Search results for "protein kinase"

showing 10 items of 1188 documents

Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism

2007

Acetylcholine may play a role in cell activation and airway inflammation. We evaluated the levels of both mRNA and protein of muscarinic M(1), M(2), M(3) receptors in human bronchial epithelial cell line (16HBE). 16HBE cells were also stimulated with acetylcholine and extracellular signal-regulated kinase1/2 (ERK1/2) and NFkB pathway activation as well as the IL-8 release was assessed in the presence or absence of the inhibitor of Protein-kinase (PKC) (GF109203X), of the inhibitor of mitogenic activated protein-kinase kinase (MAPKK) (PDO9805), of the inhibitor of kinaseB-alpha phosphorilation (pIkBalpha) (BAY11-7082), and of muscarinic receptor antagonists tiotropium bromide, 4-Diphenylacet…

medicine.medical_specialtyIndolesNeutrophilsScopolamine DerivativesBronchiMuscarinic AntagonistsBiologyPharmacologyMaleimideschemistry.chemical_compoundPiperidinesInternal medicineNitrilesMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineHumansRNA MessengerSulfonesTiotropium BromideProtein Kinase CCell Line TransformedAcetylcholine receptorFlavonoidsMitogen-Activated Protein Kinase 1PharmacologyMitogen-Activated Protein Kinase 3Gallamine TriethiodideInterleukin-8NF-kappa BMuscarinic acetylcholine receptor M3Epithelial CellsMuscarinic acetylcholine receptor M2PirenzepineMuscarinic acetylcholine receptor M1Receptors MuscarinicAcetylcholineChemotaxis LeukocyteEndocrinologychemistryTelenzepineAcetylcholinemedicine.drugEuropean Journal of Pharmacology
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Effects of Long-Term Nitroglycerin Treatment on Endothelial Nitric Oxide Synthase (NOS III) Gene Expression, NOS III–Mediated Superoxide Production, …

2000

Abstract —Long-term nitroglycerin (NTG) treatment has been shown to be associated with cross-tolerance to endothelium-dependent vasodilators. It may involve increased production of reactive oxygen species (such as superoxide, O 2 ·− ) that rapidly inactivate the nitric oxide (NO) released from the endothelial cells. It remains to be elucidated, however, whether long-term treatment with NTG alters the activity and expression of the endothelial NO synthase (NOS III) and whether this enzyme can contribute to O 2 ·− formation. We studied the influence of long-term NTG treatment on the expression of NOS III as assessed by RNase protection assay and Western blot. Tolerance was measured ex vivo i…

medicine.medical_specialtyIndolesNitric Oxide Synthase Type IIIPhysiologyCarbazolesBiological AvailabilityVasodilationArginineNitric OxideGene Expression Regulation EnzymologicTimeNitric oxideNitroglycerinchemistry.chemical_compoundAlkaloidsSuperoxidesInternal medicinemedicineAnimalsRNA MessengerLucigeninCloning MolecularEnzyme InhibitorsRats WistarCalcimycinProtein Kinase CProtein kinase CBenzophenanthridineschemistry.chemical_classificationReactive oxygen speciesSuperoxideAcetylcholinePhenanthridinesRatsVasodilationEndocrinologychemistryBiochemistryEndothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineEx vivoAcetylcholinemedicine.drugCirculation Research
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AMP-activated protein kinase (AMPK) signaling pathway: A potential mechanism involved in PAFIYAMA syndrome?

2016

medicine.medical_specialtyLeft atriumAMP-Activated Protein KinasesProtein Serine-Threonine Kinases030204 cardiovascular system & hematologyleft atrium03 medical and health sciences0302 clinical medicineAMP-activated protein kinaseFibrosisInternal medicinemedicineHumansAmpk signalingPhosphorylationPotential mechanismremodelingendurancebiologyexercisebusiness.industryfibrosismedicine.diseaseCell biologyEnzyme Activationmedicine.anatomical_structureEndocrinologybiology.proteinexercise; endurance; arrhythmias; fibrosis; remodeling; left atriumCardiology and Cardiovascular Medicinebusinessarrhythmias030217 neurology & neurosurgerySignal Transduction
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Neuroendocrine Regulation Of The IL-27-Dependent Immune Response In Macrophages

2013

Abstract The central nervous system has the ability for modulating immune responses, but the molecular mechanisms of such interactions are only partly understood. Interleukin-27 (IL-27) is a heterodimeric protein and structurally related to the IL-12 family of cytokines. IL-27 is composed of the subunits EBI3 and p28. The biological functions of IL-27 have been described as either anti-inflammatory or pro-inflammatory depending on the experimental models studied. In the current study, we investigated how production of Interleukin-27 (IL-27) is regulated by neuroendocrine hormones. We focused our work on the subunit p28, since EBI3 is also present in IL-35 and therefore is not a specific com…

medicine.medical_specialtyLipopolysaccharidebiologyp38 mitogen-activated protein kinasesmedicine.medical_treatmentImmunologyInflammationCell BiologyHematologyBiochemistrychemistry.chemical_compoundEndocrinologyCytokineImmune systemchemistryIntegrin alpha MInternal medicinemedicinebiology.proteinmedicine.symptomReceptorHormoneBlood
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Mechanisms of C-reactive protein-induced blood-brain barrier disruption.

2009

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…

medicine.medical_specialtyMyosin light-chain kinaseMyosin Light ChainsGuinea PigsBrain Edemamedicine.disease_causeBlood–brain barrierp38 Mitogen-Activated Protein KinasesMyosin light chain kinase activityTight JunctionsInternal medicineMyosinmedicineAnimalsPhosphorylationReceptorCells CulturedAdvanced and Specialized Nursingbusiness.industryReceptors IgGCoculture TechniquesCell biologyRatsStrokeEndocrinologymedicine.anatomical_structureC-Reactive ProteinBlood-Brain BarrierPhosphorylationNeurology (clinical)Endothelium VascularSignal transductionCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressSignal TransductionStroke
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NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

2021

Abstract Background and aims Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodi…

medicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilationmedicine.disease_causeEnosmedicine.arteryInternal medicineAnimalsMedicineRenal arteryProtein kinase BSistema cardiovascularMetabolic SyndromeAortaDiabetisbiologybusiness.industryModels Theoreticalmedicine.diseasebiology.organism_classificationPPAR gammaVasodilationEndocrinologyEndothelium VascularRabbitsSodium nitroprussideMetabolic syndromeCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktOxidative stressmedicine.drugAtherosclerosis
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Genetic Deletion of JNK1 and JNK2 Aggravates the DSS-Induced Colitis in Mice

2007

The c-Jun N-terminal kinases (JNKs) are considered as novel targets for therapy of inflammatory bowel diseases (IBD). However, the relevant JNK isoforms have to be elucidated. Here, we analyze the individual contribution of the JNK1 and JNK2 isoforms in a dextran sulfate sodium (DSS) model of experimental colitis. JNK1 and JNK2 knockout mice (JNK1 ko, JNK2 ko) and their wild-type controls (WT1, WT2) received three cycles of DSS treatment, each consisting of 1.7% DSS for 5 days, followed by 5 days with water. Animals were daily evaluated by a disease activity index (DAI) comprising measurement of body weight, estimation of stool consistency, and test for occult blood/gross rectal bleeding. A…

medicine.medical_specialtyPathologyCryptApoptosisMice TransgenicInflammatory bowel diseaseGastroenterologyProinflammatory cytokineMiceCecumImmune systemInternal medicineWeight LossAnimalsMitogen-Activated Protein Kinase 9MedicineMitogen-Activated Protein Kinase 8Single-Blind MethodIntestinal MucosaColitisCrosses Geneticbusiness.industryDextran SulfateColitismedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisChronic DiseaseKnockout mouseSurgeryGastrointestinal HemorrhagebusinessJournal of Investigative Surgery
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Ethanol inhibits astroglial cell proliferation by disruption of phospholipase D-mediated signaling.

2002

The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD-mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol-induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum-deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1-2%) suppressed the FCS-induced, PLD-mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration…

medicine.medical_specialtyPlatelet-derived growth factorIndolestert-Butyl Alcoholmedicine.medical_treatmentButanolsBecaplerminPhosphatidic AcidsNerve Tissue ProteinsBiologyBiochemistryCulture Media Serum-FreeCellular and Molecular Neurosciencechemistry.chemical_compound1-ButanolInternal medicineLysophosphatidic acidmedicinePhospholipase DAnimalsPhosphorylationProtein kinase APlatelet-Derived Growth FactorEndothelin-1EthanolPhospholipase DCell growthGrowth factorPhosphatidic acidDNAProto-Oncogene Proteins c-sisProtein-Tyrosine KinasesGenisteinGrowth InhibitorsCell biologyRatsEndocrinologychemistryFetal Alcohol Spectrum DisordersAstrocyteslipids (amino acids peptides and proteins)Signal transductionVanadatesProtein Processing Post-TranslationalCell DivisionSignal TransductionJournal of neurochemistry
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Acute estradiol protects CA1 neurons from ischemia-induced apoptotic cell death via the PI3K/Akt pathway

2010

Global ischemia arising during cardiac arrest or cardiac surgery causes highly selective, delayed death of hippocampal CA1 neurons. Exogenous estradiol ameliorates global ischemia-induced neuronal death and cognitive impairment in male and female rodents. However, the molecular mechanisms by which a single acute injection of estradiol administered after the ischemic event intervenes in global ischemia-induced apoptotic cell death are unclear. Here we show that acute estradiol acts via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling cascade to protect CA1 neurons in ovariectomized female rats. We demonstrate that global ischemia promotes early activation of glycogen syn…

medicine.medical_specialtyProgrammed cell deathmedicine.drug_classOvariectomyBlotting WesternIschemiaApoptosisHippocampusArticleBrain IschemiaBrain ischemiaPhosphatidylinositol 3-KinasesInternal medicinemedicineAnimalsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCaspaseNeuronsbiologyEstradiolGeneral NeuroscienceEstrogensmedicine.diseaseRatsEndocrinologyEstrogenApoptosisNerve DegenerationCancer researchbiology.proteinFemaleNeurology (clinical)Proto-Oncogene Proteins c-aktDevelopmental BiologySignal Transduction
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