Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

Dual effect of ceramide on human endothelial cells: induction of oxidative stress and transcriptional upregulation of endothelial nitric oxide syntha…

2002

Background— Generation of the second-messenger molecule ceramide by stimulated sphingomyelinase activity has been implicated in the inflammatory processes contributing to the pathogenesis of atherosclerosis. However, reports of stimulatory effects of ceramide on endothelial NO production in animal models suggest antiatherosclerotic effects of the molecule. Therefore, we investigated long-term effects of ceramide on NO generation in human endothelial cells. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and in HUVEC-derived EA.hy 926 endothelial cells, C6-ceramide ( N -hexanoyl- d -erythro-sphingosine) reduced the generation of bioactive NO (RFL-6 reporter-cell assa…

Transcriptional ActivationCeramideNitric Oxide Synthase Type IIIRNA StabilityBiologyCeramidesNitric OxideUmbilical veinCell Linechemistry.chemical_compoundDownregulation and upregulationEnosPhysiology (medical)Phosphoprotein PhosphatasesHumansEnzyme InhibitorsPromoter Regions GeneticCells CulturedDose-Response Relationship DrugLipid signalingbiology.organism_classificationCell biologyUp-RegulationNitric oxide synthaseEndothelial stem cellKineticsOxidative StressSphingomyelin PhosphodiesteraseBiochemistrychemistrybiology.proteinEndothelium VascularSignal transductionNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCirculation
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Role of reactive oxygen species in the regulation of HIF-1 by prolyl hydroxylase 2 under mild hypoxia

2012

The function and survival of eukaryotic cells depends on a constant and sufficient oxygen supply. Cells recognize and respond to hypoxia by accumulation of the transcription factor hypoxia-inducible factor 1 (HIF-1), composed of an oxygen-sensitive HIF-1α and a constitutive HIF-1β subunit. Besides physiology, HIF-1 induction is involved in major pathological processes such as cardiovascular disease, inflammation and cancer, which are associated with the formation of reactive oxygen species (ROS). ROS have been reported to affect HIF-1 activity but the role for ROS in regulating HIF-1 has not been definitely settled. In order to shed light on the redox-regulation of HIF-1 by ROS, we studied …

Transcriptional ActivationProcollagen-Proline DioxygenaseMedizinBiologyTransfectionBiochemistryHypoxia-Inducible Factor-Proline DioxygenasesTransactivationCell Line TumormedicineHumansRNA Small InterferingTranscription factorchemistry.chemical_classificationRegulation of gene expressionReactive oxygen speciesGene knockdownGeneral MedicineTransfectionHydrogen PeroxideHypoxia (medical)Cell HypoxiaCell biologyHypoxia-inducible factorschemistryBiochemistryHypoxia-Inducible Factor 1medicine.symptomReactive Oxygen SpeciesOxidation-Reduction
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Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

2003

Background— Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet. In addition, the vascular effect of histamine seems to depend critically on eNOS functionality. Therefore, we studied the effects of histamine on eNOS gene expression and function. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression. The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H 1 recep…

Transcriptional Activationmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHistamine H1 receptorNitric OxideCell LineNitric oxidechemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineHumansRNA MessengerReceptors Histamine H1Enzyme InhibitorsPromoter Regions GeneticProtein Kinase InhibitorsCells CulturedDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseKineticsOxidative StressEndocrinologymedicine.anatomical_structurechemistryEnzyme InductionCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularNitric Oxide SynthaseHistamine H3 receptorCalcium-Calmodulin-Dependent Protein Kinase Type 2Reactive Oxygen SpeciesCardiology and Cardiovascular MedicineHistamineHistamineCirculation
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RATIONALE FOR THE USE OF ANTIOXIDANT VITAMINS IN CLINICAL ORGAN TRANSPLANTATION

1996

Transplantationmedicine.medical_specialtyDiet therapybusiness.industryOrgan TransplantationAscorbic acidBioinformaticsAntioxidantsAntioxidant vitaminsOrgan transplantationSurgeryTransplantationReperfusion InjurymedicineHumansReactive Oxygen SpeciesbusinessTransplantation
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Different strategies to achieve Pb-tolerance by the two Trebouxia algae coexisting in the lichen Ramalina farinacea.

2012

Lichen thalli are permeable to airborne substances, including heavy metals, which are harmful to cell metabolism. Ramalina farinacea shows a moderate tolerance to Pb. This lichen comprises two Trebouxia phycobionts, provisionally referred to as TR1 and TR9, with distinct physiological responses to acute oxidative stress. Thus, there is a more severe decay in photosynthesis and photosynthetic pigments in TR1 than in TR9. Similarly, under oxidative stress, antioxidant enzymes and HSP70 protein decrease in TR1 but increase in TR9. Since Pb toxicity is associated with increased ROS formation, we hypothesized greater Pb tolerance in this phycobiont. Accordingly, the aim of the present study was …

TrebouxiaChlorophyllAntioxidantLichensPhysiologymedicine.medical_treatmentBOTANICAGlutathione reductasePlant SciencePhotosynthesisAntioxidantsFluorescenceLichen microalgaeRamalina farinaceaSuperoxide dismutaseElectron TransportAscorbate PeroxidasesSpecies SpecificityChlorophytaStress PhysiologicalBotanymedicineHSP70 Heat-Shock ProteinsPhotosynthesisSymbiosisChlorophyll fluorescencePlant ProteinsBIOLOGIA VEGETALbiologySuperoxide DismutaseStress responsebiology.organism_classificationAPXCatalaseOxidative StressGlutathione ReductaseBiochemistryLeadTrebouxia algaebiology.proteinReactive Oxygen SpeciesHeavy metal toleranceAgronomy and Crop ScienceJournal of plant physiology
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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Les microARN, une nouvelle voie de signalisation cellulaire empruntée par le resvératrol

2011

Les microARN (miARN), decouverts en 1993 dans le laboratoire de V. Ambros [1], ont d'abord ete identifies comme regulateurs du developpement chez Caenorhabditis elegans. Les recherches recentes confirment que ces petits ARN non codants simple-brins sont des elements de signalisation cellulaire fondamentaux dans la regulation de processus tels que le developpement, la differenciation ou la proliferation cellulaire. Ces ARN de 22 nucleotides en moyenne s'apparient de facon specifique a des ARN messagers cibles entrainant le blocage de leur traduction (en cas de complementarite parfaite) ou la degradation des transcrits (en cas de un ou quelques mesappariement[s]). Ils pourraient aussi reguler…

Tumor suppressor geneReactive oxygen species metabolismTumor cellsGeneral MedicineBiologymedicine.disease_causeMolecular biologyGeneral Biochemistry Genetics and Molecular BiologyNeoplasm geneticsGene expressionmicroRNAmedicineGene silencingCarcinogenesismédecine/sciences
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Reactive oxygen species activation of MAPK pathway results in VEGF upregulation as an undesired irradiation response

2013

Background Radioresistance limits the effectiveness of radiotherapy in head and neck squamous cell carcinoma. We previously demonstrated post-radiogenic mitogen-activated protein kinase (MAPK) pathway activation and vascular endothelial growth factor (VEGF) release resulting in reduced tumor cell response. Here, we examined the association of this mechanism with the induction of reactive oxygen species (ROS) under irradiation (IR). Methods Intracellular ROS after IR were measured. We modeled radiation-induced ROS by exposure of two SCC lines to H2O2 and evaluated the impact of irradiation and ROS on ERK phosphorylation by Western blot, immunohistochemistry, and ELISA. Results We found eleva…

Vascular Endothelial Growth Factor AMAPK/ERK pathwayCancer ResearchPathologymedicine.medical_specialtyMAP Kinase Signaling SystemBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyRadiation TolerancePathology and Forensic Medicinechemistry.chemical_compoundDownregulation and upregulationCell Line TumorNitrilesButadienesmedicineHumansEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesProtein kinase Achemistry.chemical_classificationReactive oxygen speciesHydrogen PeroxideImmunohistochemistryCytoprotectionUp-RegulationVascular endothelial growth factorVascular endothelial growth factor AOtorhinolaryngologychemistryCytoprotectionCarcinoma Squamous CellCancer researchPeriodonticsElectrophoresis Polyacrylamide GelOral SurgeryReactive Oxygen SpeciesIntracellularJournal of Oral Pathology & Medicine
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Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

2017

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases.…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtyHeart Diseasesmedicine.medical_treatmentVascular toxicity VEGF cardiotoxicity new target therapy chemotherapy radiotherapy cardio-oncologyAntineoplastic Agents030204 cardiovascular system & hematologyQT intervalCardiooncology03 medical and health scienceschemistry.chemical_compoundCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Medicine (all); Cardiology and Cardiovascular Medicine0302 clinical medicineVascularReceptorsmedicineAnimalsHumansChemotherapyEndotheliumNew target therapyChemotherapyCardiotoxicityRadiotherapybusiness.industryVascular Endothelial Growth FactorMedicine (all)Cardiooncology; Vascular toxicity; New target therapyCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Animals; Antineoplastic Agents; Cardiotoxicity; Endothelium Vascular; Heart Diseases; Humans; Reactive Oxygen Species; Receptors Vascular Endothelial Growth Factor; Vascular Endothelial Growth Factor Amedicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorRadiation therapyCardio-oncologyVascular endothelial growth factor AReceptors Vascular Endothelial Growth Factorchemistry030220 oncology & carcinogenesisHeart failureCancer researchEndothelium VascularVascular toxicityReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessTyrosine kinaseInternational Journal of Cardiology
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Oxidative stress in vascular disease: causes, defense mechanisms and potential therapies

2007

Endothelial cells control vascular homeostasis by generating paracrine factors that regulate vascular tone, inhibit platelet function, prevent adhesion of leukocytes, and limit proliferation of vascular smooth muscle. The dominant factor responsible for many of those effects is endothelium-derived nitric oxide (NO). Endothelial dysfunction characterized by enhanced inactivation or reduced synthesis of NO, alone or in combination, is seen in conjunction with risk factors for cardiovascular disease. Endothelial dysfunction can promote vasospasm, thrombosis, vascular inflammation, and proliferation of the intima. Vascular oxidative stress and increased production of reactive oxygen species con…

Vascular smooth muscleEndotheliumArteriosclerosisPharmacologyNitric Oxidemedicine.disease_causeAntioxidantsReceptor Angiotensin Type 1Superoxide dismutaseRisk FactorsmedicineHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybusiness.industryAnticholesteremic AgentsGeneral Medicinemedicine.diseaseOxidative Stressmedicine.anatomical_structureMitochondrial respiratory chainchemistryImmunologybiology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessOxidative stressNature Clinical Practice Cardiovascular Medicine
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