Search results for "Glucocorticoid receptor"

showing 10 items of 49 documents

MUC4 overexpression correlates corticoid resistance in chronic rhinosinusitis with nasal polyps

2015

Background: Some patients with chronic rhinosinusitis with nasal polyps (CRSwNP) are resistant to corticoids. Mucin 4 (MUC4) is a membrane anchored protein with a nuclear translocation domain which is modulated by corticoids. Because glucocorticoid receptor (GR) nuclear translocation is key to the anti-inflammatory effect of corticoids, we hypothesized that MUC4 is involved in the effectiveness of these drugs Objective: To analyze the role of MUC4 in corticoid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved Methods: 73 patients with CRSwNP took oral corticoids for 15 days. Corticoid resistance was evaluated by nasal endoscopy. The ex…

Gene knockdownmedicine.medical_specialtybusiness.industryMucinmedicine.diseaseBlotGlucocorticoid receptorEndocrinologyDownregulation and upregulationInternal medicineImmunologymedicineImmunohistochemistryNasal polypssense organsbusinessDexamethasonemedicine.drug5.1 Airway Pharmacology and Treatment
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Rapid acting antidepressant (2R,6R)-hydroxynorketamine (HNK) targets glucocorticoid receptor signaling: a longitudinal cerebrospinal fluid proteome s…

2020

AbstractDelayed onset of antidepressant action is a shortcoming in depression treatment. Ketamine and its metabolite (2R,6R)-hydroxynorketamine (HNK) have emerged as promising rapidacting antidepressants. However, their mechanism of action remains unknown. In this study, we first described the anxious and depression-prone inbred mouse strain, DBA/2J, as a animal model to assess the antidepressant-like effects of ketamine and HNK in vivo. To decode the molecular mechanisms mediating HNK’s rapid antidepressant effects, a longitudinal cerebrospinal fluid (CSF) proteome profiling of its acute and sustained effects was conducted using an unbiased, hypothesis-free mass spectrometry-based proteomi…

Glucocorticoid receptorHydroxynorketamineMechanism of actionNeurotrophic factorsProteomemedicineSignal transductionPharmacologyBiologymedicine.symptomProteomicsPI3K/AKT/mTOR pathway
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MUC1-CT mediates corticosteroid responses in COPD

2016

Background: Corticosteroid resistance is an acquired condition in chronic obstructive pulmonary disease (COPD) patients and a challenge to develop new anti-inflammatory therapies. In previous reports we showed that cytoplasmic tail of the membrain tethered mucin 1 (MUC1-CT) interacts with glucocorticoid receptor (GR) mediating corticosteroid anti-inflammatory efficacy. Objectives: To analyze the role of MUC1-CT as a key marker of corticosteroid efficacy in COPD Methods: The expression of MUC1-CT and the anti-inflammatory role of dexamethasone were evaluated in neutrophils and bronchial epithelial cells from healthy and COPD patients. Anti-inflammatory effects of dexamethasone and glucocorti…

Hormone response elementmedicine.medical_specialtyCOPDbusiness.industrymedicine.drug_classMucinColocalizationmedicine.diseasedigestive systembiological factorsdigestive system diseasesGlucocorticoid receptorEndocrinologyInternal medicineMedicineCorticosteroidskin and connective tissue diseasesbusinessneoplasmsMUC1Dexamethasonemedicine.drug5.1 Airway Pharmacology and Treatment
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A new p65 isoform that bind the glucocorticoid hormone and is expressed in inflammation liver diseases and COVID-19

2021

AbstractInflammation is a physiological process whose deregulation causes some diseases including cancer. Nuclear Factor kB (NF-kB) is a family of ubiquitous and inducible transcription factors, in which the p65/p50 heterodimer is the most abundant complex, that play critical roles mainly in inflammation. Glucocorticoid Receptor (GR) is a ligand-activated transcription factor and acts as an anti-inflammatory agent and immunosuppressant. Thus, NF-kB and GR are physiological antagonists in the inflammation process. Here we show that in mice and humans there is a spliced variant of p65, named p65 iso5, which binds the corticosteroid hormone dexamethasone amplifying the effect of the glucocorti…

MaleCOVID-19.Molecular biologyGene ExpressionDexamethasoneHepatitisMiceGlucocorticoid receptorAdrenal Cortex HormonesProtein IsoformsNF-kBMultidisciplinaryLiver DiseasesQLiver NeoplasmsRNF-kappa BMiddle AgedLiverMedicineFemalemedicine.symptomliver diseaseTranscriptionNFKB P65iso5 inflammationGlucocorticoidmedicine.drugAdultGene isoformCarcinoma HepatocellularScienceImmunologyInflammationBiologyGlucocorticoid ReceptorArticleReceptors GlucocorticoidmedicineAnimalsHumansGlucocorticoidsTranscription factorDexamethasoneInflammationSARS-CoV-2p65 isoformTranscription Factor RelAWild typeCOVID-19Mice Inbred C57BLAlternative SplicingSettore BIO/18 - GeneticaGene Expression RegulationLeukocytes MononuclearCancer researchHormone
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Effects of typical inducers on olfactory xenobiotic-metabolizing enzyme, transporter, and transcription factor expression in rats.

2010

International audience; Several xenobiotic-metabolizing enzymes (XMEs) have been identified in the olfactory mucosa (OM) of mammals. However, the molecular mechanisms underlying the regulation of these enzymes have been little explored. In particular, information on the expression of the transcriptional factors in this tissue is quite limited. The aim of the present study was to examine the impact of five typical inducers, Aroclor 1254, 3-methylcholanthrene, dexamethasone, phenobarbital, and ethoxyquin, on the activities and mRNA expression of several XMEs in the OM and in the liver of rats. We also evaluated the effects of these treatments on the mRNA expression of transcription factors an…

MaleLIVERMESH : Transcription FactorsMESH: Microsomes Liver[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionPharmaceutical ScienceMESH : CytochromesMESH: Down-RegulationMESH: Membrane Transport ProteinsMESH : Down-RegulationCytosol0302 clinical medicineGlucocorticoid receptorMESH : Membrane Transport ProteinsMESH: CytosolMESH: Reverse Transcriptase Polymerase Chain ReactionGene expressionConstitutive androstane receptorMESH: Up-RegulationMESH: AnimalsReceptorMESH : Up-RegulationMESH: Cytochromes0303 health sciencesPregnane X receptorMESH : Metabolic Detoxication Phase IbiologyReverse Transcriptase Polymerase Chain ReactionMESH : RatsMESH : CytosolINDUCTIONMESH : Reverse Transcriptase Polymerase Chain ReactionMESH: Transcription FactorsUp-Regulation3. Good healthMESH : Microsomes LiverHYDROCARBON HYDROXYLASE-ACTIVITYmedicine.anatomical_structurePHASE-IBiochemistryMESH: Metabolic Detoxication Phase IIEnzyme InductionMicrosomes LiverMESH: Metabolic Detoxication Phase IMESH: XenobioticsMESH: Enzyme InductionMESH: RatsMESH : MaleDown-RegulationMESH : XenobioticsPHENOL SULFOTRANSFERASEMESH : Rats WistarXenobiotics03 medical and health sciencesOlfactory mucosaOlfactory MucosamedicineAnimalsRats WistarMESH: Olfactory MucosaTranscription factor030304 developmental biologyPharmacologyMESH : Olfactory MucosaIDENTIFICATIONRECEPTORMESH : Enzyme InductionMembrane Transport ProteinsMESH : Metabolic Detoxication Phase IIUDP-GLUCURONOSYLTRANSFERASEMESH: Rats WistarAryl hydrocarbon receptorORGANIC ANION TRANSPORTERMolecular biologyMetabolic Detoxication Phase IIMESH: MaleRatsNASAL-MUCOSAbiology.proteinCytochromesMetabolic Detoxication Phase IMESH : Animals[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryTranscription Factors
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Inhibition of Proteasomal Glucocorticoid Receptor Degradation Restores Dexamethasone-Mediated Stabilization of the Blood–Brain Barrier After Traumati…

2013

To establish the molecular background for glucocorticoid insensitivity, that is, failure to reduce edema formation and to protect blood-brain barrier integrity after acute traumatic brain injury.Controlled animal study.University research laboratory.Male C57Bl/6N mice.Mechanical brain lesion by controlled cortical impact.Our study demonstrates that 1) proteasomal glucocorticoid receptor degradation is established in brain endothelial cells after traumatic brain injury as a form of posttranslational glucocorticoid receptor modification; 2) inhibition of the proteasomal degradation pathway with bortezomib (0.2 mg/kg) in combination with the glucocorticoid dexamethasone (10 mg/kg) by subcutane…

MaleProteasome Endopeptidase ComplexTraumatic brain injuryBlotting WesternBrain EdemaPharmacologyReal-Time Polymerase Chain ReactionCritical Care and Intensive Care MedicineBlood–brain barrierSensitivity and SpecificityDexamethasoneStatistics NonparametricBortezomibMiceRandom AllocationReceptors GlucocorticoidGlucocorticoid receptorReference ValuesmedicineAnimalsRNA MessengerReceptorDexamethasonebusiness.industryBortezomibmedicine.diseaseBoronic AcidsImmunohistochemistryMice Inbred C57BLBlotDisease Models Animalmedicine.anatomical_structureBlood-Brain BarrierBrain InjuriesPyrazinesMultivariate AnalysisBlood Gas AnalysisbusinessGlucocorticoidmedicine.drugCritical Care Medicine
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In vitro anti-inflammatory effects of AZD8999, a novel bifunctional muscarinic acetylcholine receptor antagonist /β2-adrenoceptor agonist (MABA) comp…

2019

Recent evidence indicates that AZD8999 (LAS190792), a novel muscarinic acetylcholine receptor antagonist and β2-adrenoceptor agonist (MABA) in development for chronic respiratory diseases, induces potent and sustained relaxant effects in human bronchi by adressing both muscarinic acetylcholine receptors and β2-adrenoceptor. However, the anti-inflammatory effects of the AZD8999 monotherapy or in combination with corticosteroids are unknown. This study investigates the anti-inflammatory effects of AZD8999 in monotherapy and combined with fluticasone propionate in neutrophils from healthy and chronic obstructive pulmonary disease (COPD) patients. Peripheral blood neutrophils from healthy and C…

MalePulmonologyNeutrophilsPhysiologyAnti-Inflammatory AgentsPharmacologyPathology and Laboratory MedicineBiochemistryPulmonary Disease Chronic ObstructiveWhite Blood CellsGlucocorticoid receptorAnimal CellsMuscarinic acetylcholine receptorMedicine and Health SciencesPost-Translational ModificationPhosphorylationReceptorImmune ResponseMultidisciplinaryPharmaceuticsQRDrug SynergismMiddle AgedReceptors MuscarinicHealthy VolunteersBody FluidsChemistryBloodPhysical SciencesQuinolinesMedicineDrug Therapy CombinationFemalemedicine.symptomCellular TypesAnatomymedicine.drugResearch ArticleSignal TransductionAgonistTransmembrane Receptorsmedicine.drug_classp38 mitogen-activated protein kinasesChronic Obstructive Pulmonary DiseaseImmune CellsScienceImmunologyInflammationMuscarinic AntagonistsThiophenesFluticasone propionateSigns and SymptomsDrug TherapyCyclohexanesDiagnostic MedicinemedicineHumansAdrenergic beta-2 Receptor AgonistsAgedInflammationBlood CellsDose-Response Relationship Drugbusiness.industryAntagonistChemical CompoundsBiology and Life SciencesProteinsCell BiologyAcetylcholine ReceptorsFluticasoneMuscarinic Acetylcholine ReceptorsReceptors Adrenergic beta-2PropionatesbusinessReceptor Antagonist TherapyPLoS ONE
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Glucocorticoid receptor knockdown decreases the antioxidant protection of B16 melanoma cells: an endocrine system-related mechanism that compromises …

2014

We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in …

MaleTumor PhysiologyGlutathione reductaseCancer TreatmentMelanoma ExperimentalGene Expressionlcsh:MedicineBiochemistryAntioxidantsMetastasisAnalytical Chemistrychemistry.chemical_compoundOxidative DamageMiceGlucocorticoid receptorSpectrum Analysis TechniquesCell SignalingNeoplasmsMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesNeoplasm Metastasislcsh:Sciencechemistry.chemical_classificationMultidisciplinaryCell DeathGlutathione peroxidaseEndocrine TherapyFlow CytometryGlutathioneChemistrymedicine.anatomical_structureOncologyResearch DesignSpectrophotometryPhysical SciencesCytophotometryGlucocorticoidmedicine.drugResearch ArticleSignal Transductionmedicine.medical_specialtyEndotheliumClinical Research DesignCell SurvivalGlutamate-Cysteine LigaseDown-RegulationEndocrine SystemBiologyResearch and Analysis MethodsCell LineReceptors GlucocorticoidInternal medicineCell Line TumormedicineGeneticsAnimalsHumansAnimal Models of DiseaseOncogenic Signalinglcsh:RBiology and Life SciencesEndothelial CellsGlutathioneCell BiologyMice Inbred C57BLEndocrinologyHEK293 CellschemistryCell cultureCancer cellAnimal Studieslcsh:QEndothelium VascularCytometryPLoS ONE
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17 beta-carboxamide steroids: highly effective inhibitors of the phytohaemagglutinin mediated blastogenesis of normal human peripheral lymphocytes.

1984

Several novel 17 beta-carboxamide analogues of dexamethasone were synthesized. The common precursor, 9-fluoro-16 alpha-methyl-11 beta,17-dihydroxy-3-oxo-1,4-androstadiene-17 beta-carboxylic acid, did not bind to the glucocorticoid receptors of rat liver and human spleen tumours. In addition, no inhibition of the mitogen-induced blastogenesis of cultured human peripheral lymphocytes was observed. The 17 beta-carboxamide analogues, however, bound with similar affinities to the glucocorticoid receptors of both tissues. They inhibited the mitogen-induced blastogenesis of peripheral lymphocytes, showing the same potency and same order of binding affinity as the natural glucocorticoids.

Malemedicine.medical_specialtyChemical Phenomenamedicine.drug_classClinical BiochemistryeducationCarboxamideBiologyIn Vitro TechniquesLymphocyte ActivationBinding CompetitiveDexamethasoneGlucocorticoid receptorCytosolReceptors GlucocorticoidInternal medicinemedicinePotencyAnimalsHumansPhytohemagglutininsBeta (finance)GlucocorticoidsDexamethasonePhytohaemagglutininBiochemistry (medical)Biological activityRats Inbred StrainsGeneral MedicineDNAPeripheralRatsChemistryEndocrinologyLiverbiology.proteinmedicine.drugThymidineJournal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie
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Correlation between the effects of retinoic acid and dexamethasone on liver tyrosine aminotransferase

1997

A single dose of 50 microg of trans-retinoic acid administered to rats significantly raised the level of hepatic tyrosine after a few hours. This effect was compared with that of dexamethasone and a possible correlation between these effectors was also investigated. An equal increase in enzyme activity level caused by retinoic acid was observed in adrenalectomized rats, leading to the suggestion that the effect of retinoic acid on liver tyrosine aminotransferase is independent of glucocorticoids. However, the study of the binding activity of the liver nuclear glucocorticoid receptors vs dexamethasone showed that this activity is favoured by retinoic acid, whereas no variation was evidenced …

Malemedicine.medical_specialtyReceptors Retinoic AcidEndocrinology Diabetes and MetabolismClinical BiochemistryTyrosine TransaminaseRetinoic acidretinoic acid receptorAntineoplastic AgentsTretinoindexamethasoneBiologyBiochemistrychemistry.chemical_compoundReceptors GlucocorticoidEndocrinologyGlucocorticoid receptorTyrosine aminotransferaseInternal medicineglucocorticoid receptorretinoic acidmedicineAnimalsRats WistarTyrosineReceptorMolecular BiologyDexamethasoneTyrosine TransaminaseBinding SitesAdrenalectomyCell BiologyRatsEndocrinologyLiverchemistryTyrosineMolecular Medicinetyrosine aminotransferaseInjections IntraperitonealGlucocorticoidmedicine.drug
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