Search results for " Type II"

showing 10 items of 542 documents

Highly efficient liposome-mediated gene transfer of inducible nitric oxide synthase in vivo and in vitro in vascular smooth muscle cells.

2000

Objective: The efficient introduction of regulatory genes into vascular smooth muscle cells (SMCs) is one of the most promising options for gene therapy of cardiovascular diseases. Cationic liposome-mediated gene transfer may become a favorable transfection technique with regard to patient’s safety for in vivo administration. However, this method until now has its limitation in a low transfection efficiency. Therefore, the present study was designed to improve cationic liposome-mediated transfection of rabbit vascular SMCs in vitro and in vivo, in order to enhance transfection efficiency and present an optimized system which may offer a potential therapeutic benefit for in vivo application.…

LipopolysaccharidesMalePathologymedicine.medical_specialtyVascular smooth musclePhysiologyTransgeneGenetic enhancementBlotting WesternGenetic VectorsGene ExpressionNitric Oxide Synthase Type IIApoptosisCoronary DiseaseBiologyMuscle Smooth VascularIn vivoPhysiology (medical)Culture TechniquesmedicineCell AdhesionAnimalsHumansRegulator geneReporter geneReverse Transcriptase Polymerase Chain ReactionGenetic transferGene Transfer TechniquesTransfectionGenetic TherapyFlow CytometryCell biologyRabbitsNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell DivisionCardiovascular research
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Beta-MSH inhibits brain inflammation via MC(3)/(4) receptors and impaired NF-kappaB signaling.

2005

The anti-inflammatory effects of melanocortin peptides have been demonstrated in different inflammation models. This is the first report describing the molecular mechanisms for the beta-MSH-induced suppression of bacterial lipopolisaccharide (LPS)-caused brain inflammation. We found that beta-MSH suppresses LPS-induced nuclear translocation of the transcription factor NF-kappaB, and inhibits the expression of inducible nitric oxide synthase, and the following nitric oxide overproduction in the brain, in vivo. Moreover, administering the preferentially MC(4) receptor selective antagonist HS014 blocked completely these effects, suggesting a tentative MC(4) receptor mediated mechanism of actio…

LipopolysaccharidesMalemedicine.medical_specialtyImmunologyNitric Oxide Synthase Type IIInflammationElectrophoretic Mobility Shift AssayNitric OxidePeptides CyclicNitric oxidechemistry.chemical_compoundMiceInternal medicinebeta-MSHmedicineImmunology and AllergyAnimalsDrug InteractionsReceptorBrain ChemistryMice Inbred ICRbiologyDose-Response Relationship DrugImmunochemistryElectron Spin Resonance SpectroscopyNF-kappa BNF-κBHormonesCell biologyNitric oxide synthaseDisease Models AnimalEndocrinologyNeurologyMechanism of actionchemistrybiology.proteinEncephalitisReceptor Melanocortin Type 4Neurology (clinical)medicine.symptomMelanocortinSignal transductionhormones hormone substitutes and hormone antagonistsReceptor Melanocortin Type 3Signal TransductionJournal of neuroimmunology
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ttCH, a selective inhibitor of inducible nitric oxide synthase expression with antiarthritic properties

2003

In a previous work, we investigated the effects of a series of dimethoxy- and trimethoxychalcone derivatives, with various patterns of fluorination, on nitric oxide production in lipopolysaccharide-stimulated murine RAW 264.7 cells. The present study was designed to determine if 2,4,6-trimethoxy-2'-trifluoromethylchalcone (ttCH) could modulate the production of nitric oxide (NO) and/or prostaglandins in vitro and in vivo. On the mouse macrophage cell line RAW 264.7, ttCH inhibited dose-dependently NO and prostaglandin E(2) production, with IC(50) in the micromolar range. This compound had no direct inhibitory effect on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities. …

LipopolysaccharidesMalemedicine.medical_treatmentBlotting WesternNitric Oxide Synthase Type IIPharmacologyCarrageenanNitric OxideDinoprostoneCell LineNitric oxideMicechemistry.chemical_compoundIn vivomedicineAnimalsEdemaEnzyme InhibitorsProstaglandin E2InflammationPharmacologybiologyChemistryMacrophagesAnti-Inflammatory Agents Non-SteroidalBiological activityArthritis ExperimentalHindlimbRatsCarrageenanIsoenzymesRadiographyNitric oxide synthaseMechanism of actionBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred Lewbiology.proteinFemaleNitric Oxide Synthasemedicine.symptomProstaglandin Emedicine.drugEuropean Journal of Pharmacology
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Interaction of dicaffeoylquinic derivatives with peroxynitrite and other reactive nitrogen species.

2008

Plant phenolic antioxidants, among them catechins and hydroxycinnamoyl conjugates, constitute a well defined class of inhibitors of reactive nitrogen species (RNS). To gain deeper insight in this field, we examined the effects of 3,5-di-O-caffeoylquinic acid (DCA), its methyl ester (DCE) and epigallocatechin gallate (EGCG) in nitrative and oxidative processes. These compounds were found to be strong inhibitors of the nitration of tyrosine residues induced by ONOO- in bovine seroalbumin, with their IC50 values (10-40 microM) notably decreasing in the presence of bicarbonate. When studied on the intracellular protein tyrosine nitration induced by ONOO- in cultured murine fibroblasts as well a…

LipopolysaccharidesNeutrophilsBicarbonateBiophysicsQuinic AcidNitric Oxide Synthase Type IIEpigallocatechin gallateBiochemistryCatechinNitric oxidechemistry.chemical_compoundInhibitory Concentration 50MiceNitrationPeroxynitrous AcidAnimalsHumansTyrosineMolecular BiologyReactive nitrogen speciesNitritesNitratesNitrotyrosineMacrophagesSerum Albumin BovineFibroblastsReactive Nitrogen SpeciesStimulation ChemicalBicarbonateschemistryBiochemistryTetradecanoylphorbol AcetateTyrosineCattleOxidation-ReductionPeroxynitriteArchives of biochemistry and biophysics
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Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene

2001

22 pages, 7 figures, 1 table.

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharideTransgeneBlotting WesternNitric Oxide Synthase Type IIApoptosisGalactosamineMice TransgenicLipopolysaccharideNitric OxideBiochemistryLiver cellsProinflammatory cytokineNitric oxidechemistry.chemical_compoundMiceInternal medicineGeneticsmedicineAnimalsTransgenesPromoter Regions GeneticMolecular BiologyLiver injurybiologyTumor Necrosis Factor-alphaNF-kappa BNitric oxide synthase 2medicine.diseaseEndotoxinsEndocrinologychemistryLiverbiology.proteinTumor necrosis factor alphaNitric Oxide SynthasePhosphoenolpyruvate carboxykinaseFood DeprivationBiotechnologyInterleukin-1
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Plasma Pro-C3 (N-terminal type III collagen propeptide) predicts fibrosis progression in patients with chronic hepatitis C.

2014

BACKGROUND & AIMS: Fibrogenesis results in release of certain extracellular matrix protein fragments into the circulation. We evaluated the diagnostic and prognostic performance of two novel serological markers, the precisely cleaved N-terminal propeptide of type III collagen (Pro-C3) and a peptide of helical collagen type III degradation (C3M), in chronic hepatitis C (CHC) patients. METHOD: Pro-C3 and C3M were measured by ELISA in plasma from CHC patients (n = 194) from a prior phase II antifibrotic trial (NCT00244751). Plasma samples and paired liver biopsies were obtained at baseline and after 1-year. Patients were stratified according to Ishak stages 2-4. Internal cross-validation w…

Liver CirrhosisCollagen Type III/bloodPathologymedicine.medical_specialtyLiver fibrosisEnzyme-Linked Immunosorbent AssayGastroenterologySerologyExtracellular matrixCohort StudiesCollagen Type IIIFibrosisPredictive Value of TestsInternal medicinemedicineHumansStage (cooking)Hepatologybusiness.industryFibroTestBiomarkerHepatitis C ChronicPrognosismedicine.diseaseCollagen Type IIIPredictive value of testsMultivariate AnalysisExtracellular matrix remodellingDisease ProgressionBiomarker (medicine)Hepatitis C Chronic/bloodbusinessLiver Cirrhosis/diagnosisBiomarkers/bloodBiomarkersLiver international : official journal of the International Association for the Study of the Liver
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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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Fibrogenesis assessed by serological type III collagen formation identifies patients with progressive liver fibrosis and responders to a potential an…

2016

There are no approved treatments for liver fibrosis. To aid development of antifibrotic therapies, noninvasive biomarkers that can identify patients with progressive fibrosis and that permit monitoring of the response to antifibrotic therapy are much needed. Samples from a phase II antifibrotic trial of the glitazone farglitazar in patients with advanced hepatitis C, with matched follow-up liver biopsies, and from a phase III study of balaglitazone in patients with late-stage Type 2 diabetes (BALLET study) were analyzed for serological Pro-C3 levels in conjunction with other disease parameters. In the farglitazar study, a predefined cutoff value for Pro-C3 as a selection criterion led to t…

Liver CirrhosisMale0301 basic medicineNonalcoholic steatohepatitisPathologymedicine.medical_specialtyPhysiologyLiver fibrosisType 2 diabetesSerology03 medical and health sciencesCollagen formation0302 clinical medicineFibrosisSerum biomarkersPhysiology (medical)Journal ArticlemedicineHumansOxazolesType III collagenHepatologybusiness.industryPatient SelectionGastroenterologyMiddle Agedmedicine.disease3. Good healthCollagen Type III030104 developmental biologyQuinazolinesTyrosineFemaleThiazolidinediones030211 gastroenterology & hepatologybusinessBiomarkersAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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The Late Endosomal Adaptor Molecule p14 (LAMTOR2) Regulates TGFβ1-Mediated Homeostasis of Langerhans Cells

2014

Langerhans cells (LCs), a sub-population of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin (mTOR) activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling regulated kinase (ERK) and the mTOR cascade. In previous work, we demonstrated that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In this study, we extended our analysis on p14 deficiency specifically in LCs. Langerin-…

MAPK/ERK pathwayMaleMAP Kinase Signaling SystemReceptor Transforming Growth Factor-beta Type IDown-Regulationchemical and pharmacologic phenomenaEndosomesDermatologyBiologyProtein Serine-Threonine KinasesDermatitis ContactBiochemistryArticleImmune toleranceImmunophenotypingTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementImmune ToleranceAnimalsHomeostasisProtein kinase AMolecular BiologyPI3K/AKT/mTOR pathway030304 developmental biologySkin0303 health sciencesintegumentary systemKinaseReceptor Transforming Growth Factor-beta Type IIPeripheral toleranceProteinshemic and immune systemsCell BiologyMice Mutant StrainsCell biologyCD11c AntigenLangerhans CellsFemaleReceptors Transforming Growth Factor beta030215 immunologyTransforming growth factorJournal of Investigative Dermatology
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Exercise and hormesis: activation of cellular antioxidant signaling pathway.

2006

Contraction-induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) kappaB and mitogen-activated protein kinases (MAPKs) are the major oxidative stress-sensitive signal transduction pathways in mammalian tissues. Activation of NF-kappaB signaling cascade has been shown to enhance the gene expression of important enzymes, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). MAPK activations are involved in a variety of cellular functions including growth, proliferation, and adap…

MAPK/ERK pathwayNitric Oxide Synthase Type IIBiologymedicine.disease_causeModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAntioxidantsGene Expression Regulation EnzymologicHistory and Philosophy of ScienceDownregulation and upregulationPhysical Conditioning AnimalmedicineAnimalsMuscle Skeletalchemistry.chemical_classificationReactive oxygen speciesKinaseSuperoxide DismutaseGeneral NeuroscienceNF-kappa BSkeletal muscleCell biologyMitochondriaNitric oxide synthaseEnzyme ActivationKineticsmedicine.anatomical_structurechemistrybiology.proteinSignal transductionMitogen-Activated Protein KinasesReactive Oxygen SpeciesOxidative stressSignal TransductionAnnals of the New York Academy of Sciences
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