntigens CD40CD40HumansCD40 AntigensMolecular BiologyMitosisCaspaseActivator protein–1Cell Line Transformedoxidant stressbiologyCell DeathCell growthCell CycleEpithelial CellsCell BiologyCell cycleCell Transformation ViralOxidantsapoptosiCell biologyTranscription Factor AP-1activator protein–1ApoptosisCytoprotectionCaspasesbiology.proteinNF- BApoptosis-inducing factorOxidant stress
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Chronological expression of Ciliated Bronchial Epithelium 1 during pulmonary development

2009

Ciliated Bronchial Epithelium (CBE) 1 is a novel gene, which is expressed in ciliated cells. As cilia are important during embryogenesis, the present authors characterised the murine homologue of CBE1 (Cbe1) and compared its temporal expression during murine and human lung development. Cbe1 cDNA was cloned and characterised using sequencing, standard PCR and Western blotting. Mouse and human embryonic/fetal lungs (HELs) were harvested for mRNA analysis and protein localisation in vivo and in vitro using RT-PCR and immunohistochemistry. The Cbe1 amino acid sequence was >75% identical with CBE1 and its alternative splicing and tissue distribution were highly conserved. Pulmonary expression of…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtyDNA ComplementaryTime FactorsBlotting WesternDNA Mutational AnalysisBiologyTransfectionStatistics NonparametricImmunoenzyme TechniquesMiceOpen Reading FramesCiliogenesisGene expressionmedicineAnimalsHumansAmino Acid SequenceRNA MessengerCloning MolecularLungDNA PrimersFetusMessenger RNALungReverse Transcriptase Polymerase Chain ReactionEmbryogenesisAlternative splicingNuclear ProteinsCell DifferentiationMolecular biologyEpitheliumDNA-Binding Proteinsmedicine.anatomical_structureBronchial epithelium Asthma DevelopmentTranscription FactorsEuropean Respiratory Journal
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The Autoimmune Regulator AIRE in Thymoma Biology: Autoimmunity and Beyond

2010

Thymomas are tumors of thymic epithelial cells. They associate more often than any other human tumors with various autoimmune diseases; myasthenia gravis is the commonest, occurring in 10-50% of thymoma patients, depending on the World Health Organization-defined histologic subtype. Most thymomas generate many polyclonal maturing T lymphocytes but in disorganized microenvironments Failure to induce self-tolerance may be a key factor leading to the export of potentially autoreactive CD4 progeny, thus predisposing to autoimmune diseases. Normally, the master Autoimmune Regulator promotes expression of peripheral tissue-restricted antigens such as insulin by medullary thymic epithelial cells a…

Pulmonary and Respiratory MedicineThymomaThymomamedicine.medical_treatmentAutoimmunitymedicine.disease_causeWorld healthAutoimmune DiseasesAutoimmunityAntigenAIREhemic and lymphatic diseasesAPS-1HumansMedicineMyasthenia gravisbusiness.industryInsulinThymus NeoplasmsAutoimmune regulatormedicine.diseaseMyasthenia gravisOncologyImmunologybusinessAPECEDTranscription FactorsJournal of Thoracic Oncology
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CD34+ progenitor to endothelial cell transition in post-pneumonectomy angiogenesis.

2012

In many species, pneumonectomy triggers compensatory lung growth that results in an increase not only in lung volume, but also in alveolar number. Whether the associated alveolar angiogenesis involves the contribution of blood-borne progenitor cells is unknown. To identify and characterize blood-borne progenitor cells contributing to lung growth after pneumonectomy in mice, we studied wild-type and wild-type/green fluorescence protein (GFP) parabiotic mice after left pneumonectomy. Within 21 days of pneumonectomy, a 3.2-fold increase occurred in the number of lung endothelial cells. This increase in total endothelial cells was temporally associated with a 7.3-fold increase in the number of …

Pulmonary and Respiratory MedicineTranscriptional ActivationPathologymedicine.medical_specialtyTime FactorsAngiogenesisCellular differentiationClinical BiochemistryGreen Fluorescent ProteinsCD34Neovascularization PhysiologicAntigens CD34Mice TransgenicBiologyMiceVasculogenesisCell MovementmedicineAnimalsRegenerationProgenitor cellPneumonectomyMolecular BiologyLungCell ProliferationStem CellsEndothelial CellsCell DifferentiationCell BiologyArticlesEndothelial stem cellVascular endothelial growth factor BMice Inbred C57BLGene Expression RegulationCancer researchStem cellAmerican journal of respiratory cell and molecular biology
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Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice.

2001

Mutations that influence the repair of oxidative DNA modifications are expected to increase the steady-state (background) levels of these modifications and thus create a mutator phenotype that predisposes to malignant transformation. We have analysed the steady-state levels and repair kinetics of oxidative DNA modifications in cells of homozygous ogg1(-/-) null mice, which are deficient in Ogg1 protein, a DNA repair glycosylase that removes the miscoding base 8-hydroxyguanine (8-oxoG) from the genome. Oxidative purine modifications including 8-oxoG were quantified by means of an alkaline elution assay in combination with Fpg protein, the bacterial functional analogue of Ogg1 protein. In pri…

PurineMaleCancer ResearchGuanineDNA RepairOxidative phosphorylationBiologymedicine.disease_causeMalignant transformationchemistry.chemical_compoundMiceTranscription (biology)medicineAnimalsN-Glycosyl HydrolasesMice KnockoutCell growthAge FactorsGeneral MedicineDNAFibroblastsMolecular biologyOxygenOxidative StresschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseOrgan SpecificityImmunologyHepatocytesOxidative stressDNACell DivisionDNA DamageCarcinogenesis
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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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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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