Search results for "Transcription Factor RelA"

showing 10 items of 38 documents

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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Paracrine in vivo inhibitory effects of adipose tissue–derived mesenchymal stromal cells in the early stages of the acute inflammatory response

2015

Abstract Background aims Excessive or unresolved inflammation leads to tissue lesions. Adipose tissue–derived mesenchymal stromal cells (AMSCs) have shown protective effects that may be dependent on the modulation of inflammation by secreted factors. Methods We used the zymosan-induced mouse air pouch model at two time points (4 h and 18 h) to evaluate the in vivo effects of AMSCs and their conditioned medium (CM) on key steps of the early inflammatory response. We assessed the effects of AMSCs and CM on leukocyte migration and myeloperoxidase activity. The levels of chemokines, cytokines and eicosanoids in exudates were measured by use of enzyme-linked immunoassay or radio-immunoassay. In …

MaleCancer ResearchChemokineLeukocyte migrationLeukotriene B4medicine.medical_treatmentInterleukin-1betaImmunologyFluorescent Antibody TechniqueAdipose tissueEnzyme-Linked Immunosorbent AssayInflammationMesenchymal Stem Cell TransplantationLeukotriene B4DinoprostoneMiceParacrine signallingchemistry.chemical_compoundCell MovementParacrine CommunicationLeukocytesmedicineAnimalsImmunology and AllergyGenetics (clinical)Prostaglandin-E SynthasesInflammationTransplantationbiologyInterleukin-6Tumor Necrosis Factor-alphaTranscription Factor RelAZymosanMesenchymal Stem CellsCell BiologyIntramolecular OxidoreductasesAdipose TissueOncologychemistryCyclooxygenase 2Culture Media ConditionedImmunologyCancer researchbiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomProstaglandin ECytotherapy
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Distinct influence of atypical 1,4-dihydropyridine compounds in azidothymidine-induced neuro- and cardiotoxicity in mice ex vivo.

2008

This study demonstrates the effective protection by compounds of atypical 1,4-dihydropyridine (DHP) series cerebrocrast, glutapyrone and tauropyrone against neuro- and cardiotoxicity caused by the model compound azidothymidine, a well-known mitochondria-compromising anti-HIV drug. In previous in vitro experiments, we have demonstrated distinct effects of these DHP compounds to influence mitochondrial functioning. In the present in vivo experiments, DHP compounds were administered intraperitoneally in mice daily for 2 weeks, per se and in combinations with azidothymidine at doses: azidothymidine 50 mg/kg; cerebrocrast 0.1 mg/kg; glutapyrone 1 mg/kg; and tauropyrone 1 mg/kg. At the end of the…

MaleDihydropyridinesHeart DiseasesRatónAnti-HIV AgentsTaurineApoptosisBiologyPharmacologyToxicologyMiceGlutamatesIn vivomedicineAnimalsPharmacologyCerebral CortexInflammationCardiotoxicityMice Inbred ICRCaspase 3DihydropyridineTranscription Factor RelAGeneral MedicineBiochemistryGene Expression RegulationEnzyme inhibitorApoptosisToxicitybiology.proteinNeurotoxicity SyndromesZidovudineEx vivomedicine.drugBasicclinical pharmacologytoxicology
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Mild Aerobic Exercise Training Hardly Affects the Diaphragm of mdx Mice

2016

In the mdx mice model of Duchenne Muscular Dystrophy (DMD), mild endurance exercise training positively affected limb skeletal muscles, whereas few and controversial data exist on the effects of training on the diaphragm. The diaphragm was examined in mdx (C57BL/10ScSn-Dmdmdx) and wild-type (WT, C57BL/10ScSc) mice under sedentary conditions (mdx-SD, WT-SD) and during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days (training: 5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed. In addition, tissue levels of the chaperonins Hsp60 and Hsp70 and the p65 subunit of nuclear factor-kB (NF-kB) were measured in diaphragm, gastrocnemius, and q…

MaleDuchenne muscular dystrophychaperoninTime FactorsDiaphragmSettore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - FisiologiaConnexinsMitochondrial ProteinsNecrosisendurance trainingAnimalsGenetic Predisposition to DiseaseHSP70 Heat-Shock Proteinsstress markersMuscle StrengthNF-kBSettore BIO/16 - Anatomia UmanaTranscription Factor RelAChaperonin 60Settore CHIM/06 - Chimica OrganicaExercise TherapyMuscular Dystrophy DuchenneDisease Models AnimalPhenotypeMice Inbred mdxPhysical Endurance
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Anti-inflammatory and antioxidant effects of muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus

2019

AbstractRecently we found that acute treatment with Oxotremorine (Oxo), a non-selective mAChRs agonist, up-regulates heat shock proteins and activates their transcription factor heat shock factor 1 in the rat hippocampus. Here we aimed to investigate: a) if acute treatment with Oxo may regulate pro-inflammatory or anti-inflammatory cytokines and oxidative stress in the rat hippocampus; b) if chronic restraint stress (CRS) induces inflammatory or oxidative alterations in the hippocampus and whether such alterations may be affected by chronic treatment with Oxo. In the acute experiment, rats were injected with single dose of Oxo (0.4 mg/kg) and sacrificed at 24 h, 48 h and 72 h. In the CRS ex…

MaleHydrocortisonemedicine.medical_treatmentInterleukin-1betaNeuroimmunologyAnti-Inflammatory Agentslcsh:MedicinePharmacologymedicine.disease_causeHippocampusSettore BIO/09 - FisiologiaAntioxidantsSuperoxide Dismutase-1Muscarinic acetylcholine receptorPhosphorylationlcsh:Sciencechemistry.chemical_classificationMultidisciplinarybiologyneurodegenerationAlzheimer's diseaseReceptors MuscarinicNeuroprotective AgentsCytokineSignal Transductionmedicine.drugRestraint PhysicalAgonistmedicine.drug_classScopolaminemuscarinic acetylcholine receptorMuscarinic AgonistsArticleOxotremorine anti-inflammatory cytokinesSuperoxide dismutaseHeat shock proteinOxotremorinemedicineAnimalsRats WistarInflammationReactive oxygen speciesInterleukin-6Superoxide DismutaseOxotremorinelcsh:RTranscription Factor RelARatsOxidative Stresschemistrybiology.proteinlcsh:QReactive Oxygen SpeciesProtein Processing Post-TranslationalOxidative stressScientific Reports
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Enhanced glomerular Toll-like receptor 4 expression and signaling in patients with type 2 diabetic nephropathy and microalbuminuria

2014

Toll-like receptor 4 (TLR4), a component of the innate immune system, is recognized to promote tubulointerstitial inflammation in overt diabetic nephropathy (DN). However, there is no information on immune activation in resident renal cells at an early stage of human DN. In order to investigate this, we studied TLR4 gene and protein expression and TLR4 downward signaling in kidney biopsies of 12 patients with type 2 diabetes and microalbuminuria, and compared them with 11 patients with overt DN, 10 with minimal change disease (MCD), and control kidneys from 13 patients undergoing surgery for a small renal mass. Both in microalbuminuria and in overt DN, TLR4 mRNA and protein were overexpress…

MaleKidney GlomerulusDiabetic nephropathyurologic and male genital diseasesDiabetic nephropathynefropatiadiabeticaDiabetic NephropathiesMinimal change diseaseChemokine CCL5KidneyMiddle AgedUp-RegulationKidney Tubulesmedicine.anatomical_structureNephrologyDisease ProgressionFemaleHumanSignal Transductionmedicine.medical_specialtyReceptors CCR5Receptors CCR2NephrosisAntigens Differentiation MyelomonocyticFollow-Up StudieNephropathyToll-like receptorAntigens CDDiabetes mellitusInternal medicinemedicineAlbuminuriaHumansRNA MessengerInflammationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryNephrosis LipoidKidney TubuleTranscription Factor RelABiomarkermedicine.diseaseImmunity InnateToll-Like Receptor 4EndocrinologyDiabetes Mellitus Type 2Diabetic NephropathieTLR4MicroalbuminuriaKidney GlomerulubusinessBiomarkersMicroalbuminuriaFollow-Up StudiesKidney International
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Patterns of Inflammatory Responses in Large and Small Airways in Smokers with and without Chronic Obstructive Pulmonary Disease

2010

<i>Background:</i> Chronic obstructive pulmonary disease (COPD) is characterised by progressive and irreversible airway obstruction. Smoking causes persistent inflammation in lung tissue. However, differences in inflammatory responses between the large and small airways have not been systematically explored among smokers with and without COPD. <i>Objectives:</i> The aim of our research was to characterise the expression and localisation of NF-ĸBp65 and histone deacetylase 2 (HDAC2) as well as inflammatory cell (macrophages, lymphocytes, neutrophils) distribution in large and small airways, in nonsmokers and in smokers with and without COPD. <i>Methods:</i&gt…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtyNeutrophilsHistone Deacetylase 2Pulmonary diseaseBronchiCell CountInflammationCD8-Positive T-Lymphocytesurologic and male genital diseasesPersistent inflammationPulmonary Disease Chronic ObstructiveRisk FactorsCarcinoma Non-Small-Cell LungInternal medicineMacrophages AlveolarCarcinomamedicineHumansLungAgedCOPDSmall airwaysbusiness.industrySmokingRespiratory diseaseTranscription Factor RelAMiddle Agedrespiratory systemAirway obstructionmedicine.diseaseImmunohistochemistryrespiratory tract diseasesImmunologyDisease ProgressionCardiologyFemalemedicine.symptombusinessRespiration
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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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Obesity causes PGC‐1α deficiency in the pancreas leading to marked IL‐6 upregulation via NF‐κB in acute pancreatitis

2019

Obesity is associated with local and systemic complications in acute pancreatitis. PPARγ coactivator 1α (PGC-1α) is a transcriptional coactivator and master regulator of mitochondrial biogenesis that exhibits dysregulation in obese subjects. Our aims were: (1) to study PGC-1α levels in pancreas from lean or obese rats and mice with acute pancreatitis; and (2) to determine the role of PGC-1α in the inflammatory response during acute pancreatitis elucidating the signaling pathways regulated by PGC-1α. Lean and obese Zucker rats and lean and obese C57BL6 mice were used first; subsequently, wild-type and PGC-1α knockout (KO) mice with cerulein-induced pancreatitis were used to assess the inflam…

MaleTaurocholic Acid0301 basic medicinemedicine.medical_specialtyPGC-1αPathology and Forensic Medicine03 medical and health sciencesDownregulation and upregulationInternal medicineAnimalsMedicineObesityPhosphorylationInterleukin 6PancreasCeruletideMice KnockoutIL-6biologyp65Interleukin-6business.industryNF-kappa BTranscription Factor RelAmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRats ZuckerUp-Regulation3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisPancreatitisbiology.proteinPancreatitisAcute pancreatitisPPARGC1AbusinessPancreasCeruletideSignal TransductionThe Journal of Pathology
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Astrocytes Protect Neurons from Aβ1-42 Peptide-Induced Neurotoxicity Increasing TFAM and PGC-1 and Decreasing PPAR-γ and SIRT-1

2015

One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated re…

MnSODProgrammed cell deathPPAR-γPeroxisome proliferator-activated receptorMitochondrionBiologyBioinformaticsmedicine.disease_causeAlzheimer's DiseaseNeurologiaPGC-1Sirtuin 1medicineAnimalsTFAMCells Culturedchemistry.chemical_classificationNeuronsAmyloid beta-PeptidesCell DeathSirtuin 1Caspase 3Superoxide DismutaseNeurotoxicityTranscription Factor RelAGeneral MedicineTFAMmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCoculture TechniquesPeptide FragmentsCell biologyMitochondriaPeroxidesRatsPPAR gammachemistryMitochondrial biogenesisNF-κB.Astrocytesbiology.proteinFisiologia humanaLipid PeroxidationOxidative stressResearch PaperTranscription FactorsInternational Journal of Medical Sciences
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