Search results for "Up-Regulation"

showing 10 items of 455 documents

The impact of alpha1-adrenoceptors up-regulation accompanied by the impairment of beta-adrenergic vasodilatation in hypertension

2008

9 pages, 7 figures, 3 tables.-- PMID: 19060223 [PubMed]

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Adrenergic receptorSystolemedia_common.quotation_subjectAdrenergicVasodilationModels BiologicalRats Inbred WKYDownregulation and upregulationHeart RateRats Inbred SHRReceptors Adrenergic alpha-1Internal medicineReceptors Adrenergic betamedicineAnimalsHumansRNA MessengerReceptorInternalizationAortamedia_commonPharmacologybiologyChemistryKinaseBeta adrenergic receptor kinaseRatsUp-RegulationVasodilationEndocrinologyHypertensionbiology.proteinMolecular Medicine
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Neurological impairment in experimental antiphospholipid syndrome is associated with increased ligand binding to hippocampal and cortical serotonergi…

2013

The antiphospholipid syndrome (APS) is an autoimmune disease where the presence of high titers of circulating autoantibodies causes thrombosis with consecutive infarcts. In experimental APS (eAPS), a mouse model of APS, behavioral abnormalities develop in the absence of vessel occlusion or infarcts. Using brain hemispheres of control and eAPS mice with documented neurological and cognitive deficits, we checked for lymphocytic infiltration, activation of glia and macrophages, as well as alterations of ligand binding densities of various neurotransmitter receptors to unravel the molecular basis of this abnormal behavior. Lymphocytic infiltrates were immunohistochemically characterized using a…

medicine.medical_specialtyImmunologyHippocampusAMPA receptorBiologySerotonergicHippocampusMiceNeurotransmitter receptorInternal medicinemedicineAnimalsImmunology and AllergyLymphocytesReceptor5-HT receptorAutoantibodiesBehavior AnimalMicrogliaGABAA receptorMacrophagesSomatosensory CortexHematologyAntiphospholipid SyndromeAntigens DifferentiationUp-RegulationDisease Models Animalmedicine.anatomical_structureEndocrinologynervous systemAstrocytesReceptor Serotonin 5-HT1ANervous System DiseasesImmunobiology
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Weaning induces NOS-2 expression through NF-κB modulation in the lactating mammary gland: importance of GSH

2005

Zaragozá, R; Miralles, VJ; Rus, AD; García, C; Carmena, R; García-Trevijano, ER; Barber, T; Pallardó, FV; Torres, L; Viña, JR. At the end of lactation the mammary gland undergoes involution, a process characterized by apoptosis of secretory cells and tissue remodelling. To gain insight into this process, we analysed the gene expression profile by oligonucleotide microarrays during lactation and after forced weaning. Up-regulation of inflammatory mediators and acute-phase response genes during weaning was found. Expression of IκBα (inhibitory κBα), a protein known to modulate NF-κB (nuclear factor-κB) nuclear translocation, was significantly up-regulated. On the other hand, there was a time-…

medicine.medical_specialtyMammary glandDown-RegulationNitric Oxide Synthase Type IIWeaninglactationBiologyBiochemistryNF-κBMammary Glands AnimalWestern blotnitric oxideInternal medicineLactationGene expressionmedicineGSHinvolutionWeaningAnimalsInvolution (medicine)Rats WistarPromoter Regions GeneticMolecular Biologymedicine.diagnostic_test:CIENCIAS DE LA VIDA::Bioquímica [UNESCO]Gene Expression ProfilingNF-kappa BUNESCO::CIENCIAS DE LA VIDA::BioquímicaCell BiologyGlutathioneRatsUp-RegulationIκBαProtein Transportmedicine.anatomical_structureEndocrinologyEnzyme InductionFemaleChromatin immunoprecipitationProtein BindingResearch Article
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Skin response to a carcinogen involves the xenobiotic receptor pregnane X receptor.

2015

Skin is in daily contact with potentially harmful molecules from the environment such as cigarette smoke, automobile emissions, industrial soot and groundwater. Pregnane X receptor (PXR) is a transcription factor expressed in liver and intestine that is activated by xenobiotic chemicals including drugs and environmental pollutants. Topical application of the tumor initiator 7,12-dimethylbenz(a)anthracene (DMBA) enhances Pxr, Cyp1a1, Cyp1b1 and Cyp3a11, but not Ahr expression in the skin. Surprisingly, DMBA-induced Pxr upregulation is largely impaired in Langerin(+) cell-depleted skin, suggesting that DMBA mainly triggers Pxr in Langerin(+) cells. Furthermore, PXR deficiency protects from DN…

medicine.medical_specialtyReceptors SteroidLangerinDNA damage910-Dimethyl-12-benzanthraceneDMBADermatologymedicine.disease_causeBiochemistrydigestive systemArticleDownregulation and upregulationCell MovementInternal medicinemedicineAnimalsMolecular BiologyCarcinogenSkinPregnane X receptorbiologyintegumentary systemPregnane X ReceptorAryl hydrocarbon receptordigestive system diseasesUp-RegulationMice Inbred C57BLEndocrinologyLangerhans CellsCancer researchbiology.proteinCarcinogensCarcinogenesisDNA DamageExperimental dermatology
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Repression of Cyclic Adenosine Monophosphate Upregulation Disarms and Expands Human Regulatory T Cells

2011

Abstract The main molecular mechanism of human regulatory T cell (Treg)-mediated suppression has not been elucidated. We show in this study that cAMP represents a key regulator of human Treg function. Repression of cAMP production by inhibition of adenylate cyclase activity or augmentation of cAMP degradation through ectopic expression of a cAMP-degrading phosphodiesterase greatly reduces the suppressive activity of human Treg in vitro and in a humanized mouse model in vivo. Notably, cAMP repression additionally abrogates the anergic state of human Treg, accompanied by nuclear translocation of NFATc1 and induction of its short isoform NFATc1/αA. Treg expanded under cAMP repression, however,…

medicine.medical_specialtyRegulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryMicechemistry.chemical_compoundInternal medicineCyclic AMPmedicineAnimalsHumansImmunology and AllergyCyclic adenosine monophosphatePsychological repressionCell ProliferationClonal AnergyNFATC Transcription FactorsClonal anergyPhosphodiesterasehemic and immune systemsUp-RegulationCell biologyEndocrinologymedicine.anatomical_structurechemistryHumanized mousecAMP-dependent pathwayCyclase activityThe Journal of Immunology
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Induction of the adrenoleukodystrophy-related gene (ABCD2) by thyromimetics.

2009

X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder caused by mutations in the ABCD1 (ALD) gene. The ABCD2 gene, its closest homolog, has been shown to compensate for ABCD1 deficiency when overexpressed. We previously demonstrated that the ABCD2 promoter contains a functional thyroid hormone response element. Thyroid hormone (T3) through its receptor TRbeta can induce hepatic Abcd2 expression in rodents and transiently normalize the VLCFA level in fibroblasts of Abcd1 null mice. In a therapeutic perspective, the use of selective agonists of TRbeta should present the advantage to be devoid of side effects, at least concerning the cardiotoxicity associated to TRalpha activation. I…

medicine.medical_specialtyThyroid HormonesEndocrinology Diabetes and MetabolismClinical BiochemistryBiologyAcetatesATP Binding Cassette Transporter Subfamily DTransfectionBiochemistryEndocrinologyDownregulation and upregulationPhenolsInternal medicinePeroxisomal disorderGene expressionChlorocebus aethiopsmedicineAnimalsHumansReceptorAdrenoleukodystrophyMolecular BiologyHormone response elementReporter geneGlyoxylatesCell BiologyTransfectionmedicine.diseaseCell biologyRatsUp-RegulationEndocrinologyCOS CellsMolecular MedicineTriiodothyronineAdrenoleukodystrophyATP-Binding Cassette TransportersThe Journal of steroid biochemistry and molecular biology
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Addition of NMDA-receptor antagonist MK801 during oxygen/glucose deprivation moderately attenuates the upregulation of glucose uptake after subsequen…

2011

During stroke the blood–brain barrier (BBB) is damaged which can result in vasogenic brain edema and inflammation. The reduced blood supply leads to decreased delivery of oxygen and glucose to affected areas of the brain. Oxygen and glucose deprivation (OGD) can cause upregulation of glucose uptake of brain endothelial cells. In this letter, we investigated the influence of MK801, a non-competitive inhibitor of the NMDA-receptor, on the regulation of the glucose uptake and of the main glucose transporters glut1 and sglt1 in murine BBB cell line cerebEND during OGD. mRNA expression of glut1 was upregulated 68.7- fold after 6 h OGD, which was significantly reduced by 10 μM MK801 to 28.9-fold.…

medicine.medical_specialtyTime FactorsSchlaganfallNMDA-RezeptorGlucose uptakeNMDA-AntagonistInflammationCarbohydrate metabolismTritiumBlood–brain barrierReceptors N-Methyl-D-AspartateMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineBlut-Hirn-SchrankeAnimalsddc:610RNA MessengerHypoxia030304 developmental biology0303 health sciencesDose-Response Relationship DrugbiologyGeneral NeuroscienceGlucosetransportproteineGlucose transporterBrainEndothelial CellsUp-RegulationOxygencarbohydrates (lipids)Glucosemedicine.anatomical_structureEndocrinologynervous systembiology.proteinNMDA receptorGLUT1Dizocilpine Maleatemedicine.symptomExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeuroscience Letters
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p53 Involvement in the control of murine hair follicle regression.

2001

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles…

medicine.medical_specialtyTumor suppressor genemedicine.medical_treatmentDown-RegulationApoptosisBiologyPathology and Forensic MedicineTelogen effluviumMiceBcl-2-associated X proteinDownregulation and upregulationInternal medicineProto-Oncogene ProteinsmedicineAnimalsbcl-2-Associated X ProteinMice Knockoutintegumentary systemGrowth factorAlopecia areatamedicine.diseaseHair follicleCell biologyUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-bcl-2Knockout mousebiology.proteinCommentaryFemaleTumor Suppressor Protein p53Hair FollicleThe American journal of pathology
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Substance P is upregulated in the serum of patients with chronic spontaneous urticaria.

2014

medicine.medical_specialtyUrticariaMEDLINESubstance PDermatologyAnxietySubstance PBiochemistrySeverity of Illness Indexchemistry.chemical_compoundText miningQuality of lifeDownregulation and upregulationInternal medicineGermanySeverity of illnessMedicineHumansMolecular Biologybusiness.industryDepressionDisease progressionCell BiologyUp-RegulationMulticenter studychemistryChronic DiseaseDisease ProgressionQuality of LifebusinessBiomarkersThe Journal of investigative dermatology
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Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells

2005

HMG-CoA reductase inhibitors (statins) exert pleiotropic physiological effects. Among others they attenuate cellular responses to genotoxic and inflammatory stress. We investigated the effect of lovastatin on the expression level of TNF receptors (TNFR) in primary human endothelial cells (HUVEC). ELISA, FACS and immunocytochemical analyses show that lovastatin selectively increases the cell surface expression of TNFR2 without affecting the expression level of TNFR1. This effect of lovastatin is independent from inhibition of cell-cycle progression since cells both in G1- and G2-phase showed elevated levels of TNFR2 after lovastatin treatment. To analyze the physiological relevance of lovast…

medicine.medical_treatmentCellBiologyDownregulation and upregulationE-selectinpolycyclic compoundsGeneticsmedicineHumansReceptors Tumor Necrosis Factor Type IILovastatinReceptorCells CulturedCell adhesion moleculeCell CycleEndothelial Cellsnutritional and metabolic diseasesGeneral MedicineFlow CytometryUp-RegulationCell biologymedicine.anatomical_structureCytokineReceptors Tumor Necrosis Factor Type ICancer researchbiology.proteinlipids (amino acids peptides and proteins)Tumor necrosis factor alphaLovastatinE-Selectinmedicine.drugInternational Journal of Molecular Medicine
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