Search results for "PROLIFERATION"

showing 10 items of 1193 documents

NFATc1 Induction in Peripheral T and B Lymphocytes

2013

Abstract NFAT transcription factors control the proliferation and survival of peripheral lymphocytes. We have reported previously that the short isoform NFATc1/αA whose generation is induced by immune receptor stimulation supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cells. We will show in this study that in novel bacterial artificial chromosome transgenic mice that express EGFP under the control of entire Nfatc1 locus the Nfatc1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripheral T and B cells. Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated in B, Th1, and Th2 cells, but…

LipopolysaccharidesGene isoformChromosomes Artificial BacterialProgrammed cell deathTransgeneGreen Fluorescent ProteinsImmunologyGene ExpressionMice TransgenicStimulationImmune receptorBiologyLymphocyte ActivationT-Lymphocytes RegulatoryAntibodiesMiceTh2 CellsGenes ReporterTransforming Growth Factor betaAnimalsProtein IsoformsImmunology and AllergyPromoter Regions GeneticTranscription factorCell ProliferationB-LymphocytesNFATC Transcription Factorsintegumentary systemNF-kappa BCD28NFATTh1 CellsMolecular biologyMice Inbred C57BLTh17 CellsThe Journal of Immunology
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A new chloroquinolinyl chalcone derivative as inhibitor of inflammatory and immune response in mice and rats

2003

AbstractThe synthetic chalcone derivative 1-(2,4-dichlorophenyl)-3-(3-(6,7-dimethoxy-2-chloroquinolinyl))-2-propen-1-one (CIDQ) was evaluated for its anti-inflammatory, analgesic and immunomodulatory efficacy in-vitro and in-vivo. CIDQ concentration-dependently inhibited the production of nitric oxide (NO) (IC50 4.3 μM) and prostaglandin E2 (PGE2) (IC50 1.8 μM) in RAW 264.7 macrophages stimulated with lipopolysaccharide. Human mononuclear cell proliferation was significantly inhibited by 10 μM CIDQ. Oral administration of CIDQ (10–30 mg kg−1) in the 24-h zymosan-stimulated mouse air-pouch model produced a dose-dependent reduction of cell migration as well as NO and PGE2 levels in exudates. …

LipopolysaccharidesLipopolysaccharidemedicine.medical_treatmentAdministration OralPharmaceutical ScienceAbdominal InjuriesPharmacologyLymphocyte ActivationMicechemistry.chemical_compoundProstaglandin E2Pain MeasurementPyridazinesCytokineFemalemedicine.symptomProstaglandin Emedicine.drugBlood PlateletsChalconeMononuclear cell proliferationPainInflammationGroup II Phospholipases A2DinoprostonePhospholipases ACell LineNitric oxideDrug HypersensitivityFormaldehydeMicrosomesmedicineAnimalsHumansNitritesInflammationPharmacologyDose-Response Relationship Drugbusiness.industryGroup IV Phospholipases A2MacrophagesZymosanArthritis ExperimentalRatsThromboxane B2Disease Models AnimalchemistryCyclooxygenase 2Rats Inbred LewImmunologyCyclooxygenase 1DinitrofluorobenzenebusinessJournal of Pharmacy and Pharmacology
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Budlein A from Viguiera robusta inhibits leukocyte-endothelial cell interactions, adhesion molecule expression and inflammatory mediators release

2009

Budlein A has been reported to exert some analgesic and anti-inflammatory properties. In this study, we have evaluated its effect on LPS-induced leukocyte recruitment in vivo and the mechanisms involved in its anti-inflammatory activity. In vivo, intravital videomicroscopy was used to determine the effects of budlein A on LPS-induced leukocyte-endothelial cell interactions in the murine cremasteric microcirculation. In vitro, the effects of budlein A on LPS-induced cytokine, chemokine and nitrites release, T-cell proliferative response as well as cell adhesion molecule expression (CAM) were evaluated. In vivo, intraperitoneal administration of budlein A (2.6 mM/kg) caused a significant redu…

LipopolysaccharidesMaleChemokineT-Lymphocytesmedicine.medical_treatmentPharmaceutical ScienceLeukocyte RollingCell CommunicationAsteraceaeNitric OxideDexamethasoneCell LineLactonesMiceIn vivoDrug DiscoverymedicineAnimalsHumansLeukocyte RollingInterleukin 8NitritesCell ProliferationPharmacologyMice Inbred BALB CbiologyPlant ExtractsCell adhesion moleculeMacrophagesMicrocirculationMonocyteEndothelial CellsCell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureCytokineComplementary and alternative medicinebiology.proteinMolecular MedicineChemokinesCell Adhesion MoleculesSesquiterpenesImmunosuppressive AgentsPhytomedicine
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New insight into the inhibition of the inflammatory response to experimental delayed-type hypersensitivity reactions in mice by scropolioside A.

2006

Scropolioside A, an iridoid isolated from Scrophularia auriculata ssp. pseudoauriculata, showed anti-inflammatory properties against different experimental models of delayed-type hypersensitivity. This iridoid reduced the oedema induced by oxazolone by 79% (72 h) at 0.5 mg/ear while reducing that induced by sheep red blood cells by 47% (18 h), 45% (24 h) and 36% (48 h) at 10 mg/kg. In vivo it reduced both oedema formation and cell infiltration whereas in vitro it reduced the proliferation of activated T-lymphocytes (IC50 of 67.74 microM). Treatment with scropolioside A (100 microM) 18 and 24 h after phytohemagglutinin stimulation increased the number of cells arrested in the subG(0) phase w…

LipopolysaccharidesNecrosisErythrocytesLeukotriene B4NeutrophilsT-LymphocytesAnti-Inflammatory AgentsStimulationInflammationApoptosisLymphocyte proliferationPharmacologyBiologyLeukotriene B4DinoprostoneNitric oxideCell LineOxazolonechemistry.chemical_compoundMiceGlucosidesmedicineAnimalsEdemaHumansHypersensitivity DelayedPyransPharmacologySheepPancreatic ElastaseCaspase 3MacrophagesOxazoloneEarAllergenschemistryDelayed hypersensitivityImmunologyCytokinesFemalemedicine.symptomEuropean journal of pharmacology
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Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis

2010

BACKGROUND AND PURPOSE Cucurbitacin R, a natural anti-inflammatory product, has been shown to exhibit activity against both adjuvant-induced arthritis and delayed-type hypersensitivity reactions induced by various agents. Previous studies have demonstrated that the effects of cucurbitacin R stem from its inhibition of both cytokine production and lymphocyte proliferation. EXPERIMENTAL APPROACHES Effects of cucurbitacin R were investigated on lipopolysaccharide-stimulated RAW 264.7 cells. Cell cycle evolution was analysed by flow cytometry, detection of apoptosis by DNA ladder, Bcl-2, p21, p53, Bax, cleaved caspase-1 (p10), caspase-9, and caspase-3, cleaved caspase (p17) and interleukin-1β d…

LipopolysaccharidesProgrammed cell deathinterleukin-1βmedicine.medical_treatmentBlotting WesternInterleukin-1betaCaspase 1caspase-1Caspase 3Lymphocyte proliferationBiologyTransfectionCell LineMiceRAW 264.7 macrophagesmedicineAnimalsBcl-2RNA Small InterferingPharmacologyMembrane Potential MitochondrialCaspase 3Reverse Transcriptase Polymerase Chain ReactionMacrophagesAnti-Inflammatory Agents Non-SteroidalCaspase 1Cell CycleapoptosisCell cycleFlow CytometryMolecular biologyResearch PapersTriterpenescucurbitacin RCytokineProto-Oncogene Proteins c-bcl-2Cell cultureApoptosis
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Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

2013

SummaryLiver fibrosis is a consequence of chronic liver diseases and thus a major cause of mortality and morbidity. Clinical evidence and animal studies suggest that local tissue homeostasis is disturbed due to immunological responses to chronic hepatocellular stress. Poorly defined stress-associated inflammatory networks are thought to mediate gradual accumulation of extracellular-matrix components, ultimately leading to fibrosis and liver failure. Here we have reported that hepatic expression of interleukin-33 (IL-33) was both required and sufficient for severe hepatic fibrosis in vivo. We have demonstrated that IL-33’s profibrotic effects related to activation and expansion of liver resi…

Liver CirrhosisLiver cytologyImmunologyBiologyLymphocyte ActivationArticle03 medical and health sciencesMice0302 clinical medicineFibrosismedicineHepatic Stellate CellsAnimalsImmunology and AllergyLymphocytesReceptors Interleukin-4 Type IIInterleukin 4Tissue homeostasisCells Cultured030304 developmental biologyCell ProliferationInflammationMice Knockout0303 health sciencesMice Inbred BALB CInterleukin-13InterleukinsInnate lymphoid cellmedicine.diseaseInterleukin-33Adoptive Transfer3. Good healthInterleukin 33Mice Inbred C57BLInfectious DiseasesLiverImmunologyHepatic stellate cellHepatic fibrosisSTAT6 Transcription Factor030215 immunologySignal TransductionImmunity
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Transformation of primary human hepatocytes in hepatocellular carcinoma

2015

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Currently, there is limited knowledge of neoplastic transformation of hepatocytes in HCC. In clinical practice, the high rate of HCC local recurrence suggests the presence of different hepatocyte populations within the liver and particularly in the tumor proximity. The present study investigated primary human hepatocyte cultures obtained from liver specimens of patients affected by cirrhosis and HCC, their proliferation and transformation. Liver samples were obtained from seven HCC cirrhotic patients and from three patients with normal liver (NL). Immediately after surgery, cell outgrowth and primary cultures were obtai…

Liver CirrhosisMale0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyCarcinoma HepatocellularCirrhosisGlypican 3Lesion03 medical and health sciences0302 clinical medicineGlypicansAntigens NeoplasmCell MovementSettore BIO/10 - BiochimicamedicineCarcinomaHumansNeoplasm InvasivenessNeoplastic transformationAgedCell ProliferationArginasebiologySettore BIO/16 - Anatomia UmanaLiver NeoplasmsCD44Hepatocellular CarcinomaMiddle AgedFlow Cytometrymedicine.diseaseImmunohistochemistrydigestive system diseasesCell Transformation NeoplasticHyaluronan Receptors030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisHepatocellular carcinomaHepatocyteHepatocytesbiology.proteinFemalemedicine.symptomInternational Journal of Oncology
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

2009

Sphingosine-1-phosphate (S1P) has been presented recently as a pro-inflammatory agent in the airway epithelium since S1P levels are increased in bronchoalveolar lavage fluid of human asthmatics. However, the effects of S1P over the alveolar epithelium and neutrophil interactions are poorly understood. Here, we show that S1P increased interleukin 8 (IL-8) gene expression and protein secretion and proliferation in alveolar epithelial cells A549 at physiological concentrations (1 microM). At the same time, S1P increased intracellular Ca2+ concentration (potency 17.91 microM, measured by epifluorescence microscopy), phospholipase D (PLD) activity (measured by chemiluminiscence method) and extra…

LuminescenceNeutrophilsIntercellular Adhesion Molecule-1Gene ExpressionBiologyPertussis toxinReceptors G-Protein-Coupled1-ButanolSphingosineCell Line TumorPhospholipase DHumansInterleukin 8PhosphorylationExtracellular Signal-Regulated MAP KinasesEgtazic AcidCell ProliferationFlavonoidsPharmacologyA549 cellCell adhesion moleculeInterleukin-8Epithelial CellsChemotaxisIntercellular Adhesion Molecule-1Intercellular adhesion moleculeMolecular biologyPulmonary AlveoliChemotaxis LeukocytePertussis ToxinBiochemistryRespiratory epitheliumCalciumlipids (amino acids peptides and proteins)LysophospholipidsEuropean Journal of Pharmacology
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Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis

2013

The mechanisms by which deregulated nuclear factor erythroid-2–related factor 2 (NRF2) and kelch-like ECH-associated protein 1 (KEAP1) signaling promote cellular proliferation and tumorigenesis are poorly understood. Using an integrated genomics and 13C-based targeted tracer fate association (TTFA) study, we found that NRF2 regulates miR-1 and miR-206 to direct carbon flux toward the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose metabolism. Sustained activation of NRF2 signaling in cancer cells attenuated miR-1 and miR-206 expression, leading to enhanced expression of PPP genes. Conversely, overexpression of miR-1 and miR-206 decreased the exp…

Lung NeoplasmsCell SurvivalNF-E2-Related Factor 2Citric Acid CycleMice NudeBiologymedicine.disease_causeMiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumormicroRNAGene expressionmedicineAnimalsHumansTranscription factor3' Untranslated RegionsCell ProliferationOligonucleotide Array Sequence AnalysisRegulation of gene expressionBinding SitesBase SequenceGeneral MedicineMolecular biologyHDAC4Cell biologyTumor BurdenGene Expression Regulation NeoplasticMicroRNAsCell Transformation NeoplasticGlucoseRNA InterferenceHistone deacetylaseCarcinogenesisTranscriptomeOxidation-ReductionNeoplasm TransplantationResearch Article
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