Search results for "coagulation"

showing 10 items of 381 documents

Paraoxonase-2 regulates coagulation activation through endothelial tissue factor

2017

Oxidative stress and inflammation of the vessel wall contribute to prothrombotic states. The antioxidative protein paraoxonase-2 (PON2) shows reduced expression in human atherosclerotic plaques and endothelial cells in particular. Supporting a direct role for PON2 in cardiovascular diseases, Pon2 deficiency in mice promotes atherogenesis through incompletely understood mechanisms. Here, we show that deregulated redox regulation in Pon2 deficiency causes vascular inflammation and abnormalities in blood coagulation. In unchallenged Pon2-/- mice, we find increased oxidative stress and endothelial dysfunction. Bone marrow transplantation experiments and studies with endothelial cells provide ev…

0301 basic medicineEndotheliumImmunologyInflammation030204 cardiovascular system & hematologymedicine.disease_causeModels BiologicalBiochemistryThromboplastinMice03 medical and health sciencesTissue factor0302 clinical medicinemedicineAnimalsHumansThromboplastinPlateletEndothelial dysfunctionBlood CoagulationInflammationMice KnockoutAryldialkylphosphataseChemistryEndothelial CellsCell BiologyHematologymedicine.diseaseEndothelial stem cellOxidative Stress030104 developmental biologymedicine.anatomical_structureCancer researchCytokinesInflammation Mediatorsmedicine.symptomOxidation-ReductionOxidative stressBlood
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Extravascular coagulation in hematopoietic stem and progenitor cell regulation

2018

Abstract The hemostatic system plays pivotal roles in injury repair, innate immunity, and adaptation to inflammatory challenges. We review the evidence that these vascular-protective mechanisms have nontraditional roles in hematopoietic stem cell (HSC) maintenance in their physiological bone marrow (BM) niches at steady-state and under stress. Expression of coagulation factors and the extrinsic coagulation initiator tissue factor by osteoblasts, tissue-resident macrophages, and megakaryocytes suggests that endosteal and vascular HSC niches are functionally regulated by extravascular coagulation. The anticoagulant endothelial protein C receptor (EPCR; Procr) is highly expressed by primitive …

0301 basic medicineImmunologyBone Marrow Cells030204 cardiovascular system & hematologyBiologyThrombomodulinBiochemistry03 medical and health sciences0302 clinical medicineBone MarrowStress PhysiologicalmedicineAnimalsHumansThromboplastinStem Cell NicheProgenitor cellBlood CoagulationEndothelial protein C receptorReview SeriesHematopoietic Stem Cell TransplantationHematopoietic stem cellCell DifferentiationCell BiologyHematologyHematopoietic Stem CellsHematopoiesisCell biologyHaematopoiesis030104 developmental biologymedicine.anatomical_structureStem cellBiomarkersFibrinolytic agentSignal TransductionBlood
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sgp120 and the contact system in hereditary angioedema: A diagnostic tool in HAE with normal C1 inhibitor

2020

Mutations in Factor XII, plasminogen gene, angiopoietin-1 gene and kininogen 1 gene have been found in some patients with hereditary angioedema with normal C1 inhibitor (HAE-nl-C1inh), but the underlying disease mechanisms remain unclear. Additionally, there are no accepted biomarkers for this disease. Because the contact system has been implicated in hereditary angioedema with C1 inhibitor deficiency (HAE-C1inh), we studied the fragmentation patterns of serum glycoprotein 120 (sgp120), a protein that is highly susceptible to cleavage by kallikrein, in 31 HAE-C1inh and 13 HAE-nl-C1inh patient plasma samples. Compared to normal controls, the majority of plasma samples from patients with HAE-…

0301 basic medicineImmunologyProteinase Inhibitory Proteins SecretoryCleavage (embryo)C1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansKaolinComplement ActivationMolecular BiologyGenechemistry.chemical_classificationChromatographyFactor XIIbiologyChemistryAngioedemas HereditaryPlasminogenKallikreinmedicine.diseaseMolecular biologyBlood Coagulation FactorsPeptide Fragments030104 developmental biologyFactor XIIProteolysisHereditary angioedemabiology.proteinBiomarker (medicine)KallikreinsGlycoproteinComplement C1 Inhibitor ProteinPlasticsBiomarkers030215 immunologyMolecular Immunology
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Tissue factor as a mediator of coagulation and signaling in cancer and chronic inflammation

2017

Thrombosis is frequently diagnosed as a first symptom in tumor patients and the clinical management of hypercoagulability in cancer patients remains challenging due to concomitant changes in risk factors for severe bleeding. It therefore remains a priority to better understand interactions of the hemostatic system with cancer biology. Specifically, further research is needed to elucidate the details and effects of new anticoagulants on extravascular coagulation and the interplay between cancer progression and chronic inflammation. In addition, it will be important to identify subgroups of cancer patients benefiting from specific modulations of the coagulation system without increasing the b…

0301 basic medicineInflammationBioinformaticsThromboplastin03 medical and health sciencesTissue factorMediatorNeoplasmsTumor MicroenvironmentmedicineHumansThromboplastinBlood CoagulationInflammationTumor microenvironmentbusiness.industryCancerHematologymedicine.diseaseThrombosis030104 developmental biologyCoagulationChronic Diseasemedicine.symptombusinessSignal TransductionThrombosis Research
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Ticagrelor, but not clopidogrel, reduces arterial thrombosis via endothelial tissue factor suppression

2017

The P2Y12 antagonist ticagrelor reduces mortality in patients with acute coronary syndrome (ACS), compared with clopidogrel, and the mechanisms underlying this effect are not clearly understood. Arterial thrombosis is the key event in ACS; however, direct vascular effects of either ticagrelor or clopidogrel with focus on arterial thrombosis and its key trigger tissue factor have not been previously investigated.Methods and results: Human aortic endothelial cells were treated with ticagrelor or clopidogrel active metabolite (CAM) and stimulated with tumour necrosis factor-alpha (TNF-α); effects on procoagulant tissue factor (TF) expression and activity, its counter-player TF pathway inhibito…

0301 basic medicineMaleTicagrelorAdenosineTime FactorsPhysiology030204 cardiovascular system & hematology2737 Physiology (medical)0302 clinical medicineP2Y12AntithromboticCells CulturedClopidogrelReceptors Purinergic P2Y123. Good healthClopidogrelmedicine.anatomical_structureCoagulation10209 Clinic for CardiologyCardiologyCardiology and Cardiovascular MedicineTicagrelormedicine.drugBlood PlateletsAcute coronary syndromemedicine.medical_specialtyProteasome Endopeptidase ComplexTiclopidineEndotheliumDown-Regulation610 Medicine & health2705 Cardiology and Cardiovascular MedicineThromboplastinEquilibrative Nucleoside Transporter 103 medical and health sciencesTissue factorFibrinolytic AgentsPhysiology (medical)Internal medicinemedicineAnimalsHumanscardiovascular diseasesBlood Coagulationbusiness.industryTumor Necrosis Factor-alphaEndothelial CellsThrombosis1314 Physiologymedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyProteolysisPurinergic P2Y Receptor AntagonistsbusinessCarotid Artery InjuriesPlatelet Aggregation Inhibitors
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Clinical Determinants of Thrombin Generation Measured in Presence and Absence of Platelets-Results from the Gutenberg Health Study.

2018

AbstractThe tendency of a plasma sample to generate thrombin, a central enzyme in blood coagulation, might be an important indicator of prothrombotic risk linked to cardiovascular disease (CVD), but the presence of platelets may be a critical determinant. Clinical data, laboratory markers and thrombin generation (TG), investigated in both platelet-rich plasma (PRP) and platelet-free plasma (PFP) at 1 pM TF, were available in 407 individuals from the Gutenberg Health Study. Given the well-known effect of anticoagulants on TG, subjects taking anticoagulants (n = 15) have been excluded resulting in 392 subjects for further analysis. Lag time, endogenous thrombin potential (ETP) and peak height…

0301 basic medicineMaleTime Factorspopulation030204 cardiovascular system & hematologyFibrinogenDISEASEHYPERCOAGULABILITYACTIVATION0302 clinical medicineRisk FactorsGermanyMedicinePlateletProspective StudiesBLOOD-COAGULATIONBlood coagulation testeducation.field_of_studybiologyPlatelet-Rich PlasmaMICROPARTICLESThrombinHematologyclinical epidemiologyMiddle AgedDEFICIENCYC-Reactive ProteinCoagulationCardiovascular Diseasesthrombin generationplateletsFemaleBlood Coagulation TestsMean Platelet Volumemedicine.drugAdultBlood Plateletsmedicine.medical_specialtyPopulationRisk AssessmentMECHANISMS03 medical and health sciencesThrombinINFLAMMATIONPredictive Value of TestsInternal medicineHumansMean platelet volumeeducationBlood CoagulationAgedVENOUS THROMBOEMBOLISMbusiness.industryPlatelet CountC-reactive proteinATHEROTHROMBOSIS030104 developmental biologyEndocrinologybiology.proteinbusinessThrombosis and haemostasis
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Determinants of the Quality of Warfarin Control after Venous Thromboembolism and Validation of the SAMe-TT2-R2 Score: An Analysis of Hokusai-VTE.

2019

Background Time in therapeutic range (TTR) measures the quality of vitamin K antagonist (VKA) anticoagulation. In patients with atrial fibrillation, the dichotomized SAMe-TT2-R2 score (≥2 vs. < 2 points) can predict if adequate TTR is unlikely to be achieved. Aims We validated the SAMe-TT2-R2 score in patients with venous thromboembolism (VTE) randomized to the warfarin arm of the Hokusai-VTE trial. Patients and Methods A total of 3,874 patients were included in the primary analysis (day 31–180 from randomization). The efficacy and safety outcomes were symptomatic recurrent VTE and major or clinically relevant non-major bleeding. Results The rates of recurrent VTE and bleeding events we…

0301 basic medicineMalevitamin K antagonistEXTERNAL VALIDATIONTime FactorsVitamin KWarfarin/therapeutic use030204 cardiovascular system & hematologyTHERAPYSeverity of Illness Indexlaw.inventionchemistry.chemical_compound0302 clinical medicineRandomized controlled trialEdoxabanlawRecurrenceAtrial FibrillationVitamin K/antagonists & inhibitorsStrokeRISKAtrial fibrillationHematologyVenous ThromboembolismVitamin K antagonistMiddle Agedrisk assessment modelTIMEPREDICTSTreatment OutcomeAnticoagulants/therapeutic useResearch DesignANTICOAGULATION CONTROLFemaleLife Sciences & Biomedicinemedicine.drugHemorrhage/drug therapyAdultmedicine.medical_specialtyRandomizationmedicine.drug_classvenous thromboembolismHemorrhageRisk AssessmentSensitivity and SpecificityEDOXABAN03 medical and health sciencesDouble-Blind MethodVITAMIN-K ANTAGONISTSInternal medicinemedicineNONVALVULAR ATRIAL-FIBRILLATIONORAL ANTICOAGULANTHumansInternational Normalized RatioBlood CoagulationScience & Technologybusiness.industryquality of treatmentWarfarinAnticoagulantsmedicine.diseasewarfarinClinical trial030104 developmental biologyPeripheral Vascular DiseasechemistryBlood Coagulation/drug effectsAtrial Fibrillation/bloodCardiovascular System & CardiologyLinear ModelsWarfarinbusinessVenous Thromboembolism/drug therapyThrombosis and haemostasis
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Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts

2018

Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs). Expert commentary: It is evident that aPL induce a proinflamma…

0301 basic medicineNeutrophilsImmunologyBioinformaticsExtracellular TrapsExtracellular vesiclesProinflammatory cytokinePathogenesisExtracellular VesiclesGenetic Heterogeneity03 medical and health sciences0302 clinical medicineimmune system diseasesAntiphospholipid syndromemicroRNAHumansImmunology and AllergyMedicineFetal lossBlood CoagulationComplement Activation030203 arthritis & rheumatologybusiness.industryNeutrophil extracellular trapsAntiphospholipid Syndromemedicine.diseaseMicroRNAs030104 developmental biologyAntibodies AntiphospholipidSignal transductionbusinessExpert Review of Clinical Immunology
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Evaluation of blood collection methods and anticoagulants for platelet function analyses on C57BL/6J laboratory mice

2019

The exploration of thrombotic mechanisms relies on the application of blood collection methods from laboratory mice with a minimal pre-activation of platelets and the clotting system. So far, very little is known on how the blood collection method and the anticoagulant used influence pre-activation of mouse platelets and coagulation. To determine the most suitable blood collection method, we systematically compared blood collection by heart puncture,

0301 basic medicinePlatelet Function TestsP-selectin030204 cardiovascular system & hematologyPharmacologyC57bl 6jMice03 medical and health sciences0302 clinical medicineAnimalsHumansMedicinePlateletPlatelet activationmedicine.diagnostic_testbusiness.industryAnticoagulantsHematologyGeneral MedicineBlood collectionThromboelastographyMice Inbred C57BL030104 developmental biologyBlood Coagulation TestsbusinessPre activationFunction (biology)Platelets
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Protease‐activated receptor signaling in intestinal permeability regulation

2019

Protease-activated receptors (PARs) are a unique class of G-protein-coupled transmembrane receptors, which revolutionized the perception of proteases from degradative enzymes to context-specific signaling factors. Although PARs are traditionally known to affect several vascular responses, recent investigations have started to pinpoint the functional role of PAR signaling in the gastrointestinal (GI) tract. This organ is exposed to the highest number of proteases, either from the gut lumen or from the mucosa. Luminal proteases include the host's digestive enzymes and the proteases released by the commensal microbiota, while mucosal proteases entail extravascular clotting factors and the enzy…

0301 basic medicineProteasesCell typeProtease-activated receptorReceptors Proteinase-ActivatedBiologyBiochemistryPermeabilityEpitheliumInflammatory bowel disease03 medical and health sciencesGastrointestinal cancer0302 clinical medicineImmune systemmedicineAnimalsHumansProtease-activated receptorIntestinal MucosaSymbiosisReceptorMolecular BiologyMicrobial proteasesGastrointestinal NeoplasmsClotting factorIntestinal permeabilityCoagulationMicrobiotaEpithelial barrier functionCell BiologyInflammatory Bowel Diseasesmedicine.diseaseIntestinal epitheliumTissue factorGastrointestinal MicrobiomeCell biologyIntestineGastrointestinal TractDisease Models Animal030104 developmental biologyGene Expression RegulationBacterial Translocation030220 oncology & carcinogenesisPeptide HydrolasesSignal Transduction
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