Search results for "fibrinolysi"

showing 10 items of 97 documents

Ectodomain shedding of L1 adhesion molecule promotes cell migration by autocrine binding to integrins.

2001

The L1 adhesion molecule plays an important role in axon guidance and cell migration in the nervous system. L1 is also expressed by many human carcinomas. In addition to cell surface expression, the L1 ectodomain can be released by a metalloproteinase, but the biological function of this process is unknown. Here we demonstrate that membrane-proximal cleavage of L1 can be detected in tumors and in the developing mouse brain. The shedding of L1 involved a disintegrin and metalloproteinase (ADAM)10, as transfection with dominant-negative ADAM10 completely abolishes L1 release. L1-transfected CHO cells (L1-CHO) showed enhanced haptotactic migration on fibronectin and laminin, which was blocked …

CytoplasmIntegrinsL1; shedding; ADAM10; cell migration; integrinsADAM10IntegrinGene ExpressionCHO CellsBiologyArticle03 medical and health sciencesParacrine signallingMice0302 clinical medicineCell MovementCricetinaeEndopeptidasesTumor Cells CulturedAnimalsAspartic Acid EndopeptidasesHumansReceptors VitronectinFibrinolysinNeural Cell Adhesion Molecules030304 developmental biology0303 health sciencesBinding SitesMembrane GlycoproteinsCell adhesion moleculeCell MembraneAntibodies MonoclonalBrainCell migrationBiological TransportCell BiologyMolecular biologyPeptide FragmentsCell biologyFibronectinAutocrine CommunicationEctodomainSolubility030220 oncology & carcinogenesisbiology.proteinNeural cell adhesion moleculeAmyloid Precursor Protein SecretasesLeukocyte L1 Antigen ComplexOligopeptidesThe Journal of cell biology
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Disseminated Intravascular Coagulation

1985

During the past decade, diffuse intravascular coagulation (DIC) has been one of the most intensively studied subjects in hematology. DIC is a dynamic pathologic process caused by the entrance of foreign material into the circulation, or by exposure to abnormal surfaces. The intravascular coagulation is triggered by activation of the clotting cascade with resultant generation of excess thrombin within the vascular system that leads to further activation of the coagulation system, shortened survival of certain hemostatic elements, deposition of fibrin in the microcirculation, and activation of the fibrinolytic system. Decreased levels of hemostatic factors, secondary fibrinolysis, and exhaust…

Disseminated intravascular coagulationExcessive Bleedingmedicine.medical_specialtyPathologyHematologybiologybusiness.industrymedicine.medical_treatmentmedicine.diseaseFibrinMicrocirculationThrombinCoagulationInternal medicineFibrinolysisbiology.proteinmedicinebusinessmedicine.drug
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Urokinase Plasminogen Activator and Gelatinases Are Associated with Membrane Vesicles Shed by Human HT1080 Fibrosarcoma Cells

1997

Membrane vesicles are shed by tumor cells both in vivo and in vitro. Although their functions are not well understood, it has been proposed that they may play multiple roles in tumor progression. We characterized membrane vesicles from human HT1080 fibrosarcoma cell cultures for the presence of proteinases involved in tumor invasion. By gelatin zymography and Western blotting, these vesicles showed major bands corresponding to the zymogen and active forms of gelatinase B (MMP-9) and gelatinase A (MMP-2) and to the MMP-9. tissue inhibitor of metalloproteinase 1 complex. Both gelatinases appeared to be associated with the vesicle membrane. HT1080 cell vesicles also showed a strong, plasminoge…

GelatinasesMacromolecular SubstancesFibrosarcomaBlotting WesternCellGelatinase ABiologyBiochemistryTumor Cells CulturedmedicineHumansCollagenasesFibrinolysinMolecular BiologyGlycoproteinsUrokinaseEnzyme PrecursorsVesicleMetalloendopeptidasesTissue Inhibitor of MetalloproteinasesCell BiologyTissue inhibitor of metalloproteinaseUrokinase-Type Plasminogen ActivatorMolecular biologyExtracellular MatrixUrokinase receptorBloodmedicine.anatomical_structureMatrix Metalloproteinase 9GelatinasesMatrix Metalloproteinase 2HT1080medicine.drugJournal of Biological Chemistry
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Crosstalk of the plasma contact system with bacteria.

2012

Activation of the plasma contact system triggers several cascade systems such as the kallikrein-kinin system, the intrinsic pathway of coagulation, the classical complement cascade and the fibrinolytic system. Recent studies have shown a critical role of the contact system for arterial and venous thrombus formation and thromboembolic disease. In contrast, the function of the contact system for host-defense reactions and its physiological functions have remained enigmatic. Experimental animal studies and clinical data have linked the contact system to bacterial infections with implications for sepsis disease. The present review summarizes the role of the contact system and its activation for…

Kallikrein-Kinin SystemVascular permeabilityBiologySepsisCapillary PermeabilitySepsismedicineAnimalsHumansComplement Pathway ClassicalThrombusBlood CoagulationFactor XIIFibrinInnate immune systemBacteriaFibrinolysisHematologyBacterial Infectionsmedicine.diseaseImmunity InnateComplement systemCrosstalk (biology)ImmunologySignal transductionSignal TransductionThrombosis research
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Plasminogen activator inhibitor‐1 augments damage by impairing fibrinolysis after traumatic brain injury

2019

Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation b…

Male0301 basic medicineTraumatic brain injurymedicine.medical_treatmentBrain damagePharmacologyLesionMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticSerpin E2FibrinolysisAnimalsMedicineThrombusResearch ArticlesIndoleacetic Acidsbusiness.industryFibrinolysisBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyNeurologychemistryPlasminogen activator inhibitor-1Neurology (clinical)medicine.symptombusinessPlasminogen activator030217 neurology & neurosurgeryIntravital microscopyResearch ArticleAnnals of Neurology
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Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

2014

International audience; Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabo…

MalePlasminlcsh:MedicineTropomyosin receptor kinase BBiochemistryMechanical Treatment of SpecimensHippocampusTissue plasminogen activator[SCCO]Cognitive scienceCell SignalingNeurotrophic factorsNeurobiology of Disease and RegenerationMedicine and Health SciencesMembrane Receptor SignalingFibrinolysinBRAINlcsh:ScienceMultidisciplinaryNeuromodulationNeurotransmitter Receptor SignalingNeurochemistryLong-term potentiationNeurotransmittersDENDRITIC GROWTHNEURONAL DEATHRECEPTORSElectroporationNeurologySpecimen DisruptionTranexamic AcidTissue Plasminogen ActivatorACTIVATORTPANMDA receptor[ SCCO ] Cognitive scienceLONG-TERM POTENTIATIONResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyN-MethylaspartateResearch and Analysis MethodsNeuropharmacologyDevelopmental NeuroscienceInternal medicinemedicineAnimalsReceptor trkBProtein PrecursorsRats WistarSPATIAL MEMORYBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factorlcsh:RBiology and Life SciencesCell BiologySYNAPTIC-PLASTICITYRetractionEndocrinologynervous systemSpecimen Preparation and TreatmentSynaptic plasticitylcsh:QMolecular NeuroscienceDizocilpine MaleateNEUROTROPHIC FACTORNeuroscienceSynaptic PlasticityPLoS ONE
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Activated thrombin activatable fibrinolysis inhibitor levels are associated with the risk of cardiovascular death in patients with coronary artery di…

2008

Summary. Background: Thrombin activatable fibrinolysis inhibitor (TAFI) attenuates fibrinolysis. Results on the association between TAFI levels and the risk of coronary artery disease (CAD) are inconsistent. Objectives: We investigated the association between TAFI levels and the risk of cardiovascular events in CAD. Patients/Methods: 1668 individuals with angiographically proven CAD at baseline were followed for a median of 2.3 years, as part of the prospective AtheroGene cohort. Fifty-six deaths from cardiovascular (CV) causes and 35 non-fatal CV events were observed. Results: At baseline, three TAFI measurements were available: one evaluating the total amount of TAFI (t-TAFI), one measuri…

MaleRiskCarboxypeptidase B2medicine.medical_specialtymedicine.medical_treatmentCoronary Artery DiseaseCoronary artery diseaseRisk FactorsInternal medicineFibrinolysismedicineHumansMyocardial infarctionAgedProportional Hazards Modelsbusiness.industryUnstable anginaProportional hazards modelHazard ratioHematologyMiddle Agedmedicine.diseaseCarboxypeptidase BDeath Sudden CardiacCohortCardiologyFemalebusinessProtein Cmedicine.drugJournal of Thrombosis and Haemostasis
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Early detection of coronary artery flow and myocardial perfusion impairment in hypertensive patients evidenced by myocardial blush grade (MBG) and th…

2012

OBJECTIVE: In hypertensive patients with typical chest pain but absence of coronary stenosis the coronary microcirculation may be impaired, thus, our study aimed to appraise, in these subjects, the role of the coronary microcirculation, assessed by Myocardial Blush Grade (MBG) and Thrombolysis in Myocardial Infarction (TIMI) Frame Count (TFC). METHODS: A total of 95 subjects with chest pain and uninjured coronary arteries were recruited into the study: 80 subjects were hypertensive while 15 subjects were normotensive. The hypertensive subjects were divided into two subgroups: hypertensive subjects with positive scintigraphy and hypertensive subjects with negative scintigraphy. The TFC, a qu…

MaleTechnetium Tc 99m SestamibiChest Painmedicine.medical_specialtymedicine.medical_treatmentMyocardial InfarctionMyocardial IschemiaCoronary AngiographyChest painScintigraphyAnginaElectrocardiographyHypertensive patients MBG TIMI frame countCoronary CirculationInternal medicineInternal MedicinemedicineHumansMyocardial infarctionAgedmedicine.diagnostic_testbusiness.industryFibrinolysisMicrocirculationElectrocardiography in myocardial infarctionGeneral MedicineThrombolysisMiddle AgedAtherosclerosismedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareCoronary arteriesmedicine.anatomical_structureEchocardiographyHypertensionExercise TestCardiologyFemaleRadiopharmaceuticalsmedicine.symptombusinessTIMI
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Captopril does not affect plasma endothelin-1 during thrombolysis and reperfusion.

1995

Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion, and that ET-1 was increased during reperfusion. This study was aimed to verify if captopril was able to reduce plasma ET-1 during thrombolysis in AMI. Seventy-three patients, hospitalized for suspected AMI within 4 h from the onset of symptoms suitable for thrombolysis (1st episode), Killip class 1-2, were randomized (double blind) into two groups: group 1 (37 pts), 8 F/29 M, received captopril, 6.25 mg, orally 15 min before thrombolysis. Group 2: (36 pts) 8 F/28 M, received placebo before thrombolysis. All patients m…

Malemedicine.medical_specialtyCaptoprilTime Factorsmedicine.medical_treatmentMyocardial InfarctionAdministration OralAngiotensin-Converting Enzyme InhibitorsBlood PressureMyocardial ReperfusionPlaceboAnginaPlacebosElectrocardiographyDouble-Blind MethodHeart RateInternal medicineFibrinolysismedicineHumansThrombolytic TherapyMyocardial infarctionAngina UnstableCreatine KinaseKillip classbusiness.industryUnstable anginaEndothelinsCaptoprilThrombolysismedicine.diseaseRecombinant ProteinsSurgeryIsoenzymesTissue Plasminogen ActivatorCardiologyFemaleCardiology and Cardiovascular Medicinebusinessmedicine.drugInternational journal of cardiology
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Genetic and environmental influences on the fibrinolytic system: a twin study.

2004

SummaryThe determination of heritability is a key issue to assess the predictive power of polymorphisms for disease in clinical studies. The aim of this study was to determine the heritability of proteins and activation markers of the fibrinolytic system in a large cohort of healthy twins. Heritability was calculated as 0.76 for thrombin activatable fibrinolysis inhibitor (TAFI), 0.44 for plasminogen activator inhibitor-1 (PAI-1), and 0.43 for tissue plasminogen activator. No significant genetic influence was observed for α2-antiplasmin-plasmin-complex and D-dimer. Heritability explained by single gene polymorphisms was 25.2% for TAFI 505G>A, 31.5% for 1542C>G, and 50.0% for combinati…

Malemedicine.medical_specialtyCarboxypeptidase B2GenotypeArteriosclerosismedicine.medical_treatmentBiologyEnvironmentTissue plasminogen activatorCohort StudiesFibrin Fibrinogen Degradation ProductsInternal medicineFibrinolysisPlasminogen Activator Inhibitor 1medicineDiseases in TwinsHumansFibrinolysinGeneGeneticsalpha-2-AntiplasminPolymorphism GeneticActivator (genetics)FibrinolysisHematologyTwins MonozygoticHeritabilityTwin studyEndocrinologyPhenotypeHaplotypesHemostasisTwin Studies as TopicFemalePlasminogen activatormedicine.drugThrombosis and haemostasis
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