Search results for "Phosphorylation"

showing 10 items of 975 documents

LACTATE, NOT GLUCOSE, UP-REGULATES MITOCHONDRIAL OXYGEN CONSUMPTION BOTHIN SHAM AND LATERAL FLUID PERCUSSED RAT BRAINS

2006

OBJECTIVE: Failure of energy metabolism after traumatic brain injury may be a major factor limiting outcome. Although glucose is the primary metabolic substrate in the healthy brain, the well documented surge in tissue lactate after traumatic brain injury suggests that lactate may provide an energy need that cannot be met by glucose. We hypothesized, therefore, that administration of lactate or the combination of lactate and supraphysiological oxygen may improve mitochondrial oxidative respiration in the brain after rat fluid percussion injury. We measured oxygen consumption (VO2) to determine what effects glucose, lactate, oxygen, and the combination of lactate and oxygen have on mitochond…

Malemedicine.medical_specialtyTraumatic brain injuryCell RespirationOxidative phosphorylationMitochondrionRats Sprague-Dawleychemistry.chemical_compoundOxygen ConsumptionFraction of inspired oxygenInternal medicineRespirationmedicineAnimalsLactic AcidDose-Response Relationship Drugbusiness.industryBrainmedicine.diseaseMitochondriaRatsUp-RegulationCartesian diverLactic acidOxygenDose–response relationshipGlucoseEndocrinologychemistryBrain InjuriesAnesthesiaSurgeryNeurology (clinical)businessNeurosurgery
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Fludarabine prevents smooth muscle proliferation in vitro and neointimal hyperplasia in vivo through specific inhibition of STAT-1 activation.

2007

Drug-eluting stents are increasingly used to reduce in-stent restenosis and adverse cardiac events after percutaneous coronary interventions. However, the race for the ideal drug-eluting stent is still on, with special regard to the best stent-coating system and the most effective and less toxic drug. Fludarabine, a nucleoside analog, has both anti-inflammatory and antiproliferative cellular effects. The aim of the present study was to assess the cellular and molecular effects of fludarabine on vascular smooth muscle cell (VSMC) growth in vitro and in vivo and the feasibility and efficacy of a fludarabine-eluting stent. To study the biomolecular effects of fludarabine on VSMC proliferation…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsPhysiologyMyocytes Smooth MusclePharmacologyProsthesis DesignTransfectionMuscle Smooth VascularRestenosisIn vivoPhysiology (medical)medicineAnimalsCarotid StenosisRNA AntisensePhosphorylationRats WistarAortaCells CulturedCell ProliferationNeointimal hyperplasiaHyperplasiaDose-Response Relationship Drugbusiness.industryCardiovascular AgentsHyperplasiaJanus Kinase 2medicine.diseaseFludarabineSurgeryRatsDisease Models AnimalSTAT1 Transcription FactorCardiovascular agentSTAT proteinFeasibility StudiesStentsRabbitsCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesTunica IntimaAngioplasty BalloonVidarabinemedicine.drug
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Enhancement of activities relative to fatty acid oxidation in the liver of rats depleted of l-carnitine by d-carnitine and a γ-butyrobetaine hydroxyl…

1995

Abstract This study was designed to examine whether the depletion of l -carnitine may induce compensatory mechanisms allowing higher fatty acid oxidative activities in liver, particularly with regard to mitochondrial carnitine palmitoyltransferase I activity and peroxisomal fatty acid oxidation. Wistar rats received d -carnitine for 2 days and 3-(2,2,2-trimethylhydrazinium)propionate (mildronate), a non-competitive inhibitor of γ-butyrobetaine hydroxylase, for 10 days. They were starved for 20 hr before being sacrificed. A dramatic reduction in carnitine concentration was observed in heart, skeletal muscles and kidneys, and to a lesser extent, in liver. Triacylglycerol content was found to …

Malemedicine.medical_specialtygamma-Butyrobetaine DioxygenaseOxidative phosphorylationBiologyMitochondrionBiochemistryMixed Function OxygenasesCarnitineInternal medicinemedicineAnimalsCarnitineRats WistarBeta oxidationPharmacologychemistry.chemical_classificationBody WeightFatty AcidsFatty acidOrgan SizePeroxisomeRatsEndocrinologyLiverchemistryKetone bodiesCarnitine palmitoyltransferase IOxidation-ReductionMethylhydrazinesmedicine.drugBiochemical Pharmacology
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Glycogen synthase kinase 3β links neuroprotection by 17β-estradiol to key Alzheimer processes

2004

Estrogen exerts many of its receptor-mediated neuroprotective functions through the activation of various intracellular signal transduction pathways including the mitogen activating protein kinase (MAPK), phospho inositol-3 kinase and protein kinase C pathways. Here we have used a hippocampal slice culture model of kainic acid-induced neurotoxic cell death to show that estrogen can protect against oxidative cell death. We have previously shown that MAPK and glycogen synthase kinase-3beta (GSK-3beta) are involved in the cell death/cell survival induced by kainic acid. In this model and other cellular and in vivo models we have shown that estrogen can also cause the phosphorylation and hence …

Malemedicine.medical_specialtymedicine.drug_classBlotting WesternTetrazolium SaltsEstrogen receptorCell Counttau Proteinsmacromolecular substancesBiologyHippocampusRats Sprague-DawleyGlycogen Synthase Kinase 3MiceOrgan Culture TechniquesPregnancyGSK-3Internal medicineExcitatory Amino Acid AgonistsSerinemedicineAnimalsDrug InteractionsPhosphorylationProtein kinase AGSK3BCells CulturedProtein kinase CEstrogen receptor betaGlycogen Synthase Kinase 3 betaKainic AcidCell DeathEstradiolKinaseGeneral NeuroscienceAntibodies MonoclonalEmbryo MammalianImmunohistochemistryRatsCell biologyMice Inbred C57BLThiazolesEndocrinologyAnimals NewbornEstrogenTyrosineFemalePropidiumNeuroscience
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats.

1997

The effects of insulin on the rates of glucose disposal were studied in soleus muscles isolated from hyper- or hypothyroid rats. Treatment with triiodothyronine for 5 or 10 days decreased the sensitivity of glycogen synthesis but increased the sensitivity of lactate formation to insulin. The sensitivity of 3-O methylglucose to insulin was increased only after 10 days of treatment and was accompanied by an increase in the sensitivity of 2-deoxyglucose phosphorylation; however, 2-deoxyglucose and glucose 6-phosphate in response to insulin remained unaltered. In hypothyroidism, insulin-stimulated rates of 3-O-methylglucose transport and 2-deoxyglucose phosphorylation were decreased; however, a…

Malemedicine.medical_specialtymedicine.medical_treatmentClinical BiochemistryBiological Transport ActiveBiologyCarbohydrate metabolismIn Vitro TechniquesBiochemistryHyperthyroidismDinoprostonechemistry.chemical_compoundHypothyroidismInternal medicinemedicineAnimalsInsulinGlycolysisDrug InteractionsLactic AcidPhosphorylationRats WistarGlycogen synthaseMuscle SkeletalHexokinaseInsulinGlucose transporterGeneral MedicineMetabolismRatsCortisoneEndocrinologyGlucosechemistryBasal (medicine)Growth Hormonebiology.proteinTriiodothyronineGlycolysisGlycogenEuropean journal of clinical investigation
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Nitric oxide metabolites, leukocyte activation markers and oxidative status in dialyzed subjects.

2008

<i>Aims:</i> Our purpose was to evaluate, in a group of 42 end-stage renal disease patients who regularly undergo hemodialysis, some indexes of leukocyte activation, nitric oxide metabolites (NOx) and other parameters that reflect the oxidative stress before and after a standard hemodialysis session. <i>Methods:</i> Elastase and myeloperoxidase (MPO) were determined by means of ELISA. The NO production was evaluated by a micromethod which measures the concentration of NOx. The oxidation of polyunsaturated fatty acids was evaluated in plasma by detection of thiobarbituric acid-reactive substances (TBARS). Total antioxidant status (TAS) was obtained using spectrophotom…

Malemedicine.medical_treatmentActivation markersOxidative phosphorylationHemodialysis Oxidative status Nitric oxide Elastase MyeloperoxidasePharmacologyNitric OxideThiobarbituric Acid Reactive SubstancesAntioxidantsNitric oxidechemistry.chemical_compoundRenal DialysisLeukocytesmedicineHumansAgedPeroxidasechemistry.chemical_classificationbiologyElastaseHematologyGeneral MedicineMiddle AgedOxidative StressEnzymechemistryNephrologyMyeloperoxidaseImmunologybiology.proteinKidney Failure ChronicFemaleHemodialysisLeukocyte Elastase
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Neuroimmune and Mu-Opioid Receptor Alterations in the Mesocorticolimbic System in a Sex-Dependent Inflammatory Pain-Induced Alcohol Relapse-Like Rat …

2021

Evidence concerning the role of alcohol-induced neuroinflammation in alcohol intake and relapse has increased in the last few years. It is also proven that mu-opioid receptors (MORs) mediate the reinforcing properties of alcohol and, interestingly, previous research suggests that neuroinflammation and MORs could be related. Our objective is to study neuroinflammatory states and microglial activation, together with adaptations on MOR expression in the mesocorticolimbic system (MCLS) during the abstinence and relapse phases. To do so, we have used a sex-dependent rat model of complete Freund’s adjuvant (CFA)-induced alcohol deprivation effect (ADE). Firstly, our results confirm that only CFA-…

Malemedicine.medical_treatmentFreund's AdjuvantReceptors Opioid mualcohol deprivation effectNitric Oxide Synthase Type IImicroglianeuroinflammationRats Sprague-DawleyRecurrenceLimbic SystemImmunology and AllergypainPhosphorylationReceptormedia_commonMicrogliaAlcohol AbstinencealcoholMicrofilament ProteinsNF-kappa BBrief Research ReportInterleukin 10AlcoholismCytokinemedicine.anatomical_structureCytokinesFemaleμ-opioid receptorInflammation Mediatorsmedicine.medical_specialtyNeuroimmunomodulationmedia_common.quotation_subjectImmunologyPrefrontal CortexSex FactorsDownregulation and upregulationInternal medicinemedicineAnimalsNeuroinflammationbusiness.industryCalcium-Binding ProteinsAbstinenceRC581-607EndocrinologyCyclooxygenase 2mu-opioid receptorImmunologic diseases. AllergybusinessFrontiers in Immunology
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A non-redundant role for OX40 in the competitive fitness of Treg in response to IL-2.

2010

OX40 stimulation is known to enhance activation of effector T cells and to inhibit induction and suppressive function of Treg. Here we uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediated promotion of Treg fitness spanned beyond lymphopenic environments, as endogenous Treg in OX40-null mice showed decreased accumulation during thymic development, enhanced susceptibility to antibody-mediated depletion and defective turnover following thymectomy. In v…

Malemedicine.medical_treatmentImmunologyBlotting Westernchemical and pharmacologic phenomenaEndogenyInflammationSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryMiceSuppressor of Cytokine Signaling 1 ProteinLymphopeniaOX40; Treg; IL-2.medicineSTAT5 Transcription FactorImmunology and AllergyAnimalsOX40PhosphorylationReceptorSTAT5Cell ProliferationMice KnockoutbiologyEffectorCell growthSuppressor of cytokine signaling 1hemic and immune systemsReceptors OX40IL-2.ColitisFlow Cytometrycytokinescompetitive fitnessSpecific Pathogen-Free OrganismsThymectomyMice Inbred C57BLTregRadiation ChimeraImmunologybiology.proteinInterleukin-2costimulatory moleculesmedicine.symptomcompetitive fitness; costimulatory molecules; cytokines; treg
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Abnormalities of mitochondrial functioning can partly explain the metabolic disorders encountered in sarcopenic gastrocnemius.

2007

International audience; Aging triggers several abnormalities in muscle glycolytic fibers including increased proteolysis, reactive oxygen species (ROS) production and apoptosis. Since the mitochondria are the main site of substrate oxidation, ROS production and programmed cell death, we tried to know whether the cellular disorders encountered in sarcopenia are due to abnormal mitochondrial functioning. Gastrocnemius mitochondria were extracted from adult (6 months) and aged (21 months) male Wistar rats. Respiration parameters, opening of the permeability transition pore and ROS production, with either glutamate (amino acid metabolism) or pyruvate (glucose metabolism) as a respiration substr…

Malemuscle atrophyMESH : Cell Aging[SDV]Life Sciences [q-bio]MESH : Reactive Oxygen SpeciesMitochondrion0302 clinical medicineGlycolysisMESH: AnimalsMESH : Muscle SkeletalMESH : Fatty AcidsCellular SenescencePhospholipidsMESH: Superoxide Dismutasereactive oxygen speciesMESH : Free Radicals0303 health sciencesMESH: Muscle SkeletalMESH : RatsFatty Acidsfatty acid profile of mitochondrial lipidsMESH: Reactive Oxygen SpeciesPyruvate dehydrogenase complexMESH: Fatty Acidsmitochondria[SDV] Life Sciences [q-bio]BiochemistryMESH: Cell AgingMESH: CalciumMESH : MitochondriaCell agingPyruvate decarboxylationmedicine.medical_specialtyFree RadicalsMESH: RatsCellular respirationMESH: MitochondriaMESH : MaleCell Respirationchemistry.chemical_elementOxidative phosphorylationBiologyCalciumMESH : Rats WistarMESH : Phospholipids03 medical and health sciencesMESH: Free RadicalsInternal medicinemedicineAnimalsMESH : Superoxide DismutaseRats WistarMuscle SkeletalMESH : Calcium030304 developmental biologyMESH: Phospholipidscalciumpermeability transition poreSuperoxide Dismutaseagingaging;calcium;fatty acid profile of mitochondrial lipids;mitochondria;muscle atrophy;permeability transition pore;reactive oxygen species;Animals;Calcium;Cell Aging;Cell Respiration;Fatty Acids;Free Radicals;Male;Mitochondria;Muscle;Skeletal;Phospholipids;Rats;Wistar;Reactive Oxygen Species;Superoxide DismutaseCell BiologyMESH: Rats WistarMESH: MaleRatsEndocrinologychemistryMESH : Cell RespirationMESH : AnimalsMESH: Cell Respiration030217 neurology & neurosurgery
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