Search results for "Receptor"

showing 10 items of 6990 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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Sox17 regulates liver lipid metabolism and adaptation to fasting.

2014

Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is …

medicine.medical_specialtyTransgeneMutantPeroxisome proliferator-activated receptorlcsh:MedicineMice TransgenicGastroenterology and HepatologyBiologyGPI-Linked ProteinsAmidohydrolasesMiceInternal medicineHMGB ProteinsMolecular Cell BiologymedicineMedicine and Health SciencesSOXF Transcription FactorsAnimalsPPAR alphalcsh:ScienceBeta oxidationchemistry.chemical_classificationMultidisciplinaryFatty liverlcsh:RBiology and Life SciencesLipid metabolismSOX9 Transcription FactorCell BiologyFastingmedicine.diseaseLipid MetabolismAdaptation Physiological3. Good healthEndocrinologychemistryPantetheinaseLiverlipids (amino acids peptides and proteins)lcsh:QTranscriptomeDrug metabolismResearch ArticlePLoS ONE
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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 reduce thromboxane production by cultured human endothelial cells.

2011

Objectives Progestogens have been poorly studied concerning their roles in endothelial physiology. Prostanoids are vasoactive compounds, such as thromboxane A2, a potent vasoconstrictor, and prostacyclin, a vasodilator. We examined the effects of two progestogens used clinically, progesterone and medroxyprogesterone acetate, on thromboxane A2 production by cultured human umbilical vein endothelial cells (HUVEC) and investigated the role of progesterone receptors and the enzymes involved in production of thromboxane A2 and prostacyclin. Methods Cells were exposed to 1‐100 nmol/l of either progesterone or medroxyprogesterone acetate, and thromboxane A2 production was measured in culture mediu…

medicine.medical_specialtyUmbilical VeinsAntineoplastic Agents HormonalThromboxaneBlotting WesternGene ExpressionProstacyclinMedroxyprogesterone AcetatePolymerase Chain ReactionProstacyclin synthaseThromboxane receptorThromboxane ProductionThromboxane A2chemistry.chemical_compoundThromboxane A2Hormone AntagonistsCytochrome P-450 Enzyme SystemInternal medicineProgesterone receptorMedicineHumansCyclooxygenase InhibitorsRNA MessengerCells CulturedProgesteronebiologyDose-Response Relationship Drugbusiness.industryObstetrics and GynecologyEndothelial CellsGeneral MedicineIntramolecular OxidoreductasesThromboxane B2MifepristoneEndocrinologychemistrycardiovascular systembiology.proteinPyrazolesThromboxane-A synthaseThromboxane-A SynthaseProgestinsbusinessmedicine.drugClimacteric : the journal of the International Menopause Society
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Gastrin induces the interaction between human mononuclear leukocytes and endothelial cells through the endothelial expression of P-selectin and VCAM-…

2009

Gastric mucosal inflammation is frequently associated with hypergastrinemia, and a correlation exists between the level of gastrin and degree of gastritis. We have previously observed that gastrin promotes leukocyte-endothelial interactions and contributes to Helicobacter -induced inflammation in the rat mesentery. In the present study, we aimed to evaluate a possible proinflammatory activity of gastrin in humans. The interaction between human leukocytes [U-937 cells, peripheral blood polymorphonuclear (PMN), and peripheral blood mononuclear (PBMC) cells] and human umbilical vein endothelial cells (HUVEC) was analyzed in static and dynamic conditions. The endothelial expression of adhesion …

medicine.medical_specialtyUmbilical VeinsEndotheliumP-selectinPhysiologyLeukocyte adhesion moleculeVascular Cell Adhesion Molecule-1Cell CommunicationBiologyCholecystokinin receptorPeripheral blood mononuclear cellchemistry.chemical_compoundInternal medicineGastrinsmedicineCell AdhesionHumansLeukocyte RollingVCAM-1Cells CulturedGastrinEndothelial CellsCell BiologyFlow CytometryReceptor Cholecystokinin BEndothelial stem cellP-Selectinmedicine.anatomical_structureEndocrinologychemistryMicroscopy FluorescenceLeukocytes MononuclearAmerican journal of physiology. Cell physiology
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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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Estradiol Stimulates Vasodilatory and Metabolic Pathways in Cultured Human Endothelial Cells

2009

Vascular effects of estradiol are being investigated because there are controversies among clinical and experimental studies. DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours. When compared to control, 187 genes were identified as differentially expressed with 1.9-fold change threshold. Supervised principal component analysis and hierarchical cluster analysis revealed the differences between control and estradiol-treated samples. Physiological concentrations of estradiol are sufficient to elicit significant changes in HUVEC gene expression. Notch signaling, actin cyt…

medicine.medical_specialtyUmbilical Veinsmedicine.drug_classScienceEstrogen receptorBiologyAmidohydrolasesTransforming Growth Factor beta1chemistry.chemical_compoundInternal medicinemedicineCluster AnalysisEstrogen Receptor betaHumansEstrogen receptor betaCell Biology/Gene ExpressionCells CulturedOligonucleotide Array Sequence AnalysisRegulation of gene expressionPrincipal Component AnalysisMultidisciplinaryEstradiolPhysiology/EndocrinologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingQPhysiology/Cardiovascular Physiology and CirculationREstrogen Receptor alphaEndothelial CellsReproducibility of ResultsActin cytoskeletonVasodilationEndocrinologychemistryGene Expression RegulationEstrogenCyclooxygenase 1MedicineSignal transductionAsymmetric dimethylarginineEstrogen receptor alphahormones hormone substitutes and hormone antagonistsMetabolic Networks and PathwaysResearch ArticleSignal TransductionPLoS ONE
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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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Pure anti-oestrogens

2000

Pure anti-oestrogens are a group of at least five new compounds which are able to antagonize the effects of oestrogen in all tissues and species studied. The mechanism by which the pure anti-oestrogens produce their effects remains in question, but all of them are competitive antagonists of the oestrogen receptors and, moreover, have been proposed to block the shuttling of oestrogen receptors into the cell nucleus. When studied in vitro, these compounds are able to block the oestrogen-stimulated growth of breast cancer cells. In animals, their ability to block the effects of oestrogen on breast, uterus, bone, cardiovascular system and other reproductive-associated tissues has been demonstra…

medicine.medical_specialtyUterusBreast NeoplasmsBreast cancerInternal medicineAnimalsHumansMedicineIn patientskin and connective tissue diseasesReceptorFulvestrantEstradiolMolecular Structurebusiness.industryEstrogen AntagonistsObstetrics and Gynecologymedicine.diseaseIn vitroClinical trialEndocrinologymedicine.anatomical_structureReproductive MedicineCancer researchFemaleBreast cancer cellsbusinessTamoxifenmedicine.drugHuman Reproduction Update
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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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