Search results for "Signaling System"

showing 10 items of 105 documents

Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Mir-4674 Regulates Angiogenesis In Tissue Injury By Targeting P38K Signaling In Endothelial Cells

2020

Neoangiogenesis is critical for tissue repair in response to injury such as myocardial ischemia or dermal wound healing. MicroRNAs are small noncoding RNAs and important regulators of angiogenesis under physiological and pathological disease states. Therefore, identification of microRNAs that may restore impaired angiogenesis in response to tissue injury may provide new targets for therapy. Using a microRNA microarray profiling approach, we identified a human-specific microRNA, miR-4674, that was significantly decreased in patients after myocardial tissue injury and had an endothelial cell (EC)-enriched expression pattern. Functionally, overexpression of miR-4674 markedly attenuated EC pro…

Male0301 basic medicineSmall interfering RNAMAP Kinase Signaling SystemPhysiologyAngiogenesisNeovascularization Physiologic030204 cardiovascular system & hematologyBiology03 medical and health sciencesOrgan Culture Techniques0302 clinical medicinemicroRNAHuman Umbilical Vein Endothelial CellsHumansProtein kinase ACell ProliferationTube formationEndothelial CellsIRAK1Cell BiologyCell biologyEndothelial stem cellMicroRNAs030104 developmental biologyFemaleWound healingResearch ArticleSignal Transduction
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High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes

2010

Introduction High mobility group box 1 (HMGB1) is released by necrotic cells or secreted in response to inflammatory stimuli. Extracellular HMGB1 may act as a pro-inflammatory cytokine in rheumatoid arthritis. We have recently reported that HMGB1 is released by osteoarthritic synoviocytes after activation with interleukin-1beta (IL-1β) The present study investigated the role of HMGB1 in synovial inflammation in osteoarthritis (OA). Methods HMGB1 was determined in human synovium using immunohistochemistry, comparing normal to OA. OA synoviocytes were incubated with HMGB1 at 15 or 25 ng/ml in the absence or presence of IL-1β (10 ng/ml). Gene expression was analyzed by quantitative PCR and pro…

MaleChemokineMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaImmunologyInflammationchemical and pharmacologic phenomenaCCL2HMGB1p38 Mitogen-Activated Protein KinasesRheumatologySynovitisMatrix Metalloproteinase 13HumansMedicineImmunology and AllergyRNA MessengerHMGB1 ProteinExtracellular Signal-Regulated MAP KinasesCells CulturedAgedbiologybusiness.industrySynovial MembraneNF-kappa BOsteoarthritis Kneemedicine.diseaseImmunohistochemistryMolecular biologyCCL20Cytokinemedicine.anatomical_structurebiology.proteinFemaleMatrix Metalloproteinase 3Matrix Metalloproteinase 1Synovial membranemedicine.symptombusinessProto-Oncogene Proteins c-aktResearch ArticleArthritis Research & Therapy
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Significant in vivo anti-inflammatory activity of Pytren4Q-Mn a superoxide dismutase 2 (SOD2) mimetic scorpiand-like Mn (II) complex.

2015

Background The clinical use of purified SOD enzymes has strong limitations due to their large molecular size, high production cost and immunogenicity. These limitations could be compensated by using instead synthetic SOD mimetic compounds of low molecular weight. Background/Methodology We have recently reported that two SOD mimetic compounds, the MnII complexes of the polyamines Pytren2Q and Pytren4Q, displayed high antioxidant activity in bacteria and yeast. Since frequently molecules with antioxidant properties or free-radical scavengers also have anti-inflammatory properties we have assessed the anti-inflammatory potential of Pytren2Q and Pytren4Q MnII complexes, in cultured macrophages …

MaleMAP Kinase Signaling Systemmedicine.drug_classAnti-Inflammatory AgentsSOD2lcsh:MedicineBiologymedicine.disease_causeAnti-inflammatoryCell LineSuperoxide dismutaseMicechemistry.chemical_compoundIn vivoChlorocebus aethiopsmedicineAnimalsHumanslcsh:ScienceVero Cellschemistry.chemical_classificationManganeseMultidisciplinarySuperoxide DismutaseSuperoxideImmunogenicityMolecular Mimicrylcsh:RMolecular mimicryEnzymechemistryBiochemistrybiology.proteinlcsh:QResearch ArticlePLoS ONE
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy

2012

Despite recent advances in the development of new cancer therapies, the treatment options for glioma remain limited, and the survival rate of patients has changed little over the past three decades. Here, we show that 2-hydroxyoleic acid (2OHOA) induces differentiation and autophagy of human glioma cells. Compared to the current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficiently and, unlike TMZ, tumor relapse was not observed following 2OHOA treatment. The novel mechanism of action of 2OHOA is associated with important changes in membrane-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glioma cells bef…

MaleProgrammed cell deathTime FactorsCell SurvivalMAP Kinase Signaling SystemCellular differentiationMice NudeAntineoplastic AgentsOleic AcidsBiologyglioma biomarkerfatty acidsMembrane LipidsMicePhosphatidylinositol 3-Kinases2-Hydroxyoleic AcidGliomaCell Line TumormedicineAutophagyTemozolomideAnimalsHumansPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinaryTemozolomideMicroscopy ConfocalDose-Response Relationship DrugCell growthCell MembraneRetinoblastoma proteinCell DifferentiationGliomaBiological Sciencesmedicine.diseaseXenograft Model Antitumor AssaysCell biologyDacarbazineProtein TransportCancer researchbiology.proteinras Proteinssphingomyelin synthaseProto-Oncogene Proteins c-aktcancer drug targetmedicine.drug
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

2014

Purpose Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. Methods Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (…

MaleRetinal Ganglion Cellsmedicine.medical_specialtyAgingSuperior ColliculiMAP Kinase Signaling SystemBlotting WesternRetinal ganglionRetinaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicinemedicineAnimalsAxonPhosphorylationMitogen-Activated Protein Kinase 7030304 developmental biologyBrain-derived neurotrophic factorMitogen-Activated Protein Kinase 10303 health sciencesRetinaMitogen-Activated Protein Kinase 3biologyChemistryBrain-Derived Neurotrophic FactorBrainAnatomyRatsmedicine.anatomical_structureEndocrinologynervous systemRetinal ganglion cellTrk receptorOptic Nerve InjuriesIntravitreal Injectionsbiology.proteinsense organsNeuroglia030217 neurology & neurosurgeryNeurotrophinInvestigative ophthalmologyvisual science
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Receptor identification and physiological characterisation of glucagon-like peptide-2 in the rat heart.

2010

Abstract Background and aims The anorexigenic glucagon-like peptide (GLP)-2 is produced by intestinal L cells and released in response to food intake. It affects intestinal function involving G-protein-coupled receptors. To verify whether GLP-2 acts as a cardiac modulator in mammals, we analysed, in the rat heart, the expression of GLP-2 receptors and the myocardial and coronary responses to GLP-2. Methods and results GLP-2 receptors were detected on ventricular extracts by quantitative real-time polymerase chain reaction (Q-RT-PCR) and Western blotting. Cardiac GLP-2 effects were analysed on Langendorff perfused hearts. Intracellular GLP-2 signalling was investigated on Langendorff perfuse…

Maleendocrine systemmedicine.medical_specialtyCardiotonic AgentsNitric Oxide Synthase Type IIIMAP Kinase Signaling SystemG proteinEndocrinology Diabetes and MetabolismBlotting WesternMedicine (miscellaneous)Enzyme-Linked Immunosorbent AssayStimulationIn Vitro TechniquesBiologyReal-Time Polymerase Chain Reactionglucagon-like peptides-2 gut peptides cardiac performanceSettore BIO/09 - FisiologiaGlucagon-Like Peptide-1 Receptorchemistry.chemical_compoundInternal medicineCyclic AMPCyclic GMP-Dependent Protein KinasesGlucagon-Like Peptide 2Receptors GlucagonmedicineAnimalsCyclic adenosine monophosphatePhosphorylationRats WistarReceptorNutrition and Dieteticsdigestive oral and skin physiologyHeartPeptide FragmentsRatsPhospholambanEndocrinologyGene Expression RegulationchemistryInotropismGlucagon-Like Peptide-2 ReceptorCardiology and Cardiovascular MedicinecGMP-dependent protein kinasehormones hormone substitutes and hormone antagonistsIntestinal L CellsSignal Transduction
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Effects of cerivastatin on adrenergic pathways, hypertrophic growth and TGFbeta expression in adult ventricular cardiomyocytes.

2010

Abstract The effects of statin treatment in the setting of heart failure have already been shown. Nevertheless, there is little knowledge about its influence on adrenergic pathways in cardiomyocytes. Therefore, this study investigated the impact of cerivastatin on adrenoceptor-mediated signalling pathways in isolated adult ventricular cardiomyocytes. It focused on two endpoints: hypertrophic growth and TGFbeta expression. Cultured cardiomyocytes were used to study rac activation (analysed by its translocation into the membrane fraction), ROS formation (H 2 DCF fluorescence) and hypertrophic growth ( 14 C-phenylalanine incorporation). Alpha- and beta-adrenoceptor stimulation showed significa…

Malemedicine.medical_specialtyHistologyAdrenergic receptorMAP Kinase Signaling SystemPyridinesp38 mitogen-activated protein kinasesHeart VentriclesAdrenergicAlpha (ethology)StimulationPharmacologyp38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineTransforming Growth Factor betaInternal medicineReceptors Adrenergic betamedicineAnimalsMyocytes CardiacRats WistarCells CulturedHeart FailurebiologyCerivastatinCell BiologyGeneral MedicineReceptors Adrenergic alphaRatsEnzyme ActivationEndocrinologyGene Expression RegulationNAD(P)H oxidaseMitogen-activated protein kinasebiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesProto-Oncogene Proteins c-aktmedicine.drugEuropean journal of cell biology
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