Search results for "type II"

showing 10 items of 607 documents

Endothelial Nitric Oxide Synthase Regulates T Cell Receptor Signaling at the Immunological Synapse

2006

The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence…

Interleukin 2CD3 ComplexNitric Oxide Synthase Type IIIT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsGolgi ApparatusBiologyLymphocyte ActivationNitric OxideNitric oxideImmunological synapseInterferon-gammaMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAntigenmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellAntigensMOLIMMUNOAntigen-presenting cellNitric Oxide Synthase Type IIIMice Mutant StrainsCell biologyInfectious DiseaseschemistryInterleukin-2CalciumSignal transductionSignal Transductionmedicine.drugImmunity
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Distribution and kinetics of superantigen-induced cytokine gene expression in mouse spleen.

1993

The polyclonal stimulation of T cells by bacterial superantigens is involved in the pathogenesis of the toxic shock syndrome in certain staphylococcal and streptococcal infections. Here we describe the onset and kinetics of superantigen-induced cytokine production in situ in spleens of normal BALB/c mice monitored at the level of cytokine mRNA expression by in situ hybridization. Messenger RNAs for interleukin 2 (IL-2), interferon gamma, and tumor necrosis factors (TNF) alpha and beta were not expressed at detectable levels in spleens of unstimulated animals but became visible already 30 min after intraperitoneal application of 50 micrograms staphylococcal enterotoxin B. All mRNA levels sho…

Interleukin 2LipopolysaccharidesSalmonella typhimuriumStaphylococcus aureusInterferon type IITranscription Geneticmedicine.medical_treatmentT cellT-LymphocytesImmunologyGene ExpressionBiologyEnterotoxinsMiceAldesleukinGene expressionmedicineSuperantigenImmunology and AllergyAnimalsInterferon gammaRNA MessengerIn Situ HybridizationMice Inbred BALB CSuperantigensTumor Necrosis Factor-alphaMacrophagesArticlesMolecular biologyKineticsCytokinemedicine.anatomical_structureCytokinesInterleukin-2Spleenmedicine.drugThe Journal of experimental medicine
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Overview of the current status of familial hypercholesterolaemia care in over 60 countries - The EAS Familial Hypercholesterolaemia Studies Collabora…

2018

PubMed: 30270054

International CooperationMÉTODOS EPIDEMIOLÓGICOS030204 cardiovascular system & hematologyNationwide surveyGlobal HealthHealth Services AccessibilityDoenças Cardio e Cérebro-vascularesMOLECULAR-GENETICS0302 clinical medicineRisk FactorsPrevalenceCARDIOVASCULAR RISK-FACTORS030212 general & internal medicineCooperative BehaviorDEFECTIVE APOLIPOPROTEIN B-100GENERAL-POPULATIONeducation.field_of_studymedicine.diagnostic_testAnticholesteremic AgentsFamilial hypercholesterolaemia; FHSC; Primary dyslipidaemia; Anticholesteremic Agents; Biomarkers; Cholesterol LDL; Cooperative Behavior; Genetic Predisposition to Disease; Health Care Surveys; Health Services Accessibility; Healthcare Disparities; Humans; Hyperlipoproteinemia Type II; Phenotype; Predictive Value of Tests; Prevalence; Risk Factors; Treatment Outcome; Blood Component Removal; Global Health; International CooperationEAS Familial Hypercholesterolaemia Studies Collaboration3. Good healthPREVALENCECholesterolPhenotypeTreatment OutcomeBlood Component RemovalCORONARY-ARTERY-DISEASENATIONWIDE SURVEYCardiology and Cardiovascular MedicineFamilial hypercholesterolaemiamedicine.medical_specialtyCardiovascular risk factorsPopulationLDL-RECEPTOR1102 Cardiovascular Medicine And HaematologyLDLHyperlipoproteinemia Type II03 medical and health sciencesPredictive Value of TestsmedicineHumans:Medicine [Science]Genetic Predisposition to DiseasePrimary dyslipidaemiaHealthcare Disparitiesfhsc; familial hypercholesterolaemia; primary dyslipidaemiaeducationGenetic testingGovernmentPublic healthEAS Familial Hypercholesterolaemia Studies Collaboration (FHSC) InvestigatorsSAFEHEART REGISTRY1103 Clinical SciencesFHSCCholesterol LDLCardiovascular System & HematologyFamily medicineHealth Care Surveys3121 General medicine internal medicine and other clinical medicineCardiovascular System & CardiologyBusinessFOLLOW-UPBiomarkers
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Role of Neutral Amino Acid Transport and Protein Breakdown for Substrate Supply of Nitric Oxide Synthase in Human Endothelial Cells

2003

Endothelial dysfunction is often associated with a relative substrate deficiency of the endothelial nitric oxide synthase (eNOS) in spite of apparently high intracellular arginine concentrations. For a better understanding of the underlying pathophysiological mechanisms, we aimed to characterize the intracellular arginine sources of eNOS. Our previous studies in human endothelial EA.hy926 cells suggested the existence of two arginine pools: pool I can be depleted by extracellular lysine, whereas pool II is not freely exchangeable with the extracellular space, but accessible to eNOS. In this study, we demonstrate that the eNOS accessible pool II is also present in human umbilical vein endoth…

Intracellular FluidUmbilical VeinsNitric Oxide Synthase Type IIIArginineEndotheliumPhysiologyGlutamineArginineTransfectionSubstrate Specificitychemistry.chemical_compoundEnosNeutral amino acid transportCitrullinemedicineAnimalsHumansAmino AcidsCells CulturedbiologyCarcinomaMembrane Transport ProteinsProteinsNitric Oxide Synthase Type IIIBiological Transportbiology.organism_classificationRatsEndothelial stem cellNitric oxide synthaseAmino Acid Transport Systems NeutralAmino Acids Neutralmedicine.anatomical_structureUrinary Bladder NeoplasmsBiochemistrychemistrybiology.proteinCitrullineEndothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineCirculation Research
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Effects of chronic exercise on myocardial refractoriness: a study on isolated rabbit heart

2008

Aim:  To determine whether chronic physical training increases atrial and ventricular refractoriness in isolated rabbit heart. Methods:  Trained rabbits were submitted to a protocol of treadmill running. The electrophysiological parameters of refractoriness investigated in an isolated heart preparation were: (1) atrial effective refractory period (AERP) and atrial functional refractory period and ventricular effective and functional refractory periods (VERP and VFRP) using the extrastimulus technique at four different pacing cycle lengths; (2) the dominant frequency (DF) of ventricular fibrillation (VF). A multi-electrode plaque containing 256 electrodes and a spectral method were used to o…

Isolated Heart Preparationmedicine.medical_specialtyRefractory Period ElectrophysiologicalPhysiologyRefractory periodNitric Oxide Synthase Type IIPhysical exerciseMotor ActivityOrgan Culture TechniquesHeart RatePhysical Conditioning AnimalInternal medicineHeart ratemedicineAnimalsVentricular FunctionLagomorphabiologybusiness.industryMyocardiumHeartChaperonin 60Organ SizeAtrial Functionbiology.organism_classificationmedicine.diseaseSurgeryElectrophysiologyVentricular FibrillationVentricular fibrillationCirculatory systemcardiovascular systemCardiologyRabbitsbusinessActa Physiologica
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Expression of a dominant negative type II TGF-β receptor in mouse skin results in an increase in carcinoma incidence and an acceleration of carcinoma…

1998

The role of Transforming growth factor beta (TGF-beta) in carcinogenesis is complex. There are reports on both tumor inhibition and tumor promotion by TGF-beta. To elucidate the complex role of TGF-beta in epithelial carcinogenesis, we generated transgenic mice overexpressing a dominant negative type II TGF-beta receptor in the basal cell compartment and in follicular cells of the skin. Despite the reduced responsiveness of transgenic keratinocytes to TGF-beta, both proliferation and differentiation were normal in non-irritated epidermis of these transgenic mice. Thus, interruption of signaling of all three isoforms of TGF-beta in basal and follicular cells does not disturb tissue homeostas…

KeratinocytesCancer Researchmedicine.medical_specialtySkin NeoplasmsRatónMice TransgenicProtein Serine-Threonine KinasesBiologyMiceTransforming Growth Factor betaInternal medicineGene expressionGeneticsCarcinomamedicineAnimalsHumansReceptorMolecular BiologyGeneCells CulturedSkinIncidenceIncidence (epidemiology)Receptor Transforming Growth Factor-beta Type IImedicine.diseaseEndocrinologyTumor progressionCarcinoma Squamous CellCancer researchReceptors Transforming Growth Factor betaCell DivisionSignal TransductionTransforming growth factorOncogene
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Processing of procollagen III by meprins: new players in extracellular matrix assembly?

2010

Meprins α and β, a subgroup of zinc metalloproteinases belonging to the astacin family, are known to cleave components of the extracellular matrix, either during physiological remodeling or in pathological situations. In this study we present a new role for meprins in matrix assembly, namely the proteolytic processing of procollagens. Both meprins α and β release the N- and C-propeptides from procollagen III, with such processing events being critical steps in collagen fibril formation. In addition, both meprins cleave procollagen III at exactly the same site as the procollagen C-proteinases, including bone morphogenetic protein-1 (BMP-1) and other members of the tolloid proteinase family. …

Keratinocytesmacromolecular substancesDermatologyMatrix metalloproteinaseCleavage (embryo)BiochemistryBone Morphogenetic Protein 1Substrate SpecificityExtracellular matrix03 medical and health sciencesDermismedicineHumansEnhancerMolecular BiologyCells Cultured030304 developmental biology0303 health sciencesExtracellular Matrix Proteinsintegumentary systemChemistryExtracellular matrix assembly030302 biochemistry & molecular biologyMetalloendopeptidasesCell BiologyDermisFibroblastsFibrosisProcollagen peptidasemedicine.anatomical_structureCollagen Type IIIHEK293 CellsBiochemistryKeloidAstacinThe Journal of investigative dermatology
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Transforming growth factor beta1 T29C gene polymorphism and hypertension: relationship with cardiovascular and renal damage.

2008

Distribution of T29C TGFb1 gene polymorphism was analysed in 260 hypertensive and 134 normotensive subjects. Circulating TGFb1 and procollagen type III levels, microalbuminuria, left ventricular geometry and function were evaluated in all the hypertensives subgrouped according to T29C TGFb1 gene polymorphism. Circulating TGFb1by ELISA technique, procollagen type III by a specific radioimmunoassay, microalbuminuria by radioimmunoassay, left ventricular geometry and function by echocardiography were determined. All groups were comparable for gender, age and sex. Regarding T29C TGFb1 gene polymorphism, prevalence of TC or CC genotypes was significantly (pv0.05) higher in hypertensives than nor…

Key Words: Circulating TGFb1 hypertension left ventricular hypertrophy microalbuminuria procollagen type III TGFb1 gene polymorphism.
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[Apoptosis of human leukemic cells induced by topoisomerase I and II inhibitors].

1996

International audience; Comparison between five human leukemic lines (BV173, HL60, U937, K562, KCL22) suggest that the main determinant of their sensitivity to topoisomerase I (camptothecin) and II (VP-16) inhibitors is their ability to regulate cell cycle progression in response to specific DNA damage, then to die through apoptosis: the more the cells inhibit cell cycle progression, the less sensitive they are. The final pathway of apoptosis induction involves a cytoplasmic signal, active at neutral pH, needing magnesium, sensitive to various protease inhibitors and activated directly by staurosporine. Modulators of intracellular signaling (calcium chelators, calmodulin inhibitors, PKC mod…

Leukemia[SDV]Life Sciences [q-bio]Cell CycleApoptosisCell DifferentiationDNA Neoplasm[SDV.BC]Life Sciences [q-bio]/Cellular BiologyStaurosporine[SDV] Life Sciences [q-bio]AlkaloidsDNA Topoisomerases Type IIDNA Topoisomerases Type ITumor Cells CulturedHumansTopoisomerase II InhibitorsCamptothecinTopoisomerase I Inhibitors[SDV.BC] Life Sciences [q-bio]/Cellular BiologyProtein Kinase CEtoposideSignal Transduction
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Anti-inflammatory effects of annexin-1: stimulation of IL-10 release and inhibition of nitric oxide synthesis.

2003

Annexin-1 (ANX-1) is an anti-inflammatory protein induced by glucocorticoids. Like glucocorticoids, ANX-1 and derived peptides inhibit eicosanoid synthesis, block leukocyte migration and induce apoptosis of inflammatory cells. Cytokines may possess either pro-inflammatory, i.e. interleukin(IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12 or anti-inflammatory properties, i.e. IL-4, IL-10. The experiments described in the present study have been performed to answer the question whether the anti-inflammatory action of ANX-1 may be mediated, at least in part, by the release of IL-10. In macrophage (J774) cell line cultures primed with lipolysaccharide (LPS), recombinant ANX-1 stimulated IL-1…

Leukocyte migrationCell SurvivalImmunologyAnti-Inflammatory AgentsNitric Oxide Synthase Type IINitric OxideNitric oxideCell Linechemistry.chemical_compoundMiceAnnexinImmunology and AllergyAnimalsRNA MessengerEnzyme InhibitorsAnnexin A1PharmacologybiologyReverse Transcriptase Polymerase Chain ReactionMacrophagesInterleukinPeptide FragmentsRecombinant ProteinsCell biologyInterleukin-10Nitric oxide synthasechemistryBiochemistryApoptosisbiology.proteinTumor necrosis factor alphaNitric Oxide SynthaseAnnexin A1International immunopharmacology
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