Search results for "Forskolin"

showing 10 items of 37 documents

Desensitization of cAMP Accumulation via Human β3-Adrenoceptors Expressed in Human Embryonic Kidney Cells by Full, Partial, and Biased Agonists

2019

β3-Adrenoceptors couple not only to cAMP formation but, at least in some cell types, also to alternative signaling pathways such as phosphorylation of extracellular signal-regulated kinase (ERK). β3-Adrenoceptor agonists are used in long-term symptomatic treatment of the overactive bladder syndrome; it is only poorly understood which signaling pathway mediates the clinical response and whether it undergoes agonist-induced desensitization. Therefore, we used human embryonic kidney cells stably transfected with human β3-adrenoceptors to compare coupling of ligands with various degrees of efficacy, including biased agonists, to cAMP formation and ERK phosphorylation, particularly regarding des…

0301 basic medicineAgonistMAPK/ERK pathwaymedicine.drug_classmedicine.medical_treatmentdesensitization03 medical and health scienceschemistry.chemical_compoundpartial agonism0302 clinical medicinecAMPIsoprenalinemedicinePharmacology (medical)β3-adrenoceptorOriginal ResearchDesensitization (medicine)PharmacologyForskolinKinaselcsh:RM1-950extracellular signal-related kinaseCell biologylcsh:Therapeutics. Pharmacology030104 developmental biologybiased agonismchemistry030220 oncology & carcinogenesisPhosphorylationSignal transductionmedicine.drugFrontiers in Pharmacology
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Activation of PPARβ/δ prevents hyperglycaemia-induced impairment of Kv7 channels and cAMP-mediated relaxation in rat coronary arteries.

2016

PPARβ/δ activation protects against endothelial dysfunction in diabetic models. Elevated glucose is known to impair cAMP-induced relaxation and Kv channel function in coronary arteries (CA). Herein, we aimed to analyse the possible protective effects of the PPARβ/δ agonist GW0742 on the hyperglycaemic-induced impairment of cAMP-induced relaxation and Kv channel function in rat CA. As compared with low glucose (LG), incubation under high glucose (HG) conditions attenuated the relaxation induced by the adenylate cyclase activator forskolin in CA and this was prevented by GW0742. The protective effect of GW0742 was supressed by a PPARβ/δ antagonist. In myocytes isolated from CA under LG, forsk…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPDK4Protein Serine-Threonine Kinasesmedicine.disease_causeGW0742Diabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineCyclic AMPAnimalsHumansPPAR deltaRats WistarPPAR-betaForskolinAntagonistPyruvate Dehydrogenase Acetyl-Transferring KinaseGeneral MedicineHyperpolarization (biology)Coronary VesselsPotassium channelRatsVasodilationThiazoles030104 developmental biologyEndocrinologychemistryHyperglycemiaKCNQ1 Potassium ChannelReactive Oxygen SpeciesOxidative stressClinical science (London, England : 1979)
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Activity of the adenylyl cyclase in lymphocytes of male alcoholic patients is state dependent.

1998

A decreased basal and/or stimulated activity of the G-protein/adenylyl cyclase (AC) system in peripheral blood cells has been proposed to represent a trait marker for alcoholism. However, AC activity may underlie state-dependent changes, which may impair a proper interpretation of AC activity measurements. Our study examined systematically the AC activity in peripheral lymphocytes of 73 male alcohol-dependent patients (according to DSM-IV criteria) at three different time points of measurement during the clinical course of detoxification (day 0 = at admission, while still ethanol-affected; day 2 = at the presumed peak of withdrawal symptoms; day E = after detoxification). Basal and stimulat…

AdultMalemedicine.medical_specialtyLymphocyteGTPgammaSMedicine (miscellaneous)ToxicologyAdenylyl cyclaseAlcohol Withdrawal Deliriumchemistry.chemical_compoundBasal (phylogenetics)Reference ValuesInternal medicineDetoxificationmedicineHumansLymphocytesAgedForskolinbusiness.industryMiddle AgedPeripheralPsychiatry and Mental healthAlcoholismmedicine.anatomical_structureEndocrinologychemistryToxicitybusinessBiomarkersAdenylyl CyclasesAlcoholism, clinical and experimental research
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Blood ethanol levels and adenylyl cyclase activity in lymphocytes of alcoholic patients

1999

Abstract Background: The adenylyl cyclase (AC) signal transduction pathway is a target of acute and chronic ethanol actions. This study examined whether AC activity in lymphocyte membranes of male alcoholic patients correlated with blood concentrations of ethanol. Methods: Patients ( n = 13; mean age: 40 ± 8 years) were studied on the day of admission (day 0) and 2 days later under detoxification. Moreover, 13 age-matched male healthy controls (mean age 40 ± 9 years) were included. Lymphocyte membranes were prepared by differential centrifugation whereby blood ethanol was washed out. As a measure of AC activity the formation of cyclic adenosine monophosphate (cAMP) from adenosine triphospha…

AdultMalemedicine.medical_specialtyLymphocyteStimulationGuanosine triphosphateAdenylyl cyclasechemistry.chemical_compoundAdenosine TriphosphateInternal medicineCyclic AMPmedicineHumansCyclic adenosine monophosphateLongitudinal StudiesLymphocytesBiological PsychiatryEthanolForskolinDose-Response Relationship DrugEthanolColforsinMiddle AgedAlcoholismmedicine.anatomical_structureEndocrinologychemistryCase-Control StudiesGuanosine TriphosphatePhosphorus RadioisotopesAdenosine triphosphateAdenylyl CyclasesSignal TransductionBiological Psychiatry
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Relaxation induced by milrinone and rolipram in human penile arteries and veins

2002

Abstract We studied the relaxant effects of milrinone, an inhibitor of phosphodiesterase 3, and rolipram, an inhibitor of phosphodiesterase 4, on contracted human penile dorsal artery and deep dorsal vein. Vascular rings from 12 multi-organ donors were suspended in organ baths for isometric recording of tension. Both milrinone and rolipram inhibited (100%) the contraction induced by noradrenaline and shifted the relaxation–response curves to the cAMP forming agents prostaglandin E1 and forskolin to the left. The findings indicate that the cAMP pathway appears to be a main determinant of relaxation in human penile vessels.

AdultMalemedicine.medical_specialtyPhosphodiesterase InhibitorsPhosphodiesterase 3Penile arteryBiologyMuscle Smooth Vascularchemistry.chemical_compoundInternal medicinemedicineHumansDrug InteractionsChildProstaglandin E1RolipramPharmacologyForskolinDose-Response Relationship DrugColforsinMiddle AgedVasodilationEndocrinologymedicine.anatomical_structurechemistryCirculatory systemMilrinoneRolipramMilrinonePenisBlood vesselmedicine.drugEuropean Journal of Pharmacology
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Biphasic Erk1/2 activation sequentially involving Gs and Gi signaling is required in beta3-adrenergic receptor-induced primary smooth muscle cell pro…

2013

Abstract The beta3 adrenergic receptor (B3-AR) reportedly induces cell proliferation, but the signaling pathways that were proposed, involving either Gs or Gi coupling, remain controversial. To further investigate the role of G protein coupling in B3-AR induced proliferation, we stimulated primary human myometrial smooth muscle cells with SAR150640 (B3-AR agonist) in the absence or presence of variable G-protein inhibitors. Specific B3-AR stimulation led to an Erk1/2 induced proliferation. We observed that the proliferative effects of B3-AR require two Erk1/2 activation peaks (the first after 3 min, the second at 8 h). Erk1/2 activation at 3 min was mimicked by forskolin (adenylyl-cyclase a…

Beta-3 adrenergic receptorGs alpha subunitMAP Kinase Signaling SystemMyocytes Smooth MuscleProliferationG protein coupled receptorBiologyGTP-Binding Protein alpha Subunits Gi-GoPertussis toxinchemistry.chemical_compoundErk1/2Protein kinasesCyclinsReceptors Adrenergic betaGTP-Binding Protein alpha Subunits GsHumansMolecular BiologyPI3K/AKT/mTOR pathwayCells CulturedG protein-coupled receptorCell ProliferationForskolinColforsinBeta-3 adrenergic receptorCell BiologyCell biologychemistryGene Expression RegulationPertussis ToxinMyometriumFemaleSignal transductionProto-oncogene tyrosine-protein kinase SrcBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Synergistic interaction of adenylate cyclase activators and nitric oxide donor SIN-1 on platelet cyclic AMP

1995

Abstract The molecular mechanism of the synergistic platelet inhibition by activators of adenylate cyclase and guanylate cyclase in human platelets was investigated. The adenylate cyclase activators iloprost and prostaglandin E 1 and the guanylate cyclase activator 3-morpholino-synonimine (SIN-1) dose-dependently inhibited thrombin-induced aggregation of washed human platelets. Furthermore, SIN-1 at a concentration inhibiting platelet aggregation by only 10% shifted the IC 50 values of iloprost and prostaglandin E 1 by one order of magnitude to the left, indicating a synergistic action of adenylate cyclase and guanylate cyclase activators. Iloprost and prostaglandin E 1 dose-dependently ele…

Blood Plateletsmedicine.medical_specialtyGUCY1B3Platelet Aggregationmedicine.medical_treatmentAdenylate kinaseIn Vitro TechniquesNitric OxideCyclasechemistry.chemical_compoundInternal medicineCyclic AMPmedicineHumansPlateletIloprostAlprostadilCyclic GMPPharmacologyForskolinGUCY1A3PhosphodiesteraseDrug SynergismEnzyme ActivationEndocrinologychemistryGuanylate CyclaseMolsidominelipids (amino acids peptides and proteins)Platelet Aggregation InhibitorsAdenylyl CyclasesProstaglandin EEuropean Journal of Pharmacology: Molecular Pharmacology
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Decrease of mRNA levels and biosynthesis of sucrase-isomaltase but not dipeptidylpeptidase IV in forskolin or monensin-treated Caco-2 cells.

1991

International audience; Treatment for 48 h of differentiated, confluent Caco-2 cells with 2.5 10(-5) M forskolin or 10(-6) M monensin, which produces a significant decrease of the de novo biosynthesis of sucrase-isomaltase, does not change quantitatively the de novo biosynthesis of dipeptidylpeptidase IV. Western blot analysis and silver nitrate staining indicate that neither drug induces any modification in the steady state expression of these two brush border hydrolases. Northern blot analysis shows that the level of dipeptidylpeptidase IV mRNA does not change in treated as compared to control Caco-2 cells. In contrast, forskolin and monensin dramatically decrease the level of sucrase-iso…

Brush borderDipeptidyl Peptidase 4Blotting WesternAdenocarcinomaBiology03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundWestern blot[ CHIM.ORGA ] Chemical Sciences/Organic chemistryCyclic AMPTumor Cells CulturedmedicineHumansRNA MessengerNorthern blotMonensinDipeptidyl-Peptidases and Tripeptidyl-PeptidasesMolecular Biology030304 developmental biologyPharmacology0303 health sciencesForskolinmedicine.diagnostic_test[CHIM.ORGA]Chemical Sciences/Organic chemistryColforsin030302 biochemistry & molecular biologyMonensinAntibodies MonoclonalCell BiologyMetabolismBlotting Northern[CHIM.ORGA] Chemical Sciences/Organic chemistrySucrase-Isomaltase ComplexGlucosechemistryBiochemistryCell cultureColonic NeoplasmsMolecular MedicineSucrase-isomaltase
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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Comparison of a Novel Homogeneous Cyclic Amp Assay and a Luciferase Assay for Measuring Stimulating Thyrotropin-Receptor Autoantibodies.

2019

Objective: Stimulating thyrotropin-receptor antibodies (TSAb) cause Graves’ disease (GD). We tested a novel homogeneous fluorescent 3′,5′ cyclic adenine monophosphate (cAMP) assay for the detection of TSAb in a bioassay. Methods: Chinese hamster ovary (CHO) cell lines expressing either a chimeric (MC4) or wild-type (WT) TSH-R were incubated with the adenyl cyclase activator forskolin, a human TSAb monoclonal antibody (M22), and with sera from GD patients. Intracellular cAMP levels were measured using a Bridge-It® cAMP assay, and the results were compared with a luciferase-based bioassay. Results: Both cell lines were stimulated with forskolin concentrations (0.006–200 µM) in a dose-dependen…

Forskolinbusiness.industryActivator (genetics)Endocrinology Diabetes and MetabolismLigand binding assayChinese hamster ovary cell030209 endocrinology & metabolismMolecular biologyThyrotropin receptor03 medical and health scienceschemistry.chemical_compound0302 clinical medicinechemistryCell culture030220 oncology & carcinogenesisMedicineBioassayLuciferasebusinessTranslational Thyroidology / Research ArticleEuropean thyroid journal
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