Search results for "ACTIVATION"

showing 10 items of 2079 documents

Pentoxifylline Prevents Loss of PP2A Phosphatase Activity and Recruitment of Histone Acetyltransferases to Proinflammatory Genes in Acute Pancreatitis

2009

Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production. Our aim was to elucidate the mechanism of action of pentoxifylline as an anti-inflammatory agent in acute pancreatitis. Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied. Phosphorylation of ERK and ERK kinase (MEK1/2), as well as PP2A, PP2B, and PP2C serine/threonine phosphatase activiti…

MaleMAPK/ERK pathwayChromatin ImmunoprecipitationPhosphodiesterase InhibitorsBlotting WesternPhosphataseAnti-Inflammatory AgentsPharmacologyBiologyCell LinePentoxifyllineProinflammatory cytokineCyclic AMPPhosphoprotein PhosphatasesmedicineAnimalsPentoxifyllineRats WistarExtracellular Signal-Regulated MAP KinasesHistone AcetyltransferasesInflammationPharmacologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaProtein phosphatase 2medicine.diseaseCyclic Nucleotide Phosphodiesterases Type 2RatsEnzyme ActivationPancreatitisBiochemistryAcute DiseaseRNAMolecular MedicinePhosphorylationPancreatitisMitogen-Activated Protein KinasesChromatin immunoprecipitationmedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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Strength training in old age: adaptation of antagonist muscles at the ankle joint.

2005

The purpose of this study was to determine whether strength training could reduce the deficit in plantarflexion (PF) maximal voluntary contraction (MVC) torque observed in previous studies in older subjects relative to young adults. Accordingly, the effects of a 6-month strength training program on the muscle and neural properties of the major muscle groups around the ankle were examined. PF and dorsiflexion (DF) isometric MVC torques were measured and surface electromyographic activity of the triceps surae and tibialis anterior muscles was recorded. The strength training program was very effective in improving strength in PF (+24.5%), and it thus reduced the DF-to-PF MVC torque ratio; in a…

MaleMESH : Ankle Joint[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]MESH : Electric StimulationPhysiologyMESH: Muscle ContractionMESH : AgedMESH: Physical FitnessIsometric exerciseElectromyographyMESH: Research Support Non-U.S. Gov'tMESH : Research Support Non-U.S. Gov't0302 clinical medicineTriceps surae muscleMESH: Ankle JointMESH : FemaleMESH : Muscle SkeletalMESH : Adaptation PhysiologicalMESH : AlgorithmsMESH: AgedMESH: Muscle SkeletalMESH: Middle Agedmedicine.diagnostic_test[ SDV.MHEP.PHY ] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]MESH: Electric StimulationMiddle AgedAdaptation PhysiologicalCoactivationmedicine.anatomical_structureData Interpretation StatisticalMESH : ElectromyographyFemalemedicine.symptomMESH : Physical FitnessAlgorithmsMuscle ContractionMuscle contractionmedicine.medical_specialtyWeight LiftingStrength trainingMESH : MaleJoint stabilityMESH: AlgorithmsMESH: Electromyography03 medical and health sciencesCellular and Molecular NeurosciencePhysical medicine and rehabilitationPhysiology (medical)medicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansMESH : Middle AgedMESH : Data Interpretation StatisticalMuscle SkeletalAgedMESH: HumansElectromyographybusiness.industryMESH : Humans030229 sport sciencesMESH: Adaptation PhysiologicalElectric StimulationMESH: MalePhysical FitnessPhysical therapyMESH : Muscle ContractionNeurology (clinical)AnklebusinessMESH: Data Interpretation StatisticalMESH: FemaleAnkle Joint030217 neurology & neurosurgery
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Dietary polyunsaturated fatty acids reduce retinal stress induced by an elevation of intraocular pressure in rats.

2011

International audience; N-6 and n-3 polyunsaturated fatty acids (PUFAs) have been shown to prevent tissue release of inflammatory molecules. We have shown that a combination of n-6 and n-3 PUFAs is more efficient than single supplementations on the long-term consequences of intraocular pressure elevation. We hypothesized that such an association is also more effective during early retinal stress by modifying retinal proinflammatory prostaglandin and cytokine productions. Rats were supplemented for 3 months with n-6 PUFAs, n-3 PUFAs, or both n-6 and n-3 PUFAs. After 3 months, a surgical elevation of intraocular pressure was induced. Retinal morphometry and glial cell activation were evaluate…

MaleMESH : RNA MessengerMESH: Eicosapentaenoic AcidEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betaMESH: Dietary SupplementsMESH: Rats Sprague-DawleyRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: Interleukin-1betaratMESH: AnimalsProstaglandin E2Prostaglandin E1MESH : Tumor Necrosis Factor-alphaMESH : Intraocular Pressure0303 health sciencesNutrition and DieteticsMESH : RatsMESH : NeurogliaMESH: RetinaMESH: Dinoprostonepression intraoculaireMESH: AlprostadilMESH: Docosahexaenoic AcidsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidlipids (amino acids peptides and proteins)MESH: NeurogliaProstaglandin D2Cell activationNeurogliaMESH : Alprostadilmedicine.drugProstaglandin Emedicine.medical_specialtyMESH : DinoprostoneMESH : Interleukin-6Docosahexaenoic AcidsMESH: RatsMESH : MaleProstaglandinBiologyMESH : Interleukin-1betaDinoprostoneRetinaMESH : Diet03 medical and health sciencesMESH: DietMESH: Intraocular PressureInternal medicinemedicineMESH : Eicosapentaenoic AcidAnimalsMESH : Dietary SupplementsRNA MessengerAlprostadilprostanoids030304 developmental biologyMESH: RNA MessengerInterleukin-6Tumor Necrosis Factor-alphadietary polyunsatured fatty acidretinal stressMESH : RetinaRetinalN-6MESH: Interleukin-6MESH : Rats Sprague-Dawleyeye diseasesMESH: MaleMESH : Docosahexaenoic AcidsDietRatsN-3EndocrinologychemistryMESH: Tumor Necrosis Factor-alphaDietary Supplements030221 ophthalmology & optometryMESH : Animalssense organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionintraocular pressure
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The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
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Constitutive activation of JAK2 in mammary epithelium elevates Stat5 signalling, promotes alveologenesis and resistance to cell death, and contribute…

2011

Signalling through the janus kinase (JAK)/signal transducer and activator of transcription (Stat) pathway is required at different stages of mammary gland development, and this pathway is frequently hyper-activated in cancer, including tumours of the breast. Stats 3, 5 and 6 have important roles in the differentiation and survival of mammary alveolar cells, but somewhat paradoxically, both Stat3 and 5 can have oncogenic activity in the mammary gland. Constitutive activation of JAK2 could be anticipated to result in hyper-activation of Stats 1, 3, 5 and 6 with concomitant cell transformation, although the outcome is difficult to envisage, particularly since Stats 3 and 5 play opposing roles …

MaleMammary glandTransplantation HeterologousMutation MissenseMice NudeBreast NeoplasmsMammary Neoplasms AnimalMiceMammary Glands AnimalPregnancyhemic and lymphatic diseasesCell Line TumormedicineSTAT5 Transcription FactorAnimalsHumansLactationSTAT3Mammary Glands HumanMolecular BiologySTAT5Mice KnockoutOriginal PaperJanus kinase 2biologyCell DeathCell growthCell BiologyJanus Kinase 2Enzyme Activationmedicine.anatomical_structureCell Transformation Neoplasticbiology.proteinSTAT proteinCancer researchFemaleSignal transductionJanus kinaseNeoplasm TransplantationSignal Transduction
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The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats

2006

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by i…

MaleMethyl Ethersmedicine.medical_specialtyH&E stainIschemiaCell CountHippocampal formationHippocampusNeuroprotectionSevofluraneBrain IschemiaRats Sprague-DawleySevofluraneInternal medicineEosinophilicmedicineAnimalsNeuronsCaspase 3business.industrymedicine.diseaseImmunohistochemistryRatsEnzyme ActivationNeuroprotective AgentsAnesthesiology and Pain MedicineBlood pressureEndocrinologyCaspasesCerebrovascular CirculationReperfusion InjuryAnesthesiaAnesthetics InhalationApoptosis Regulatory ProteinsbusinessBlood Flow VelocityImmunostainingmedicine.drugAnesthesia & Analgesia
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Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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The Choice of the Filtering Method in Microarrays Affects the Inference Regarding Dosage Compensation of the Active X-Chromosome

2011

BackgroundThe hypothesis of dosage compensation of genes of the X chromosome, supported by previous microarray studies, was recently challenged by RNA-sequencing data. It was suggested that microarray studies were biased toward an over-estimation of X-linked expression levels as a consequence of the filtering of genes below the detection threshold of microarrays.Methodology/principal findingsTo investigate this hypothesis, we used microarray expression data from circulating monocytes in 1,467 individuals. In total, 25,349 and 1,156 probes were unambiguously assigned to autosomes and the X chromosome, respectively. Globally, there was a clear shift of X-linked expressions toward lower levels…

MaleMicroarrayMicroarraysScienceGene ExpressionBiologyMonocytesGenomic ImprintingMiceX Chromosome InactivationGenes X-LinkedDosage Compensation GeneticMolecular Cell BiologyGeneticsAnimalsHumansRNA MessengerBiologyX-linked recessive inheritanceX chromosomeOligonucleotide Array Sequence AnalysisGeneticsChromosomes Human XMultidisciplinaryDosage compensationAutosomeModels GeneticChromosome BiologyGene Expression ProfilingQRComputational BiologyGenomicsGene expression profilingHEK293 CellsMedicineEpigeneticsFemaleDNA microarrayGenomic imprintingGenome Expression AnalysisResearch ArticlePLoS ONE
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Bilobalide, a constituent of Ginkgo biloba , inhibits NMDA-induced phospholipase A 2 activation and phospholipid breakdown in rat hippocampus

2000

In rat hippocampal slices superfused with magnesium-free buffer, glutamate (1 mM) caused the release of large amounts of choline due to phospholipid breakdown. This phenomenon was mimicked by N-methyl-D-aspartate (NMDA) in a calcium-sensitive manner and was blocked by NMDA receptor antagonists such as MK-801 and 7-chlorokynurenate. The NMDA-induced release of choline was not caused by activation of phospholipase D but was mediated by phospholipase A2 (PLA2) activation as the release of choline was accompanied by the formation of lyso-phosphatidylcholine (lyso-PC) and glycerophospho-choline (GPCh) and was blocked by 5-[2-(2-carboxyethyl)-4-dodecanoyl-3,5-dimethylpyrrol-1-yl]pentano ic acid, …

MaleMicrodialysisN-MethylaspartateMicrodialysisGlycineCyclopentanesPharmacologyHippocampal formationHippocampusReceptors N-Methyl-D-AspartatePhospholipases ACholinechemistry.chemical_compoundPhospholipase A2BilobalideSeizuresAnimalsCholineRats WistarFuransCells CulturedPhospholipidsPharmacologyPlants MedicinalDose-Response Relationship DrugbiologyPhospholipase DGlutamate receptorGinkgo bilobaLysophosphatidylcholinesGeneral MedicineGlycerylphosphorylcholineRatsEnzyme ActivationPhospholipases A2Ginkgolideschemistrybiology.proteinNMDA receptorDiterpenesNaunyn-Schmiedeberg's Archives of Pharmacology
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