Search results for " PAR-1"

showing 5 items of 5 documents

Signal transduction pathways involved in the mechanical responses to protease-activated receptors in rat colon.

2002

Recording simultaneously in vitro the changes of endoluminal pressure (index of circular muscle activity) and isometric tension (index of longitudinal muscle activity), we examined the mechanisms responsible for the apamin-sensitive relaxant and contractile responses induced by protease-activated receptor (PAR)-1 and PAR-2 activating peptides, SFLLRN-NH2 and SLIGRL-NH2, respectively, in rat colon. In the circular muscle, the inhibitory effects of SFLLRN-NH2 and SLIGRL-NH2 were significantly reduced by ryanodine, an inhibitor of Ca2+ release from the sarcoplasmic reticulum, but unaffected by 1-[6-[[17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122), a phosph…

Intracellular FluidMalemedicine.medical_specialtyColonGenisteinBiologyIn Vitro Techniqueschemistry.chemical_compoundInternal medicinemedicineAnimalsReceptor PAR-2Receptor PAR-1Rats WistarReceptorProtein kinase CPharmacologyPhospholipase CRyanodine receptorNeural InhibitionRatsEndocrinologychemistryType C PhospholipasesMolecular MedicineCalciumReceptors ThrombinSignal transductionmedicine.symptomExtracellular SpaceTyrosine kinaseMuscle contractionMuscle ContractionSignal TransductionThe Journal of pharmacology and experimental therapeutics
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Vorapaxar in the secondary prevention of atherothrombotic events

2012

BACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients …

MalePyridines[SDV]Life Sciences [q-bio]Myocardial InfarctionMedizinKaplan-Meier Estimate030204 cardiovascular system & hematologyBrain IschemiaLactones0302 clinical medicineMESH: Peripheral Arterial DiseaseSecondary PreventionMESH: Double-Blind Method030212 general & internal medicineMyocardial infarctionStrokeVorapaxarMESH: AgedAspirinMESH: Middle AgedMESH: RiskCardiovascular diseases [NCEBP 14]MESH: Secondary PreventionHazard ratioMESH: Brain IschemiaGeneral MedicineMiddle AgedClopidogrel3. Good healthStrokeMESH: Receptor PAR-1MESH: Myocardial Infarctionvorapaxar secondary prevention atherothrombotic eventsCardiovascular DiseasesMESH: Platelet Aggregation InhibitorsAnesthesiaRetreatmentPlatelet aggregation inhibitorFemaleIntracranial HemorrhagesMESH: HemorrhageMESH: Intracranial HemorrhagesMESH: Lactonescirculatory and respiratory physiologymedicine.drugRiskISQUEMIA CEREBRALHemorrhagePlaceboMESH: StrokePeripheral Arterial Disease03 medical and health sciencesDouble-Blind Method[INFO.INFO-IM]Computer Science [cs]/Medical ImagingmedicineHumansReceptor PAR-1MESH: RetreatmentMESH: Kaplan-Meier EstimateAgedMESH: Humansbusiness.industryMESH: PyridinesMESH: Cardiovascular Diseasesmedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareMESH: MalebusinessMESH: FemalePlatelet Aggregation Inhibitors
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Human neutrophil elastase induces endothelial cell apoptosis by activating the PERK‐CHOP branch of the unfolded protein response

2017

Human neutrophil elastase impacts on atherosclerotic plaque stability by inducing apoptosis in endothelial cells. Our aim was to investigate the proapoptotic mechanism of elastase on endothelial cells and to evaluate the presence of elastase in human plaque material. Human endothelial cells were treated with purified human neutrophil elastase. Apoptosis was assayed by capsase-3/7 activation, TUNEL, and sub-G1 assay. Activation of unfolded protein response (UPR) effector molecules binding Ig protein, soluble X-binding protein-1, protein kinase RNA-like ER kinase (PERK), and C/EBP-homologous protein (CHOP) was analyzed by RT-PCR, immunocytochemistry, and Western blot. Genetic silencing of CHO…

0301 basic medicineSmall interfering RNACell SurvivalApoptosisCHOPBiochemistryGene Expression Regulation EnzymologicCell LineeIF-2 Kinase03 medical and health sciencesGeneticsHumansReceptor PAR-2Receptor PAR-1Protein kinase AMolecular BiologyCaspase 7Caspase 3KinaseChemistryElastaseEndothelial CellsAtherosclerosisMolecular biologyEndothelial stem cellCarotid Arteries030104 developmental biologyApoptosisUnfolded Protein ResponseUnfolded protein responseLeukocyte ElastaseTranscription Factor CHOPBiotechnologyThe FASEB Journal
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Glypican-3 and Hep Par-1 are Useful Biomarkers in the Cytologic Assessment of Ascites.

2018

Till date, the utility of cytologic assessment of ascites for the identification of hepatocellular carcinoma (HCC) cells is still debated and the usefulness of immunocytochemistry for glypican-3 (GPC3) and Hep Par-1 in this setting has not been reported. Liquid-based cytology of ascitic fluid of 28 cirrhotic patients was performed and the spots obtained were stained with hematoxylin and eosin, papanicolau, and with GPC3 and Hep Par-1 antibodies. GPC3 and Hep Par-1 antibodies stained positively the atypical cells in the ascites of 2 patients with HCC showing an exophytic growth pattern. The specimens of the patients with nonexophytic HCC, other non-HCC cancers, or cirrhosis stained negativel…

0301 basic medicinePathologymedicine.medical_specialtyHistologyCirrhosisCarcinoma HepatocellularH&E stainneoplastic asciteGlypican 3EpitheliumPathology and Forensic Medicineperitoneal effusionDiagnosis Differential03 medical and health sciencesimmunocytochemistry0302 clinical medicineGlypicansCytologyAscitesCarcinomaMedicineHumansProspective StudiesHCCneoplasmsReceptors Eph Familybusiness.industryLiver NeoplasmsAsciteshepatocellular carcinomamedicine.diseaseFibrosisImmunohistochemistryglypican-3digestive system diseasesMedical Laboratory Technology030104 developmental biologyLiver030220 oncology & carcinogenesisHepatocellular carcinomaImmunohistochemistrymedicine.symptomHep Par-1businessApplied immunohistochemistrymolecular morphology : AIMM
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PAR1 signaling regulates the retention and recruitment of EPCR-expressing bone marrow hematopoietic stem cells

2015

Retention of long-term repopulating hematopoietic stem cells (LT-HSCs) in the bone marrow is essential for hematopoiesis and for protection from myelotoxic injury. We report that signaling cascades that are traditionally viewed as coagulation related also control retention of endothelial protein C receptor-positive (EPCR(+)) LT-HSCs in the bone marrow and their recruitment to the blood via two pathways mediated by protease activated receptor 1 (PAR1). Thrombin-PAR1 signaling induces nitric oxide (NO) production, leading to EPCR shedding mediated by tumor necrosis factor-α-converting enzyme (TACE), enhanced CXCL12-CXCR4-induced motility and rapid stem and progenitor cell mobilization. Conver…

Receptors CXCR4Receptors Cell SurfaceADAM17 ProteinIntegrin alpha4beta1BiologyNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyMiceBone MarrowCell MovementCell AdhesionmedicineAnimalsReceptor PAR-1Progenitor cellcdc42 GTP-Binding ProteinCell adhesionEndothelial protein C receptorThrombinEndothelial Protein C ReceptorGeneral MedicineHematopoietic Stem CellsChemokine CXCL12Cell biologyMice Inbred C57BLTransplantationADAM ProteinsHaematopoiesismedicine.anatomical_structureCdc42 GTP-Binding ProteinImmunologyBone marrowStem cellProtein CSignal TransductionNature Medicine
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