Search results for "RECEPTORS"

showing 10 items of 3254 documents

Regulation of PTHrP and PTH/PTHrP receptor by extracellular Ca2+ concentration and hormones in the breast cancer cell line 8701-BC.

2000

AbstractIt was previously reported that 8701-BC breast tumour cells express the gene for parathyroid hormonerelated peptide (PTHrP) and PTH/PTHrP receptor (PTHrPR) and release immunoreactive PTHrP (iPTHrP) into the extracellular medium. Since the regulation of PTHrP and PTHrPR by breast cancer cells has been poorly investigated so far, we have chosen the 8701- BC cell line as a model system to investigate whether alterations in the extracellular Ca[2+] concentration ([Ca[2+]]) and treatment with some wellknown differentiation agents for breast cells, such as dimethyl sulfoxide, hydrocortisone, progesterone, prolactin, alltrans retinoic acid and transforming growth factorβ1 might (i) modulat…

medicine.medical_specialtyTranscription GeneticRNA SplicingClinical BiochemistryRetinoic acidCodon InitiatorBreast NeoplasmsTretinoinBiochemistrychemistry.chemical_compoundTranscription (biology)Transforming Growth Factor betaInternal medicinemedicineExtracellularTumor Cells CulturedHumansProtein IsoformsRNA MessengerPromoter Regions GeneticMolecular BiologyGeneChemistryParathyroid Hormone-Related ProteinProteinsProlactinHormonesNeoplasm ProteinsEndocrinologyGene Expression RegulationCell cultureRNA splicingReceptors Parathyroid HormoneCalciumExtracellular Spacehormones hormone substitutes and hormone antagonistsHormoneBiological chemistry
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Proliferative effect of acetylcholine on rat trachea epithelial cells is mediated by nicotinic receptors and muscarinic receptors of the M1-subtype.

2003

Acetylcholine (ACh), synthesized in mammalian non-neuronal cells such as epithelial cells of the airways, digestive tract and skin, is involved in the regulation of basic cell functions (so-called non-neuronal cholinergic system). In the present experiments rat trachea epithelial cells have been cultured to study the proliferative effect of applied ACh by [3H]thymidine incorporation. ACh (exposure time 24 h) caused a concentration-dependent increase in cell proliferation with a doubling of the [3H]thymidine incorporation at a concentration of 0.1 microM. This effect was partly reduced by 30 microM tubocurarine and completely abolished by the additional application of 1 microM atropine. The …

medicine.medical_specialtyTubocurarineMuscarinic AntagonistsNicotinic AntagonistsBiologyReceptors NicotinicGeneral Biochemistry Genetics and Molecular BiologyRats Sprague-DawleyInternal medicineMuscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsGeneral Pharmacology Toxicology and PharmaceuticsNicotinic AntagonistReceptor Muscarinic M1Muscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Epithelial CellsGeneral MedicineMolecular biologyPirenzepineReceptors MuscarinicAcetylcholineRatsTracheaAtropineEndocrinologyAcetylcholineCell Divisionmedicine.drugThymidineLife sciences
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Progestogens stimulate prostacyclin production by human endothelial cells.

2005

BACKGROUND: The effects of progestogens on endothelial physiology are poorly studied. Prostacyclin is a potent vasodilator synthesized by two isoforms of cyclooxygenase (COX) in endothelium. We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes. METHODS: Cells were exposed to 1-100 nmol/l of either progesterone or MPA and prostacyclin production was measured in culture medium. RESULTS: Both progestogens significantly increased prostacyclin release in a time- and dose-dependent man…

medicine.medical_specialtyUmbilical VeinsEndotheliumProstacyclinMedroxyprogesterone AcetateUmbilical veinInternal medicineProgesterone receptormedicineMedroxyprogesterone acetateHumansCyclooxygenase InhibitorsReceptorCells CulturedNitrobenzenesProgesteroneSulfonamidesbiologyCyclooxygenase 2 InhibitorsDose-Response Relationship DrugEstradiolRehabilitationObstetrics and GynecologyEndothelial CellsMembrane ProteinsEpoprostenolEndothelial stem cellMifepristoneEndocrinologymedicine.anatomical_structureReproductive MedicineCyclooxygenase 2Prostaglandin-Endoperoxide Synthasescardiovascular systembiology.proteinCyclooxygenase 1PyrazolesCyclooxygenaseEndothelium VascularProgestinsReceptors Progesteronemedicine.drugHuman reproduction (Oxford, England)
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The pharmacological rationale for combining muscarinic receptor antagonists and beta-adrenoceptor agonists in the treatment of airway and bladder dis…

2014

Highlights • Muscarinic receptors increase smooth muscle tone in airways and urinary bladder. • β-Adrenoceptors relax smooth muscle tone and oppose muscarinic contraction. • Opposition involves transmitter release, signal transduction and receptor expression. • This supports the combined use of muscarinic antagonists and β-adrenoceptor agonists.

medicine.medical_specialtyUrologyDiseaseMuscarinic AntagonistsPharmacologyArticleβ adrenoceptorchemistry.chemical_compoundInternal medicineReceptors Adrenergic betaMuscarinic acetylcholine receptorDrug DiscoveryMuscarinic acetylcholine receptor M4RAT URINARY-BLADDERMedicineAnimalsHumansCyclic adenosine monophosphateADRENERGIC RELAXATIONLung Diseases ObstructivePROTEIN-KINASE-CReceptorTRACHEAL SMOOTH-MUSCLEPharmacologybusiness.industryUrinary Bladder DiseasesMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2ACETYLCHOLINE-RELEASEAdrenergic beta-Agonistsmedicine.diseaseReceptors MuscarinicEndocrinologyNONNEURONAL CHOLINERGIC SYSTEMchemistryGUINEA-PIG TRACHEADrug Therapy CombinationCYCLIC ADENOSINE-MONOPHOSPHATECA2+-ACTIVATED K+ CHANNELAirwaybusinessUrinary bladder diseaseAUTORADIOGRAPHIC VISUALIZATIONAcetylcholinemedicine.drug
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Dopaminergic modulation of evoked vasopressin release from the isolated neurohypophysis of the rat

1982

1. Neurointermediate lobes of rat pituitaries were incubated in Locke or Krebs solution, and the vasopressin released into the medium was assayed on the blood pressure of the pithed rat or by a radioimmunological procedure. Release of vasopressin over resting levels was evoked either by incubation with 60 mM KCl (high K) solution or by electrical stimulation of the pituitary stalk. Two different kinds of electrical stimulation were carried out. Procedure A (1 ms, 10 Hz, 5 times for 1 min within 10 min) induced a vasopressin overflow which was greatly calcium-dependent but only insignificantly sensitive to tetrodotoxin (TTX). Procedure B (0.2 ms, 15 Hz, 10 s trains with 10 s intervals for 10…

medicine.medical_specialtyVasopressinApomorphineVasopressinsDopamineStimulationTetrodotoxinIn Vitro TechniquesReceptors DopaminePituitary Gland PosteriorDopamineInternal medicinemedicineAnimalsBromocriptineEndogenous opioidPharmacologyNaloxoneChemistryDopaminergicRats Inbred StrainsGeneral MedicineElectric StimulationRatsFlupenthixolApomorphineEndocrinologyDopamine receptorFemaleEndorphinsSulpirideSulpiridemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Dietary cholate increases plasma levels of apolipoprotein B in mice by posttranscriptional mechanisms

2001

To induce atherogenesis in mice, a high fat (HF) diet is supplemented with cholic acid (CA), which increases apoB-containing particles and lower apoA-I-containing particles. HF diet without CA increases levels of both HDL and LDL, suggesting that CA may be responsible for the elevation of LDL and lowering of HDL. The mechanism of dietary CA-induced lowering of apoA-I-containing particles has recently been reported. In this study, we examined the mechanism of CA- and HF-induced elevation of apoB-containing lipoproteins in mice. Mice were fed the following four diets: control chow (C), high fat high cholesterol, (HF), control and 0.5% cholate (CA), and HF + CA. Dietary CA increased the plasma…

medicine.medical_specialtyVery low-density lipoproteinSettore MED/09 - Medicina InternaMouseApolipoprotein Bmedicine.medical_treatmentDown-RegulationCholic AcidLipoproteins VLDLBiochemistryDietary cholateMicechemistry.chemical_compoundApolipoproteins ERibonucleasesDownregulation and upregulationInternal medicinemedicineAnimalsVitamin ERNA MessengerRNA Processing Post-TranscriptionalReceptorApolipoproteins BbiologyChemistryVitamin ECholic acidnutritional and metabolic diseasesCell BiologyBlotting NorthernDietLipoproteins LDLMice Inbred C57BLCholesterolEndocrinologyLiverReceptors LDLLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Gene expressionHepatic lipaseApolipoprotein BCholatesDietary fatThe International Journal of Biochemistry & Cell Biology
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Changes in neurophysiologic markers of visual processing following beneficial anti-VEGF treatment in macular degeneration

2013

Pasi Vottonen,1 Kai Kaarniranta,1,2 Ari Pääkkönen,3 Ina M Tarkka41Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland; 2Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland; 3Department of Clinical Neurophysiology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland; 4Department of Health Sciences, University of Jyväskylä, Jyväskylä, FinlandPurpose: Antivascular endothelial growth factor (VEGF) agents have been shown to improve visual acuity and prevent vision loss in exudative age-related macular degeneration. As the vision im…

medicine.medical_specialtyVisual acuityexudative age-related macular degenerationvisual acuitygenetic structuresvisual evoked potentialsVEGF receptorsta3112Cortical processingVisual processingText miningOphthalmologymedicinescalp-recorded EEGage-related eye diseasesOriginal Researchbiologybusiness.industryta3141Clinical OphthalmologyMacular degenerationmedicine.diseaseeye diseasesOphthalmologybiology.proteinElectrophysiological markerssense organsAnti vegf treatmentmedicine.symptombusinessClinical Ophthalmology
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Molecular Analysis of the Androgen Receptor Gene in 52 Patients with Complete or Partial Androgen Insensitivity Syndrome: A Collaborative Study

1992

In patients with androgen insensitivity syndrome (AIS), RFLP study of the androgen receptor gene made it possible to analyze whether deletions or mutations could be responsible for abnormalities in androgen responsiveness. We studied RFLPs of DNA from 25 46,XY patients with partial AIS (PAIS), defined as a concentration of androgen receptor in genital-skin fibroblasts less than 340 fmol/mg DNA, and DNA from 27 46,XY patients with complete AIS (CAIS) with no detectable androgen receptor site. DNA samples were digested with BamHI, EcoRI, HindIII and TaqI restriction enzymes and hybridized with three cDNA probes covering the three domains of the androgen receptor. When we had the maternal and …

medicine.medical_specialtyX Chromosomemedicine.drug_classEndocrinology Diabetes and MetabolismMolecular Sequence DataDeoxyribonuclease HindIIIBiologyurologic and male genital diseasesPolymerase Chain Reactionchemistry.chemical_compoundEndocrinologyInternal medicinemedicineHumansPartial androgen insensitivity syndromeGeneSex Chromosome AberrationsBase SequenceAndrogen Receptor GeneDNASyndromeMetribolonemedicine.diseaseAndrogenMolecular analysisEndocrinologychemistryReceptors AndrogenMutationAndrogensAndrogen insensitivity syndromeRestriction fragment length polymorphismPolymorphism Restriction Fragment LengthDNAHormone Research
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Selected peptides targeted to the NMDA receptor channel protect neurons from excitotoxic death

1998

Excitotoxic neuronal death, associated with neurodegeneration and stroke, is triggered primarily by massive Ca2+ influx arising from overactivation of glutamate receptor channels of the N-methyl-D-aspartate (NMDA) subtype. To search for channel blockers, synthetic combinatorial libraries were assayed for block of agonist-evoked currents by the human NR1-NR2A NMDA receptor subunits expressed in amphibian oocytes. A set of arginine-rich hexapeptides selectively blocked the NMDA receptor channel with IC50 approximately 100 nM, a potency similar to clinically tolerated blockers such as memantine, and only marginally blocked on non-NMDA glutamate receptors. These peptides prevent neuronal cell d…

medicine.medical_specialtyXenopusDrug Evaluation PreclinicalBiomedical EngineeringBioengineeringHippocampal formationBiologyPharmacologyArginineBinding CompetitiveHippocampusReceptors N-Methyl-D-AspartateApplied Microbiology and BiotechnologySubstrate SpecificityInternal medicinemedicineAnimalsHumansChannel blockerReceptorNeuronsCell DeathNeurodegenerationGlutamate receptorMemantinemedicine.diseaseRatsEndocrinologymedicine.anatomical_structurenervous systemDrug DesignOocytesMolecular MedicineNMDA receptorFemaleNeuronPeptidesBiotechnologymedicine.drugNature Biotechnology
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