Search results for "Transcription"

showing 10 items of 2278 documents

In vivo GSH depletion induces c-myc expression by modulation of chromatin protein complexes.

2009

Abstract We hypothesize that glutathione (GSH) fluctuations could have a prominent role in the modulation of c-myc expression through a mechanism affecting chromatin remodeling complexes. This could lead to an open chromatin structure accessible to transcription factors. We studied the in vivo effect of GSH depletion on these complexes bound to the c-myc promoter in the liver of l-buthionine-(S,R)-sulfoximine (BSO)-treated rats. Using chromatin immunoprecipitation we found that 3 h after BSO treatment the repressing complexes Id2 and Sin3A (part of a histone–deacetylase complex) were released from the c-myc promoter. STAT3 was phosphorylated and associated with its coactivator p300 with int…

MaleSTAT3 Transcription FactorTranscriptional ActivationTime FactorsBiologyBiochemistryChromatin remodelingHistone DeacetylasesProto-Oncogene Proteins c-mycHistone H3Physiology (medical)Gene expressionCoactivatorTranscriptional regulationAnimalsp300-CBP Transcription FactorsPhosphorylationRats WistarTranscription factorButhionine SulfoximineInhibitor of Differentiation Protein 2AcetylationChromatin Assembly and DisassemblyMolecular biologyGlutathioneChromatinRatsRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexGene Expression RegulationLiverChromatin immunoprecipitationProtein BindingFree radical biologymedicine
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Anti-inflammatory and joint protective effects of extra-virgin olive-oil polyphenol extract in experimental arthritis

2014

The consumption of extra virgin olive oil (EVOO) in Mediterranean countries has shown beneficial effects. A wide range of evidence indicates that phenolic compounds present in EVOO are endowed with anti-inflammatory properties. In this work, we evaluated the effects of EVOO-polyphenol extract (PE) in a model of rheumatoid arthritis, the collagen-induced arthritis model in mice. On day 0, DBA-1/J mice were immunized with bovine type II collagen. On day 21, mice received a booster injection. PE (100 and 200 mg/kg) was orally administered once a day from days 29 to 41 to arthritic mice. We have demonstrated that PE decreases joint edema, cell migration, cartilage degradation and bone erosion. …

MaleSTAT3 Transcription Factormedicine.drug_classEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryAnti-Inflammatory AgentsType II collagenAdministration OralDown-RegulationArthritisPharmacologyp38 Mitogen-Activated Protein KinasesBiochemistryDinoprostoneAnti-inflammatoryProinflammatory cytokineMiceEdemamedicineAnimalsPlant OilsPhosphorylationProstaglandin E2Olive OilMolecular BiologyProstaglandin-E SynthasesActivating Transcription Factor 3Nutrition and DieteticsChemistryJNK Mitogen-Activated Protein KinasesNF-kappa BPolyphenolsmedicine.diseaseArthritis ExperimentalIntramolecular OxidoreductasesCyclooxygenase 2Mice Inbred DBARheumatoid arthritisImmunologyCytokinesmedicine.symptomSignal TransductionProstaglandin Emedicine.drugThe Journal of Nutritional Biochemistry
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The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism.

2008

Macrophages play key roles in obesity-associated pathophysiology, including inflammation, atherosclerosis, and cancer, and processes that affect the survival-death balance of macrophages may have an important impact on obesity-related diseases. Adipocytes and other cells secrete a protein called extracellular nicotinamide phosphoribosyltransferase (eNampt; also known as pre-B cell colony enhancing factor or visfatin), and plasma levels of eNampt increase in obesity. Herein we tested the hypothesis that eNampt could promote cell survival in macrophages subjected to endoplasmic reticulum (ER) stress, a process associated with obesity and obesity-associated diseases. We show that eNampt potent…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCell SurvivalNicotinamide phosphoribosyltransferaseApoptosisBiologyEndoplasmic ReticulumBiochemistryStat3 Signaling Pathwaychemistry.chemical_compoundParacrine signallingMicePiperidinesInternal medicinemedicineAnimalsSecretionAutocrine signallingSTAT3Nicotinamide PhosphoribosyltransferaseMolecular BiologyNicotinamide MononucleotideNicotinamide mononucleotideAcrylamidesInterleukin-6MacrophagesMechanisms of Signal TransductionCell BiologyCell biologyMice Inbred C57BLEndocrinologychemistryGene Expression Regulationbiology.proteinCytokinesSignal transductionSignal TransductionThe Journal of biological chemistry
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

2011

BackgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.Methods and resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between th…

MaleSTRESSPulmonologyChronic Obstructive Pulmonary DiseasesNeutrophilsBiopsyGene ExpressionCD8-Positive T-Lymphocytesmedicine.disease_causeBiochemistryEpitheliumPulmonary function testingPathogenesisACTIVATIONPulmonary Disease Chronic ObstructiveMolecular Cell BiologyLungCOPDMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCOPD Hsp60QRCOPD heat shock proteins inflammationMiddle AgedImmunohistochemistrymedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMedicineFemalemedicine.symptomInflammation MediatorsSPINAL-CORDResearch ArticleEXPRESSIONanimal structuresCOPD; heat shock proteins; inflammationScienceImmunologyMolecular Sequence DataInflammationBronchichemical and pharmacologic phenomenaHEAT-SHOCK-PROTEIN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ACUTE LUNG INJURY SPINAL-CORD CELL-DEATH KAPPA-B HEAT-SHOCK-PROTEIN-60 STRESS EXPRESSION ACTIVATIONKAPPA-BBiologyHEAT-SHOCK-PROTEINMicrobiologycomplex mixturesCell LineACUTE LUNG INJURYMolecular GeneticsIn vivoStress PhysiologicalHeat shock proteinmedicineGeneticsHumansCOPDRNA MessengerBiologyAgedLungMucous MembraneBase SequenceSettore BIO/16 - Anatomia UmanaMacrophagesfungiImmunityTranscription Factor RelAProteinsComputational BiologyChaperonin 60medicine.diseaseChaperone Proteinsrespiratory tract diseasesGene Expression RegulationCELL-DEATHHEAT-SHOCK-PROTEIN-60inflammationImmunologyheat shock proteinsClinical ImmunologyOxidative stressBiomarkers
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Interleukin (IL)-22 receptor 1 is over-expressed in primary Sjogren's syndrome and Sjögren-associated non-Hodgkin lymphomas and is regulated by IL-18.

2015

Summary The aim of this study was to elucidate more clearly the role of interleukin (IL)-18 in modulating the IL-22 pathway in primary Sjögren's syndrome (pSS) patients and in pSS-associated lymphomas. Minor salivary glands (MSGs) from patients with pSS and non-specific chronic sialoadenitis (nSCS), parotid glands biopsies from non-Hodgkin lymphomas (NHL) developed in pSS patients, were evaluated for IL-18, IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and signal transducer and activator of transcription-3 (STAT-3) expression. MSGs IL-22R1-expressing cells were characterized by confocal microscopy and flow cytometry in pSS, nSCS and healthy controls. The effect of recom…

MaleSalivary Glandslaw.inventionInterleukin 22lawIL-22Immunology and AllergyMyeloid CellsIL-22R1Receptormedicine.diagnostic_testnon-Hodgkin lymphomaLymphoma Non-HodgkinInterleukin-17TranslationalInterleukin-18Lacrimal ApparatusInterleukinMiddle AgedHaematopoiesisSjogren's SyndromeIL-22BPRecombinant DNASjögren's syndromeInterleukin 18FemaleIL-18Signal TransductionAdultSTAT3 Transcription FactorImmunologyPrimary Cell CultureBiologyPeripheral blood mononuclear cellIL-18; IL-22; IL-22BP; IL-22R1; Sjögren's syndrome; non-Hodgkin lymphomaSialadenitisFlow cytometrystomatognathic systemmedicineHumansAgedInterleukinsMacrophagesReceptors InterleukinSettore MED/16 - Reumatologiastomatognathic diseasesGene Expression RegulationImmunologyLeukocytes MononuclearClinical and experimental immunology
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Cholinergic Control of Synchronized Seminal Emissions in Drosophila

2004

0960-9822 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; In many animal species, copulation involves the coordinated release of both sperm and seminal fluid, including substances that change female fertility and postmating behavior. In Drosophila melanogaster, these substances increase female fertility and prevent mating with a second male. By using a PGal4 strain, we targeted together with other cells a dozen cholinergic neurons found only in the male abdominal ganglion (Abg-MAch). Genetic feminization apparently deleted these neurons in males and significantly increased their copulation duration, blocked their fertility in 60% of cases, and only weakly repress…

MaleSemen/*metabolismSexual Behavior Animal0302 clinical medicineHuman fertilizationDrosophila ProteinsMatingmedia_commonGenetics0303 health sciencesAgricultural and Biological Sciences(all)ReproductionNuclear ProteinsImmunohistochemistryCell biologyDrosophila melanogasterCholinergic FibersFemaleDrosophila melanogasterGeneral Agricultural and Biological SciencesDrosophila melanogaster/genetics/*metabolism/physiologymedia_common.quotation_subjectFeminization (biology)Sexual BehaviorInvertebrate/physiologyTranscription Factors/geneticsFertilityBiologyCrossesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesGeneticSemenCholinergic Fibers/*metabolism/physiologyAnimalsFeminizationCholinergic neuronReproduction/physiologyCrosses Genetic030304 developmental biologyBiochemistry Genetics and Molecular Biology(all)Animalbiology.organism_classificationSpermGanglia InvertebrateNuclear Proteins/geneticsCholinergicGangliaFeminization/*genetics030217 neurology & neurosurgeryTranscription FactorsCurrent Biology
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p-Chlorophenylalanine treatment depresses the number of synaptic ribbon profiles in the rat pineal gland, but does not abolish their day-night rhythm

1995

It is largely unknown as to how the day/night rhythm of pineal synaptic ribbon number is regulated. Transcriptional events related to the nocturnal formation of new synaptic ribbons occur early in the morning, when pineal serotonin levels begin to increase. The present study was carried out in order to elucidate as to how altered serotonin levels affect the day/night changes in the number of synaptic ribbon profiles. To this end, male Sprague-Dawley rats received a single dose of p-chlorophenylalanine (pCPA, 300 mg/kg body weight, 72 hours before sacrifice), which depresses tryptophan hydroxylase activity and hence pineal serotonin levels. Control animals received saline injections. Experim…

MaleSerotoninendocrine systemmedicine.medical_specialtyTranscription GeneticArylamine N-AcetyltransferaseTryptophan HydroxylaseBiologyPineal GlandRats Sprague-DawleyMelatoninPineal glandReference ValuesInternal medicinemedicineFenclonineAnimalsCircadian rhythmSynaptic ribbonP chlorophenylalanineFenclonineGeneral MedicineTryptophan hydroxylaseCircadian RhythmRatsMicroscopy Electronmedicine.anatomical_structureEndocrinologynervous systemSynapsessense organsSerotoninAnatomyhormones hormone substitutes and hormone antagonistsDevelopmental Biologymedicine.drugAnnals of Anatomy - Anatomischer Anzeiger
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Neurotransmitter receptor density changes in Pitx3ak mice – A model relevant to Parkinson’s disease

2014

Abstract Parkinson’s disease (PD) is the second most common neurodegenerative disorder, characterized by alterations of nigrostriatal dopaminergic neurotransmission. Compared to the wealth of data on the impairment of the dopamine system, relatively limited evidence is available concerning the role of major non-dopaminergic neurotransmitter systems in PD. Therefore, we comprehensively investigated the density and distribution of neurotransmitter receptors for glutamate, GABA, acetylcholine, adrenaline, serotonin, dopamine and adenosine in brains of homozygous aphakia mice being characterized by mutations affecting the Pitx3 gene. This genetic model exhibits crucial hallmarks of PD on the ne…

MaleSerotoninmedicine.medical_specialtyAdenosineEpinephrineDopamineMice TransgenicD1-like receptorKainate receptorBiologySerotonergicParkinsonian DisordersNeurotransmitter receptorInternal medicinemedicineAnimalsReceptorgamma-Aminobutyric Acid5-HT receptorHomeodomain ProteinsGeneral NeuroscienceHomozygoteGlutamate receptorBrainAcetylcholineReceptors NeurotransmitterMice Inbred C57BLEndocrinology5-HT6 receptorNeuroscienceTranscription FactorsNeuroscience
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