Search results for "Up-Regulation"

showing 10 items of 455 documents

Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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Protective role of nuclear factor of activated T cells 2 in CD8+ long-lived memory T cells in an allergy model

2007

Background The transcriptional regulation of cytokines released and controlled by memory T cells is not well understood. Defective IFN-γ production in allergic asthma correlates in human beings with the risk of wheezing in childhood. Objective To understand the role of the transcription factor nuclear factor of activated T cells 2 (NFATc2) in memory and effector T cells in the airways in experimental allergic asthma. Methods We used murine models of allergic asthma and adoptive cell transfer of fluorescence-activated sorted cells in a disease model. Results Mice lacking NFATc2 developed an increase in airway hyperresponsiveness (AHR), remodeling, and serum IgE levels on ovalbumin sensitizat…

MaleInterleukin 2Adoptive cell transferImmunologyMice SCIDCD8-Positive T-LymphocytesInterferon-gammaMiceInterleukin 21T-Lymphocyte SubsetsHypersensitivitymedicineAnimalsImmunology and AllergyCytotoxic T cellInterleukin-7 receptorLungMice KnockoutMice Inbred BALB CReceptors Interleukin-7NFATC Transcription Factorsbusiness.industryInterleukin-17Cell Differentiationrespiratory systemAdoptive TransferMolecular biologyGrowth InhibitorsUp-Regulationrespiratory tract diseasesInterleukin-2 Receptor beta SubunitInterleukin 10ImmunologyFemaleInterleukin 17Bronchial HyperreactivitybusinessImmunologic MemoryCD8medicine.drugJournal of Allergy and Clinical Immunology
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Mild-stretch mechanical ventilation upregulates toll-like receptor 2 and sensitizes the lung to bacterial lipopeptide.

2011

Introduction Mechanical ventilation (MV) could prime the lung toward an inflammatory response if exposed to another insult such as bacterial invasion. The underlying mechanisms are not so far clear. Toll-like receptors (TLRs) allow the host to recognize selectively bacterial pathogens and in turn to trigger an immune response. We therefore hypothesized that MV modulates TLR2 expression and in turn modifies responsiveness to agonists such as bacterial lipopeptide (BLP). Method Both in vitro and in vivo experiments were conducted. First, TLR2 expression and protein were measured in the A549 pulmonary epithelial cell line submitted to 8-hour cyclic stretch (20% elongation; 20/minute rate). Aft…

MaleInterleukin-6/metabolismCell Culture TechniquesRespiration Artificial/methodsBiologyLung injuryCritical Care and Intensive Care MedicineReal-Time Polymerase Chain Reaction03 medical and health scienceschemistry.chemical_compoundLipopeptidesToll-Like Receptor 2/analysis/genetics/metabolism0302 clinical medicineImmune systemLipopeptides/metabolismDownregulation and upregulationAnimalsReceptorLung030304 developmental biologyddc:616A549 cell0303 health sciencesToll-like receptorEpithelial Cells/metabolism/microbiologyddc:617BacteriaInterleukin-6ResearchInterleukin-8Lipopeptide030208 emergency & critical care medicineEpithelial CellsSequence Analysis DNArespiratory systemFlow CytometryRespiration ArtificialLung/immunology/metabolismToll-Like Receptor 23. Good healthCell biologyUp-RegulationTLR2chemistryInterleukin-8/metabolismBacteria/metabolismImmunologyRabbitsCritical care (London, England)
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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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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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Changing the General Factor of Personality and the c-fos Gene Expression with Methylphenidate and Self-Regulation Therapy

2012

[EN] A deepening in the biological nature of the general factor of personality (GFP) is suggested: the activation level of the stress system is here represented by the gene expression of c-fos. The results of a single case experimental design are reported. A model of four coupled differential equations that explains the human personality dynamics as a consequence of a single stimulant drug intake has been fitted to psychological and biological experimental data. The stimulant-drug conditioning and its adaptation to the considered mathematical model is also studied for both kinds of measures. The dynamics of the cfos expression presents a similar pattern to the dynamics of the psychological …

MaleLinguistics and LanguageSubjective variablesmedia_common.quotation_subjectGene ExpressionModels PsychologicalHierarchical structure of the Big Fivec-FosDynamic modelLanguage and LinguisticsDevelopmental psychologyTerapia de auto-regulaciónGene expressionConditioning PsychologicalSelf-regulation therapymedicinePersonalityHumansPersonalidadGeneral Psychologymedia_commonModelo dinámicobiologyC-fosMethylphenidateGenes fosMiddle AgedUp-RegulationCoupled differential equationsExpression (architecture)biology.proteinMethylphenidateFactor general de personalidadCentral Nervous System StimulantsGeneral factor of personalityPsychologyMATEMATICA APLICADANeuroscienceProto-Oncogene Proteins c-fosMetilfenidatomedicine.drugPersonality
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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Local salsolinol modulates dopamine extracellular levels from rat nucleus accumbens: shell/core differences.

2008

Salsolinol (SAL), a condensation product of dopamine and acetaldehyde that appears in the rat and human brain after ethanol ingestion, has been largely implicated in the aetiology of alcoholism. Although the behavioural consequences of systemic or intracerebral SAL administrations have been described, the neurochemical effects of pharmacologically relevant doses of SAL and other tetrahydroisoquinolines (THIQs) in the brain areas involved in alcohol addiction are practically unknown. To gain an insight into this topic, male Wistar rats were stereotaxically implanted with one concentric microdialysis probe in either the shell or the core of the nucleus accumbens (NAc). Treatments involved loc…

MaleMicrodialysisDopamineMicrodialysisDown-RegulationAcetaldehydePharmacologyNucleus accumbensSynaptic TransmissionNucleus AccumbensCellular and Molecular Neurosciencechemistry.chemical_compoundNeurochemicalAlcohol-Induced Disorders Nervous SystemRewardDopamineparasitic diseasesBasal gangliamedicineAnimalsEthanol metabolismRats WistarNeurotransmitterChromatography High Pressure LiquidDose-Response Relationship DrugEthanolChemistryExtracellular FluidCell BiologyIsoquinolinesRatsUp-RegulationAlcoholismCatecholamineNeurosciencemedicine.drugNeurochemistry international
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Acute intermittent nicotine treatment induces fibroblast growth factor-2 in the subventricular zone of the adult rat brain and enhances neuronal prec…

2007

Abstract Over the past years, evidence has accumulated that stem cells are present in the adult brain, and generate neurons and/or glia from two active germinal zones: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus. This study shows that acute intermittent nicotine treatment significantly enhances neuronal precursor cell proliferation in the SVZ of adult rat brain, but not in the SGZ of the hippocampus, and pre-treatment with mecamylamine, a nonselective nAChR antagonist, blocks the enhanced precursor proliferation by nicotine. This effect is supported by up-regulation of fibroblast growth factor-2 (FGF-2) mRNA …

MaleNicotinemedicine.medical_specialtyBasic fibroblast growth factorSubventricular zoneNicotinic AntagonistsReceptors NicotinicBiologyFibroblast growth factorSettore BIO/09 - FisiologiaHippocampusSubgranular zonechemistry.chemical_compoundLateral VentriclesInternal medicinePrecursor cellmedicineAnimalsPyrrolesNicotinic AgonistsRNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarCell ProliferationNeuronsNeuronal PlasticityStem CellsGeneral NeuroscienceFibroblast growth factor receptor 1Dentate gyrusNeurogenesisCell DifferentiationNerve RegenerationRatsUp-RegulationCell biologymedicine.anatomical_structureEndocrinologynervous systemchemistryneurogenesis FGF-2 FGFR-1 subventricular zone nicotineFibroblast Growth Factor 2Neuroscience
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Regulation of α4β2α5 nicotinic acetylcholinergic receptors in rat cerebral cortex in early and late adolescence: Sex differences in response to chron…

2013

Chronic nicotine administration in animals, and smoking in humans, causes up-regulation of α4β2* neuronal nicotinic receptors (nAChRs), which has been hypothesized to contribute to the addictive actions of nicotine. We used a rat model to test whether such up-regulatory effects differ in adolescents versus adults, and in males versus females. Following chronic treatment with nicotine or saline via subcutaneous osmotic minipumps, we measured α4β2 and α4β2α5 nAChRs in cerebral cortex using [3H]epibatidine to label assembled nAChRs, and selective antibodies to measure the individual subunits via immunoprecipitation. For the first time, we provide a detailed characterization of the response of …

MaleNicotinemedicine.medical_specialtyPyridinesmedia_common.quotation_subjectReceptors NicotinicTritiumArticleRats Sprague-DawleyNicotineCellular and Molecular NeuroscienceDownregulation and upregulationInternal medicinemedicineAnimalsImmunoprecipitationNicotinic AgonistsReceptormedia_commonCerebral CortexPharmacologySex CharacteristicsBinding SitesAddictionBridged Bicyclo Compounds HeterocyclicUp-RegulationNicotinic agonistEndocrinologymedicine.anatomical_structureCerebral cortexEpibatidineFemalePsychologymedicine.drugSex characteristicsNeuropharmacology
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