Search results for "type II"

showing 10 items of 607 documents

Dexamethasone lacks effect on blood pressure in mice with a disrupted endothelial NO synthase gene.

2003

Cushing's syndrome and systemic administration of glucocorticoids are associated with hypertension, but the underlying molecular mechanism is only partially understood. We have shown previously that dexamethasone downregulates the expression of the endothelial NO synthase (eNOS) gene in human endothelial cells and in the rat and that this may contribute to the blood pressure-raising effect of the steroid [Proc. Natl. Acad. Sci. USA 96 (1999) 13357]. In the current communication, we demonstrated that dexamethasone increased mean arterial blood pressure in wild-type C-57 Bl6 mice (eNOS+/+ mice), but had no effect on blood pressure in mice with a disrupted eNOS gene (eNOS-/- mice) derived from…

Cancer Researchmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryNitric Oxide Synthase Type IIBlood PressureBiologyKidneyNitric OxideBiochemistryDexamethasoneMiceDownregulation and upregulationEnosInternal medicinemedicineAnimalsEnzyme InhibitorsDexamethasoneMice KnockoutKidneyMyocardiumNitric Oxide Synthase Type IIIbiology.organism_classificationmedicine.anatomical_structureBlood pressureEndocrinologyLiverPharmacogeneticsHypertensionSystemic administrationNitric Oxide Synthasemedicine.drugNitric oxide : biology and chemistry
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Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs.

2002

In many types of cardiovascular pathophysiology such as hypercholesterolemia and atherosclerosis, diabetes, cigarette smoking, or hypertension (with its sequelae stroke and heart failure) the expression of endothelial NO synthase (eNOS) is altered. Both up- and downregulation of eNOS have been observed, depending on the underlying disease. When eNOS is upregulated, the upregulation is often futile and goes along with a reduction in bioactive NO. This is due to an increased production of superoxide generated by NAD(P)H oxidase and by an uncoupled eNOS. A number of drugs with favorable effects on cardiovascular disease upregulate eNOS expression. The resulting increase in vascular NO producti…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryPharmacologymedicine.disease_causeNitric OxideBiochemistrychemistry.chemical_compoundDownregulation and upregulationMetabolic DiseasesEnosInternal medicineDiabetes mellitusmedicineAnimalsHumansEndothelial dysfunctionAngiotensin II receptor type 1biologybusiness.industrySuperoxidemedicine.diseasebiology.organism_classificationEndocrinologychemistryGene Expression RegulationErythropoietinCardiovascular DiseasesNitric Oxide SynthasebusinessOxidative stressmedicine.drugNitric oxide : biology and chemistry
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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Local transient myocardial liposomal gene transfer of inducible nitric oxide synthase does not aggravate myocardial function and fibrosis and leads t…

2010

Microcirculation (2010) 17, 69–78. doi: 10.1111/j.1549-8719.2010.00002.x Abstract Background:  This study was designed to explore the effect of transient inducible nitric oxide synthase (iNOS) overexpression via cationic liposome-mediated gene transfer on cardiac function, fibrosis, and microvascular perfusion in a porcine model of chronic ischemia. Methods and Results:  Chronic myocardial ischemia was induced using a minimally invasive model in 23 landrace pigs. Upon demonstration of heart failure, 10 animals were treated with liposome-mediated iNOS-gene-transfer by local intramyocardial injection and 13 animals received a sham procedure to serve as control. The efficacy of this iNOS-gene-…

Cardiac function curveMalemedicine.medical_specialtyPhysiologySus scrofaIschemiaMyocardial IschemiaGene ExpressionNitric Oxide Synthase Type IINitric OxideVentricular Function LeftNeovascularizationFibrosisPhysiology (medical)Internal medicinemedicineAnimalsHumansMolecular BiologyEjection fractionbiologyNeovascularization Pathologicbusiness.industryMyocardiumGene Transfer Techniquesmedicine.diseaseFibrosisMagnetic Resonance ImagingRecombinant ProteinsNitric oxide synthaseArteriolesHeart failureLiposomesCardiologybiology.proteinDobutamineFemalemedicine.symptomCardiology and Cardiovascular Medicinebusinessmedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Mechanisms of Increased Vascular Superoxide Production in an Experimental Model of Idiopathic Dilated Cardiomyopathy

2005

Objective— In the present study, we sought to identify mechanisms underlying increased oxidative stress in vascular tissue in an experimental animal model of chronic congestive heart failure (CHF). Methods and Results— Superoxide and nitric oxide (NO) was measured in vessels from cardiomyopathic hamsters (CHF hamsters) and golden Syrian hamsters. We also determined expression of endothelial nitric oxide synthase (NOSIII), the soluble guanylyl cyclase, the cGMP-dependent kinase, and the NADPH oxidase. To analyze the contribution of the renin-angiotensin system to oxidative stress, CHF hamsters were treated with the angiotensin-converting enzyme inhibitor captopril for 200 days (120 mg · kg …

Cardiomyopathy DilatedMalemedicine.medical_specialtyCaptoprilNitric Oxide Synthase Type IIIReceptors Cytoplasmic and NuclearAngiotensin-Converting Enzyme InhibitorsNitric Oxidemedicine.disease_causeNitric oxideRenin-Angiotensin Systemchemistry.chemical_compoundSoluble Guanylyl CyclaseSuperoxidesCricetinaeInternal medicineIdiopathic dilated cardiomyopathymedicineAnimalsHeart FailureNADPH oxidaseMesocricetusbiologybusiness.industrySuperoxideMyocardiumBody WeightMicrofilament ProteinsNADPH OxidasesCaptoprilOrgan SizePhosphoproteinsDisease Models AnimalOxidative StressEndocrinologychemistryGuanylate CyclaseACE inhibitorbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessSoluble guanylyl cyclaseCell Adhesion MoleculesOxidative stressmedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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Polyvascular subclinical atherosclerosis in familial hypercholesterolemia: The role of cholesterol burden and gender

2019

International audience; BACKGROUND AND AIM:Heterozygous familial hypercholesterolemia (HeFH) is a genetic disease characterized by a heterogeneous phenotype. The assessment of cardiovascular (CV) risk is challenging for HeFH. Cholesterol burden (CB) allows to estimate the lifelong exposure to high levels of cholesterol. The aim of this study was to analyze the distribution of subclinical atherosclerosis and the relationship between atherosclerosis and the CB in a sample of HeFH patients, focusing on sex-related differences.METHODS AND RESULTS:154 asymptomatic HeFH subjects underwent coronary-artery-calcium score (CACs) and Doppler ultrasound of carotid and femoral arteries. Yearly lipid pro…

Carotid Artery DiseasesMaleCarotid atherosclerosisPeripheral arterial atherosclerosisTime Factors[SDV]Life Sciences [q-bio]Endocrinology Diabetes and MetabolismMedicine (miscellaneous)Coronary Artery DiseaseDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologySeverity of Illness Indexchemistry.chemical_compound0302 clinical medicineRisk FactorsAtherosclerosis; Calcium score; Cardiovascular disease; Cardiovascular risk; Cholesterol burden; Coronary artery calcium; Familial hypercholesterolemia; Peripheral arterial atherosclerosis; Adult; Aged; Asymptomatic Diseases; Biomarkers; Carotid Artery Diseases; Cholesterol; Coronary Artery Disease; Cross-Sectional Studies; Female; Femoral Artery; Genetic Predisposition to Disease; Humans; Hyperlipoproteinemia Type II; Male; Middle Aged; Paris; Peripheral Arterial Disease; Phenotype; Prevalence; Prognosis; Risk Assessment; Risk Factors; Severity of Illness Index; Sex Factors; Time Factors; Young AdultPrevalenceMedicineNutrition and Dietetics[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedPrognosisCardiovascular diseaseCalcium score3. Good healthFemoral ArteryCholesterol burdenCholesterolPhenotypeAtherosclerosiCardiologyPopulation studyFemalemedicine.symptomCardiology and Cardiovascular MedicineAdultParismedicine.medical_specialtyFamilial hypercholesterolemia030209 endocrinology & metabolismRisk AssessmentAsymptomaticCoronary artery calciumHigh cholesterolHyperlipoproteinemia Type IIPeripheral Arterial DiseaseYoung Adult03 medical and health sciencesSex Factors[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineHumansGenetic Predisposition to DiseaseAgedbusiness.industryCholesterolAtherosclerosismedicine.diseaseCardiovascular riskCross-Sectional StudieschemistrySubclinical atherosclerosisAsymptomatic DiseasesbusinessBiomarkers
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In vitro 30 nm silver nanoparticles promote chondrogenesis of human mesenchymal stem cells

2015

Silver nanoparticles (Ag NPs) are one of the most widely used products in nano-medicine due to their broad-spectrum antimicrobial activity. In tissue engineering, Ag NPs are often incorporated as antibacterial agents in scaffolds, which are subsequently loaded with human bone marrow-derived mesenchymal stem cells (hMSCs). In this study, we investigated the effect of Ag NPs on chondrogenesis of hMSCs. The synthesized Ag NPs were spherical in shape, with a mean diameter of ∼30 nm. After 24 h exposure, Ag NPs were taken up into hMSCs and mainly distributed in the cytoplasm, the nucleus and different sized vesicles. We examined the chondrogenesis through several methods, including glycosaminogl…

Cartilage oligomeric matrix proteinbiologyChemistryGeneral Chemical EngineeringMesenchymal stem cellType II collagenGeneral ChemistryChondrogenesisSilver nanoparticleGlycosaminoglycanTissue engineeringBiophysicsbiology.proteinAggrecanRSC Advances
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Haem oxygenase-1 regulates catabolic and anabolic processes in osteoarthritic chondrocytes

2007

Pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro-inflammatory cytokines such as interleukin-1β (IL-1β) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase-1 (HO-1) is down-regulated by pro-inflammatory cytokines and up-regulated by IL-10 in OA chondrocytes. The aim of this study was to determine whether HO-1 can modify the catabolic effects of IL-1β in OA cartilage and chondrocytes. Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1β in OA …

Cartilage ArticularMaleMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaProtoporphyrinsMatrix metalloproteinaseChondrocytePathology and Forensic MedicineExtracellular matrixChondrocytesmedicineExtracellularHumansInsulin-Like Growth Factor ICollagen Type IICells CulturedAggrecanAgedbiologyChemistryCartilageGrowth factorOsteoarthritis KneeMatrix MetalloproteinasesCell biologymedicine.anatomical_structureProteoglycanImmunologybiology.proteinFemaleProteoglycansHeme Oxygenase-1The Journal of Pathology
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Haem oxygenase-1 induction reverses the actions of interleukin-1β on hypoxia-inducible transcription factors and human chondrocyte metabolism in hypo…

2013

HO-1 (haem oxygenase-1) catalyses the degradation of haem and possesses anti-inflammatory and cytoprotective properties. The role of inflammatory mediators in the pathogenesis of OA (osteoarthritis) is becoming increasingly appreciated. In the present study, we investigated the effects of HO-1 induction in OA and healthy HACs (human articular chondrocytes) in response to inflammatory cytokine IL-1 β (interleukin-1β) under hypoxic conditions. Hypoxia was investigated as it is a more physiological condition of the avascular cartilage. Hypoxic signalling is mediated by HIFs (hypoxia-inducible factors), of which there are two main isoforms, HIF-1α and HIF-2α. Normal and OA chondrocytes were sti…

Cartilage ArticularMaleSmall interfering RNAmedicine.medical_treatmentInterleukin-1betaBiologyMatrix metalloproteinaseChondrocytesOsteoarthritisBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaCollagen Type IITranscription factorAgedTumor Necrosis Factor-alphaCatabolismSOX9 Transcription FactorGeneral MedicineMiddle AgedHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCOPPMatrix MetalloproteinasesCell biologyCytokineBiochemistryFemaleTumor necrosis factor alphamedicine.symptomHeme Oxygenase-1Clinical Science
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