Search results for "HEME OXYGENASE"

showing 10 items of 90 documents

Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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Heme oxygenase-1: a novel key player in the development of tolerance in response to organic nitrates.

2007

Objective— Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling. We tested whether differences in their capacity to induce heme oxygenase-1 (HO-1) might explain why PETN and not GTN therapy is devoid of nitrate and cross-tolerance. Methods and Results— Wistar rats were treated with PETN or GTN (10.5 or 6.6 μg/kg/min for 4 days). In contrast to GTN, PETN did not induce nitrate tolerance or cross-tolerance as assess…

MaleEndotheliumPharmacologySensitivity and SpecificityNitric oxidechemistry.chemical_compoundNitroglycerinRandom AllocationDrug toleranceReference ValuesmedicineAnimalsPentaerythritol TetranitrateRats WistarHemeCyclic GMPChromatography High Pressure LiquidProbabilitychemistry.chemical_classificationReactive oxygen speciesbiologyDrug ToleranceFree Radical ScavengersAldehyde DehydrogenaseRatsHeme oxygenaseFerritinDisease Models Animalmedicine.anatomical_structurechemistryBiochemistrycardiovascular systembiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineReactive Oxygen SpeciesHeme Oxygenase-1HeminArteriosclerosis, thrombosis, and vascular biology
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Hemin, an inducer of heme oxygenase-1, lowers intraocular pressure in rabbits.

2007

Carbon monoxide (CO) generated from heme may induce vasodilation and exert cyto-protective properties in the eye. This study was undertaken to investigate the effects of hemin, a potent inducer of heme oxygenase-1 (HO-1), on models of ocular hypertension in rabbits.Ocular hypertension was induced by injecting alpha-chymotrypsin in both eyes under local anesthesia. Only rabbits with an intraocular pressure (IOP) of 25 mmHg or more were used. The dose-response study of the hemin effect on IOP was made by an intravenous injection of the drug (50, 75, and 100 mg/kg) and subsequent IOP monitoring every 6 h. A separate set of animals was pretreated with the HO-1 inhibitor, zinc protoporphyrin-IX …

MaleIntraocular pressuregenetic structuresmedicine.drug_classOcular hypertensionProtoporphyrinsVasodilationPharmacologyBetamethasonechemistry.chemical_compoundRandom AllocationmedicineAnimalsChymotrypsinPharmacology (medical)Enzyme inducerIntraocular PressurePharmacologyAnalysis of VariancebiologyDose-Response Relationship Drugmedicine.diseaseeye diseasesHeme oxygenaseOphthalmologyDisease Models AnimalchemistryAnesthesiaEnzyme InductionInjections Intravenousbiology.proteinCorticosteroidBetamethasoneHeminOcular Hypertensionsense organsRabbitsHeme Oxygenase-1Heminmedicine.drugJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
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Expression of heme oxygenase-1 and regulation by cytokines in human osteoarthritic chondrocytes

2003

Heme oxygenase-1 (HO-1) is implicated in the protection against tissue injury. We investigated the expression of this protein in cartilage sections and chondrocytes obtained from osteoarthritic patients. HO-1 was immunodetected in preparations from cartilage and also in chondrocytes cultured in the absence of stimulation. We found that HO-1 can be modulated by cytokines since the pro-inflammatory cytokines interleukin (IL)-1beta, IL-17 and tumour necrosis factor-alpha (TNF-alpha) down-regulated this protein, whereas the anti-inflammatory cytokine IL-10 exerted the opposite effect. Our results suggest a role for HO-1 as part of protective mechanisms against tissue injury in human cartilage.

MaleNecrosismedicine.medical_treatmentBiochemistryGene Expression Regulation EnzymologicChondrocytechemistry.chemical_compoundChondrocytesOsteoarthritismedicineHumansHemeAgedPharmacologyRegulation of gene expressionbusiness.industryCartilageInterleukin-17Membrane ProteinsInterleukinInterleukin-10Cell biologyHeme oxygenasemedicine.anatomical_structureCytokinechemistryHeme Oxygenase (Decyclizing)ImmunologyCytokinesFemalemedicine.symptombusinessHeme Oxygenase-1Interleukin-1Biochemical Pharmacology
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Beneficial effect of dipyridyl, a liposoluble iron chelator against focal cerebral ischemia: In vivo and in vitro evidence of protection of cerebral …

2007

Whereas iron chelators were shown to induce neuroprotection against brain injury, the effect of iron chelators on ischemia-induced damage of cerebral endothelium is largely unknown. Our objective was to explore the endothelioprotective effect of the lipophilic iron chelator dipyridyl (DP) (i) in vitro on the death of cerebral endothelial cells (CECs) subjected to intracellular iron loading and (ii) in vivo on the ischemia-induced blood-brain barrier (BBB) disruption. When given shortly after iron exposure or brain ischemia, DP prevented the death of CECs and diminished BBB disruption, respectively, whereas a delayed administration of DP was associated with a lower CECs protection. Interesti…

MaleProgrammed cell deathTime FactorsIronIschemiaPharmacologymedicine.disease_causeBlood–brain barrierIron Chelating AgentsTransfectionNeuroprotectionStatistics NonparametricBrain IschemiaBrain ischemiaMice22'-DipyridylIn vivoIschemiamedicineAnimalsPROTECTIONMolecular BiologyCells CulturedtherapyCell DeathDose-Response Relationship DrugChemistrySuperoxide DismutaseGeneral NeuroscienceLEDEndothelial CellsBrainProteinscellmedicine.diseaseEndothelial stem cellIn VitroDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain InjuriesImmunologyCELLScardiovascular systemNeurology (clinical)Oxidative stressHeme Oxygenase-1Developmental Biology
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Heme oxygenase-1 regulates the progression of K/BxN serum transfer arthritis.

2012

Background Heme oxygenase-1 (HO-1) is induced in many cell types as a defense mechanism against stress. We have investigated the possible role of endogenous HO-1 in the effector phase of arthritis using the K/BxN serum transfer model of arthritis in HO-1 heterozygous and homozygous knock-out mice. Methodology/Principal Findings Arthritis was induced in C57/Black-6 xFVB (HO-1+/+, HO-1+/− and HO-1−/−) mice by intraperitoneal injection of 150 µl serum from arthritic K/BxN mice at days 0 and 2. Blood was collected and animals were sacrificed at day 10. Histological analysis was performed in ankle sections. The levels of inflammatory mediators were measured in serum and paw homogenates by enzyme…

MaleTime FactorsAnatomy and PhysiologyMouseNon-Clinical MedicineArthritislcsh:MedicineEndogenyBiochemistryAntioxidantsMicechemistry.chemical_compoundDrug Discoverylcsh:ScienceMusculoskeletal SystemHemeRegulation of gene expressionMultidisciplinaryEffectorSystems BiologyAnimal ModelsEnzymesDisease ProgressionMedicineMatrix Metalloproteinase 3Inflammation Mediatorsmedicine.symptomResearch ArticleCell typeOsteocalcinRheumatoid ArthritisInflammationModel OrganismsRheumatologymedicineAnimalsBiologyBlood CellsRANK Ligandlcsh:Rmedicine.diseaseArthritis ExperimentalMolecular biologyMice Inbred C57BLHeme oxygenaseDisease Models AnimalGene Expression RegulationchemistryImmunologylcsh:QAnkle JointHeme Oxygenase-1PLoS ONE
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Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

2004

Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyp…

MaleVascular Endothelial Growth Factor AOsteolysisAngiogenesisNitric Oxide Synthase Type IIProtoporphyrinsArthritisInflammationPharmacologyNitric OxidePathology and Forensic MedicineSynovitismedicineAnimalsEnzyme InhibitorsMolecular BiologyHeat-Shock ProteinsbiologyTumor Necrosis Factor-alphabusiness.industryLysineCell Biologymedicine.diseaseArthritis ExperimentalHindlimbRatsUp-RegulationNitric oxide synthaseHeme oxygenaseDisease Models AnimalCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred LewHeme Oxygenase (Decyclizing)ImmunologyOxygenasesbiology.proteinNitric Oxide Synthasemedicine.symptomVascular endothelial growth factor productionbusinessLaboratory Investigation
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Maternal Treatment of Spontaneously Hypertensive Rats With Pentaerythritol Tetranitrate Reduces Blood Pressure in Female Offspring

2014

Pentaerythritol tetranitrate is devoid of nitrate tolerance and shows no reproductive or developmental toxicity in animal studies. Recently, pentaerythritol tetranitrate has been demonstrated to reduce the risk of intrauterine growth restriction and the risk of preterm birth in women with abnormal placental perfusion. This study was conducted to test the perinatal programming effect of pentaerythritol tetranitrate in spontaneously hypertensive rats, a rat model of genetic hypertension. Parental spontaneously hypertensive rats were treated with pentaerythritol tetranitrate (50 mg/kg per day) during pregnancy and lactation periods; the offspring received standard chow without pentaerythritol …

Malemedicine.medical_specialtyGPX1Nitric Oxide Synthase Type IIIOffspringVasodilator AgentsDevelopmental toxicityBlood PressureVasodilationPentaerythritol tetranitratePentaerythritolchemistry.chemical_compoundPregnancyRats Inbred SHRInternal medicineInternal MedicinemedicineAnimalsPentaerythritol Tetranitratebusiness.industryGene Expression Regulation DevelopmentalDNARatsVasodilationHeme oxygenaseEndocrinologyBlood pressureAnimals NewbornchemistryMaternal ExposureHypertensionPregnancy AnimalFemaleEndothelium VascularbusinessHypertension
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Atorvastatin treatment increases plasma bilirubin but not HMOX1 expression in stable angina patients.

2015

In vitro and animal studies indicate that statins increase heme oxygenase-1 gene (HMOX1) expression, which then, presumably, increases plasma bilirubin concentration. However, clinical confirmation that statins concomitantly increase HMOX1 expression and plasma bilirubin concentration is lacking. We hypothesized that in patients with stable angina atorvastatin therapy (20 mg/day for 10 weeks) concomitantly increases total bilirubin concentration and HMOX1 expression, as assessed non-invasively by plasma analysis.In 44 patients with stable angina plasma concentrations of total bilirubin, HMOX1 mRNA and HMOX1 protein were measured before and after the statin treatment, as well as plasma conce…

Malemedicine.medical_specialtyHMOX1BilirubinAtorvastatinClinical BiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundInternal medicinemedicineAtorvastatinHumanscardiovascular diseasesAngina StableRNA MessengerIncreased total bilirubinHemeBilirubinGeneral MedicineMiddle AgedMalondialdehydeEndocrinologychemistryProteolysislipids (amino acids peptides and proteins)FemaleAnimal studiesHeme Oxygenase-1Lipoproteinmedicine.drugScandinavian journal of clinical and laboratory investigation
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Heme oxygenase-1 mediates protective effects on inflammatory, catabolic and senescence responses induced by interleukin-1β in osteoarthritic osteobla…

2011

Osteoarthritis (OA) is a chronic degenerative joint disease showing altered bone metabolism. Osteoblasts contribute to the regulation of cartilage metabolism and bone remodeling. We have shown previously that induction of heme oxygenase-1 (HO-1) protects OA cartilage against inflammatory and degradative responses. In this study, we investigated the effects of HO-1 induction on OA osteoblast metabolism. HO-1 was induced with cobalt protoporphyrin IX (CoPP) and by transduction with LV-HO-1. In osteoblasts stimulated with interleukin (IL)-1β, CoPP enhanced mineralization, the expression of a number of markers of osteoblast differentiation such as Runx2, bone morphogenetic protein-2, osteocalci…

Malemedicine.medical_specialtyInterleukin-1betaCartilage metabolismBiochemistryBone remodelingOsteoprotegerinInternal medicineOsteoarthritismedicineHumansCells CulturedCellular SenescenceOsteitisAgedPharmacologyOsteoblastsbiologyChemistryInterleukinOsteoblastMiddle AgedCOPPHeme oxygenaseMetabolismmedicine.anatomical_structureEndocrinologyOsteocalcinbiology.proteinFemaleInflammation MediatorsHeme Oxygenase-1Biochemical Pharmacology
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