Search results for "DPH"

showing 10 items of 361 documents

Neutrophil Extracellular Traps as a Drug Target to Counteract Chronic and Acute Inflammation

2019

Neutrophil extracellular traps (NET), extruded decondensated chromatin entangled with neutrophil proteases, have been first identified in neutrophils stimulated with bacteria or phorbol myristate acetate (PMA) via activation of NADPH oxidase and the generation of reactive oxygen species. Although the first findings demonstrated the beneficial role of NET formation by trapping the bacteria and limiting their dissemination, numerous studies in the recent decade revealed the multifunctional aspects of NET formation which manifests itself not only in the context of anti-microbial effect but also as a pathological trigger. Uncontrolled and exaggerated NET formation or inability to digest and rem…

ProteasesNeutrophilsPharmaceutical ScienceInflammationExtracellular TrapsmedicineHumansMolecular Targeted TherapyInflammationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyNADPH OxidasesNeutrophil extracellular trapsChromatinCell biologyHistonechemistryAcute DiseaseChronic Diseasebiology.proteinSignal transductionmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionSignal TransductionBiotechnologyCurrent Pharmaceutical Biotechnology
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Missense mutations of dual oxidase 2 (DUOX2) implicated in congenital hypothyroidism have impaired trafficking in cells reconstituted with DUOX2 matu…

2007

Abstract Dual oxidase 2 (DUOX2), a reduced NAD phosphate:O2 oxidoreductase flavoprotein, is a component of the thyrocyte H2O2 generator required for hormone synthesis at the apical plasma membrane. We recently identified a specific DUOX2 maturation factor (DUOXA2) that is necessary and sufficient for expression of functional DUOX2 in mammalian cell lines. We have now used a DUOXA2 reconstituted system to provide the first characterization of natural DUOX2 missense variants (Q36H, R376W, D506N) at the molecular level, analyzing their impact on H2O2 generation, trafficking, stability, folding, and DUOXA2 interaction. The Q36H and R376W mutations completely prevent routing of DUOX2 to the cell…

Protein FoldingMutantMutation MissenseBiologyEndoplasmic ReticulumCell membranesymbols.namesakeEndocrinologyMutant proteinPolysaccharidesCalnexinmedicineCongenital HypothyroidismAnimalsHumansMolecular BiologyCells CulturedFlavoproteinsOxidative foldingEndoplasmic reticulumCell MembraneMembrane ProteinsNADPH OxidasesDual oxidase 2General MedicineHydrogen PeroxideGolgi apparatusDual OxidasesRatsProtein Transportmedicine.anatomical_structureMannosyl-Glycoprotein Endo-beta-N-AcetylglucosaminidaseBiochemistrysymbolsOxidation-ReductionMolecular endocrinology (Baltimore, Md.)
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Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

2012

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX3CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX3CL1 expression. Neutralisation of CX3CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interferi…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyEndotheliumPeripheral blood mononuclear cellMiceInternal medicineCX3CR1Cell AdhesionMedicineAnimalsHumansEndothelial dysfunctionRNA Small InterferingCell adhesionNADPH oxidasebiologybusiness.industryChemokine CX3CL1MicrocirculationSmokingNOX4Membrane ProteinsNADPH Oxidasesmedicine.diseaseUp-RegulationEndothelial stem cellmedicine.anatomical_structureEndocrinologyNADPH Oxidase 5Immunologybiology.proteinEndothelium VascularbusinessThorax
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Synthesis of pyrido[2,1-a]isoquinolin-4-ones and oxazino[2,3-a]isoquinolin-4-ones: New inhibitors of mitochondrial respiratory chain

2013

International audience; Benzo[a]quinolizine is an important heterocyclic framework that can be found in numerous bioactive compounds. The general scheme for the synthesis of these compounds was based on the preparation of the appropriate dihydroisoquinolines by Bischler-Napieralski cyclization with good yields, followed by the Pemberton method to form the oxazinones or pyridones derivatives via acyl-ketene imine cyclocondensation. All the synthesized compounds were assayed in vitro for their ability to inhibit mitochondrial respiratory chain. Most of the tested compounds were able to inhibit the integrated electron transfer chain, measured as NADH oxidation, which includes complexes I, III …

PyridonesStereochemistryImine010402 general chemistryRing (chemistry)01 natural sciencesMitochondria HeartElectron TransportStructure-Activity Relationshipchemistry.chemical_compoundMultienzyme ComplexesFuranOxazinesDrug DiscoveryAnimalsNADH NADPH OxidoreductasesCytotoxicityPharmacologyDose-Response Relationship DrugMolecular Structure[CHIM.ORGA]Chemical Sciences/Organic chemistry010405 organic chemistryOrganic ChemistryQuinolizineBiological activityGeneral MedicineIsoquinolinesElectron transport chain3. Good health0104 chemical sciencesMitochondrial respiratory chainchemistryCattleEuropean Journal of Medicinal Chemistry
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Inhibition of Rac1 GTPase Decreases Vascular Oxidative Stress, Improves Endothelial Function, and Attenuates Atherosclerosis Development in Mice

2021

Aims: Oxidative stress and inflammation contribute to atherogenesis. Rac1 GTPase regulates pro-oxidant NADPH oxidase activity, reactive oxygen species (ROS) formation, actin cytoskeleton organization and monocyte adhesion. We investigated the vascular effects of pharmacological inhibition of Rac1 GTPase in mice.Methods and Results: We treated wild-type and apolipoprotein E-deficient (ApoE−/−) mice with Clostridium sordellii lethal toxin (LT), a Rac1 inhibitor, and assessed vascular oxidative stress, expression and activity of involved proteins, endothelial function, macrophage infiltration, and atherosclerosis development. LT-treated wild-type mice displayed decreased vascular NADPH oxidase…

RHOAInflammationVascular permeabilityfree radicalsPharmacologyCardiovascular Medicinemedicine.disease_causeActin cytoskeleton organizationendothelial functionmedicineoxidative stressDiseases of the circulatory (Cardiovascular) systemddc:610Endothelial dysfunctionOriginal Researchchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseGTPasesbiologymedicine.diseasechemistryatherosclerosis endothelial function oxidative stress free radicals Rac1 GTPasesRC666-701biology.proteinmedicine.symptomatherosclerosisCardiology and Cardiovascular MedicineOxidative stressRac1Frontiers in Cardiovascular Medicine
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Factors affecting the amount and the mode of merocyanine 540 binding to the membrane of human erythrocytes. A comparison with the binding to leukemia…

1995

Abstract In the presence of albumin Merocyanine 540 (MC540) exhibits a very limited binding to the outer surface of the membrane of normal erythrocytes, whereas pronounced binding is observed to leukemia cells. To find out whether this difference is due to differences in the composition or structural organization of the cell membrane we analyzed effects of a number of covalent and non-covalent perturbations of the red cell membrane on the binding and fluorescence characteristics of membrane-bound MC540. It is shown that exposure of the cells to cationic chlorpromazine, neuraminidase or photodynamic treatment with AlPcS 4 as sensitizer caused a limited increase (30–50%) of MC540 binding, tog…

Radiation-Sensitizing AgentsTMA-DPHHot TemperatureIndolesBSALightChlorpromazineLipid BilayersBiophysicsPhospholipidNeuraminidaseQuantum yieldPyrimidinonesBiochemistryCell membranechemistry.chemical_compoundt-BuOOHOrganometallic CompoundsTumor Cells CulturedmedicineMerocyanine 540HumansPBSCell MembraneErythrocyte MembraneMembrane structureCell Biologymedicine.diseasePEGFluorescenceDIDSLeukemiaLeukemia cellAlPcS4CholesterolSpectrometry FluorescenceMembranemedicine.anatomical_structureBNML cellsBiochemistrychemistryLeukemia MyeloidCovalent bondBiophysicsMC540Biochimica et Biophysica Acta (BBA) - Biomembranes
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Short-Time Ocular Ischemia Induces Vascular Endothelial Dysfunction and Ganglion Cell Loss in the Pig Retina

2019

Visual impairment and blindness are often caused by retinal ischemia-reperfusion (I/R) injury. We aimed to characterize a new model of I/R in pigs, in which the intraocular pathways were not manipulated by invasive methods on the ocular system. After 12 min of ischemia followed by 20 h of reperfusion, reactivity of retinal arterioles was measured in vitro by video microscopy. Dihydroethidium (DHE) staining, qPCR, immunohistochemistry, quantification of neurons in the retinal ganglion cell layer, and histological examination was performed. Retinal arterioles of I/R-treated pigs displayed marked attenuation in response to the endothelium-dependent vasodilator, bradykinin, compared to sham-tre…

Retinal Ganglion CellsVascular Endothelial Growth Factor A0301 basic medicinePathologySwineNitric Oxide Synthase Type IIVasodilationendothelial dysfunctionlcsh:Chemistrychemistry.chemical_compound0302 clinical medicineIschemiaEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyGeneral MedicineComputer Science ApplicationsArteriolesmedicine.anatomical_structureRetinal ganglion cellReperfusion InjuryNADPH Oxidase 2medicine.medical_specialtyEndotheliumRetinal ArteryI/R injuryIschemiaretinal arteriolesBradykininRetinal ganglionRetinaArticleCatalysisganglion cell lossInorganic Chemistry03 medical and health sciencesmedicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyRetinabusiness.industryOrganic ChemistryRetinalHypoxia-Inducible Factor 1 alpha Subunitmedicine.disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometryEndothelium VascularReactive Oxygen SpeciesbusinessInternational Journal of Molecular Sciences
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Pharmacological prevention of eNOS uncoupling.

2013

Under physiological conditions, nitric oxide (NO) is produced in the vasculature mainly by the endothelial NO synthase (eNOS). This endothelium-derived NO is a protective molecule with antihypertensive, antithrombotic and anti-atherosclerotic properties. Cardiovascular risk factors such as hypertension, hypercholesterolemia, cigarette smoking and diabetes mellitus induce oxidative stress mostly by stimulation of the NADPH oxidase. Overproduction of reactive oxygen species leads to oxidation of tetrahydrobiopterin (BH4), the essential cofactor of eNOS. In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide- producing enzyme. Consequently, NO …

SepiapterinNitric Oxide Synthase Type IIImedicine.drug_classPharmacologymedicine.disease_causeNitric OxideRenin inhibitorNitric oxidechemistry.chemical_compoundEnosDrug DiscoverymedicineHumansPharmacologyNADPH oxidasebiologyEndothelial CellsTetrahydrobiopterinAliskirenbiology.organism_classificationOxidative StresschemistryCardiovascular Diseasesbiology.proteinReactive Oxygen SpeciesOxidative stressmedicine.drugCurrent pharmaceutical design
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Downregulation of myogenic microRNAs in sub-chronic but not in sub-acute model of daunorubicin-induced cardiomyopathy

2016

Cardiac muscle-related microRNAs play important roles in cardiac development and disease by translational silencing of mRNAs, the dominant mechanism of microRNA action. To test whether they could be involved in daunorubicin-associated cardiomyopathy (DACM), we determined expression patterns of myomiRs in two distinct models of DACM. We used 10–12 weeks old male Wistar rats. In the sub-acute model, rats were administered with six doses of daunorubicin (DAU-A, 3 mg/kg, i.p., every 48 h). Rats were sacrificed two days after the last dose. In the sub-chronic model, anaesthetized rats were administered a single dose of daunorubicin (15 mg/kg, i.v., DAU-C). Age-matched controls (CON) receive…

Settore BIO/17 - IstologiaMale0301 basic medicinemedicine.medical_specialtyAnthracyclineCardiomyopathyDaunorubicinClinical BiochemistryCardiomyopathyDown-RegulationMuscle ProteinsAnthracyclineBiology03 medical and health sciencesDownregulation and upregulationInternal medicineGene expressionmedicineAnimalsRats WistarMolecular BiologyNADPH oxidaseNADPH oxidaseDaunorubicinMyosin heavy chain isoformMicroRNACell BiologyGeneral Medicinemedicine.diseaseRatsDisease Models AnimalMicroRNAs030104 developmental biologyEndocrinologybiology.proteinMYH7Gene expressionMYH6Cardiomyopathiesmedicine.drugMolecular and Cellular Biochemistry
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Environmental Noise and the Cardiovascular System

2018

Abstract Noise has been found associated with annoyance, stress, sleep disturbance, and impaired cognitive performance. Furthermore, epidemiological studies have found that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, heart failure, and stroke. Observational and translational studies indicate that especially nighttime noise increases levels of stress hormones and vascular oxidative stress, which may lead to endothelial dysfunction and arterial hypertension. Novel experimental studies found aircraft noise to be associated with oxidative stress–induced vascular damage, mediated by activation of the NADPH oxidase, uncoupling of …

Sleep Wake Disordersmedicine.medical_specialtyBlood Pressure030204 cardiovascular system & hematology010501 environmental sciencesmedicine.disease_cause01 natural sciencesTranscriptome03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicinemedicineAnimalsHumansMyocardial infarctionEndothelial dysfunctionStroke0105 earth and related environmental sciencesNADPH oxidasebiologybusiness.industryEnvironmental Exposuremedicine.diseaseOxidative StressCardiovascular DiseasesHeart failurebiology.proteinCardiologyCardiology and Cardiovascular MedicinebusinessNoiseOxidative stressHormone
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