Search results for "Plasminogen"

showing 10 items of 142 documents

Enzymatic modification of low-density lipoprotein in the arterial wall: a new role for plasmin and matrix metalloproteinases in atherogenesis.

2004

Objective— Functionally interactive proteases of the plasminogen/plasmin and the matrix metalloproteinase (MMP) system degrade and reorganize the extracellular matrix of the vessel wall in atherosclerosis. Here we investigated whether such proteases are able to confer atherogenic properties onto low density lipoprotein by nonoxidative modification. Methods and Results— Similar to the recently described enzymatically-modified low-density lipoprotein (E-LDL), native LDL exposed to plasmin or matrix MMP-2 or MMP-9 and cholesterylester-hydrolase (CEH) showed extensive deesterification, with ratios of free cholesterol to total cholesterol rising to 0.8 compared with 0.2 in native LDL. When the …

AdultLipoprotein modificationProteasesAdolescentPlasminArteriosclerosisBlotting WesternMatrix metalloproteinaseComplement Hemolytic Activity AssayMonocyteschemistry.chemical_compoundmedicineHumansTrypsinFibrinolysinComplement ActivationCells CulturedAgedbiologyMacrophagesAntibodies MonoclonalSodium Dodecyl SulfateLipoprotein(a)Middle AgedSterol EsteraseCell biologyLipoproteins LDLC-Reactive ProteinchemistryBiochemistryMatrix Metalloproteinase 9Low-density lipoproteinbiology.proteinMatrix Metalloproteinase 2lipids (amino acids peptides and proteins)Electrophoresis Polyacrylamide GelCardiology and Cardiovascular MedicinePlasminogen activatormedicine.drugLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

2016

Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells.…

AdultMale0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosisanimal structuresT-LymphocytesScienceMedizinGeneral Physics and AstronomyKininsCoagulation Factor XIIAdaptive ImmunityBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyReceptors Urokinase Plasminogen ActivatorAutoimmunityYoung Adult03 medical and health sciencesImmune systemddc:570medicineAnimalsHumansddc:610cardiovascular diseasesNeuroinflammationAgedFactor XIIMultidisciplinaryInterleukin-17QExperimental autoimmune encephalomyelitisCell DifferentiationDendritic CellsGeneral ChemistryMiddle Agedmedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyNeuroimmunologyFactor XIIImmunologyFemaleKallikreinscirculatory and respiratory physiologyNature Communications
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Hereditary angioedema with a mutation in the plasminogen gene

2017

Background Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or functional mutations in other genes that are still unknown. We sought to identify and characterize a hitherto unknown type of HAE with normal C1-INH and without mutation in the F12 gene. Methods The study comprised analysis of whole-exome sequencing, Sanger sequencing, and clinical data of patients. Results We detected a mutation in the plasminogen (PLG) gene in patients with HAEnCI. The mutation c.9886A>G was located in exon 9 leading to the missense mutation p.Lys330Glu (K330E) in the kringle 3 domain of the PLG protein. The mutation…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAdolescentImmunologyMutation MissenseGene mutationBiologyYoung Adult03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGermanyExome SequencingmedicineHumansImmunology and AllergyMissense mutationChildExome sequencingAgedSanger sequencingAngioedemas HereditaryAutosomal dominant traitPlasminogenMiddle Agedmedicine.disease030104 developmental biology030228 respiratory systemChild PreschoolMutationMutation (genetic algorithm)Hereditary angioedemasymbolsFemaleAllergy
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Prognostic value of soluble urokinase plasminogen activator receptor in patients presenting to the emergency department with chest pain suggestive of…

2021

International audience; INTRODUCTION: Soluble urokinase plasminogen activator receptor (suPAR) is a prognostic biomarker of cardiovascular disease. OBJECTIVES: We aimed to evaluate the early prognostic value of suPAR in patients presenting to the emergency department (ED) with chest pain suggestive of acute coronary syndrome (ACS). PATIENTS AND METHODS: In a post-hoc analysis from a multicenter study including patients with a chest pain < 6 h, suPAR concentrations at ED admission were studied according to the outcome at 30-days. RESULTS: 198 patients (median age 56 years) in whom 16% had an ACS, were included. Fifteen (7.3%) patients presented a 30-day event. At ED admission, median (IQR…

AdultMale030213 general clinical medicineAcute coronary syndromemedicine.medical_specialty[SDV]Life Sciences [q-bio]Clinical BiochemistrySoluble urokinase plasminogen activator receptorDisease030204 cardiovascular system & hematologyChest painPrognosticGastroenterologyReceptors Urokinase Plasminogen ActivatorsuPARChest pain03 medical and health sciences0302 clinical medicinePredictive Value of TestsInternal medicinemedicineHumansIn patientAcute Coronary SyndromeReceptorAgedOutcomeAged 80 and overbusiness.industryEmergency departmentGeneral MedicineEmergency departmentMiddle Agedmedicine.diseasePrognosisED30-day event3. Good health[SDV] Life Sciences [q-bio]SuPARBiomarker (medicine)Femalemedicine.symptombusinessEmergency Service HospitalBiomarkers
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Hereditary angioedema in a single family with specific mutations in both plasminogen and SERPING1 genes

2019

BACKGROUND Hereditary angioedema (HAE) is a group of genetic diseases characterized by recurrent, painful and potentially lethal tissue swelling. The most common form results from mutations in the SERPING1 gene, leading to reduced function of complement 1 inhibitor (C1-INH). Rarer forms with normal C1-INH may arise from mutations in the coagulation factor F12 gene, but mostly the genetic background is unknown. Recently, a novel HAE mutation in the plasminogen (PLG) gene was shown. PATIENTS AND METHODS We analyzed the various clinical manifestations of HAE in 14 related patients using clinical data, biochemical analysis for C1-INH and C4 as well as gene sequencing. RESULTS Patients' symptoms…

AdultMaleAdolescentMutation MissenseDermatologymedicine.disease_causeYoung Adult030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineTonguemedicineHumansFamilyChildGeneSingle familyMutationGastrointestinal tractbusiness.industryAngioedemas HereditaryPlasminogenMiddle Agedmedicine.diseasePhenotype3. Good healthPhenotypemedicine.anatomical_structureCoagulationChild PreschoolMutationHereditary angioedemaImmunologyFemalebusinessComplement C1 Inhibitor ProteinJDDG: Journal der Deutschen Dermatologischen Gesellschaft
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PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.

1998

Abstract —Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion ( I )/deletion ( D ) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels we…

AdultMaleAgingmedicine.medical_specialtyAlcohol DrinkingGenotypePopulationPeptidyl-Dipeptidase ABody Mass Indexchemistry.chemical_compoundInsulin resistanceGene FrequencyInternal medicinePlasminogen Activator Inhibitor 1Blood plasmaGenotypemedicineHumanseducationAllele frequencyTriglyceridesAgedSex Characteristicseducation.field_of_studyPolymorphism GeneticbiologySmokingAngiotensin-converting enzymeMiddle Agedmedicine.diseaseCholesterolEndocrinologychemistryPlasminogen activator inhibitor-1Hypertensionbiology.proteinFemaleCardiology and Cardiovascular MedicineBody mass indexGene Deletion
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Kallikrein–kinin system and fibrinolysis in hereditary angioedema due to factor XII gene mutation Thr309Lys

2009

In a subgroup of hereditary angioedema (HAE) patients with normal C1-esterase inhibitor levels, HAE is caused by a Thr309Lys mutation in the coagulation factor XII (F12) gene. The aim of this study was to examine elements of the kallikrein-kinin system ('contact system') and the downstream-linked coagulation, complement and fibrinolytic systems in the plasma of six patients with HAE caused by the Thr309Lys mutation and healthy probands. Blood samples were taken from participants during the symptom-free interval between attacks. Samples were analyzed for activity and concentrations of components of the kallikrein-kinin system and linked enzyme systems. The mean FXII clotting activity was 90%…

AdultMalemedicine.medical_specialtyAdolescentMutation MissenseKininsCoagulation Factor XIIFactor XIIaGene mutationYoung AdultInternal medicinemedicineHumansPoint MutationHereditary Angioedema Type IIIComplement Pathway ClassicalAgedAged 80 and overFactor XIIAngioedemaChemistryFibrinolysisDextran SulfateAngioedemas HereditaryPrekallikreinPrekallikreinBlood ProteinsHematologyGeneral MedicineMiddle AgedSilicon Dioxidemedicine.diseaseEnzyme ActivationEndocrinologyAmino Acid SubstitutionChromogenic CompoundsCoagulationTissue Plasminogen ActivatorHereditary angioedemaImmunologyFemaleKallikreinsmedicine.symptomcirculatory and respiratory physiologyBlood Coagulation & Fibrinolysis
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Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina

1991

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and sign…

AdultMalemedicine.medical_specialtyAntithrombin IIICoronary DiseaseStable anginaAngina PectorisFibrin Fibrinogen Degradation ProductsCoronary artery diseaseThrombinAntigenDiabetes mellitusInternal medicinemedicineHumanscardiovascular diseasesAgedbusiness.industryFibrinolysisPlasminogen activator inhibitor antigenAntithrombinFibrinogenHematologyGeneral MedicineMiddle Agedmedicine.diseaseObesityPlasminogen InactivatorsEndocrinologyDiabetes Mellitus Type 2Tissue Plasminogen ActivatorExercise TestbusinessPeptide Hydrolasesmedicine.drugBlood Coagulation & Fibrinolysis
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The PAI-1 gene locus 4G/5G polymorphism is associated with a family history of coronary artery disease.

1998

Abstract —A family history of ischemic events is a major determinant of coronary artery disease (CAD). Plasma levels of plasminogen activator inhibitor 1 (PAI-1) modulate this risk. A deletion/insertion polymorphism within the PAI-1 locus (4G/5G) affects the expression of this gene. We investigated the relationship between the PAI-1 4G/5G polymorphism in 1179 healthy employees of our institution and the occurrence of CAD in their first-degree relatives. A family history of documented ischemic coronary disease was assessed by a modified WHO questionnaire. The PAI-1 4G/5G polymorphism was evaluated by polymerase chain reaction and endonuclease digestion. The group with a first-degree relativ…

AdultMalemedicine.medical_specialtyCoronary DiseaseLocus (genetics)BiologyGastroenterologyMedical RecordsGenetic determinismCohort StudiesCoronary artery diseasechemistry.chemical_compoundRisk FactorsInternal medicinePlasminogen Activator Inhibitor 1medicineHumansFamily historyAlleleAgedGeneticsPolymorphism GeneticChromosome MappingOdds ratioMiddle Agedmedicine.diseasechemistryPlasminogen activator inhibitor-1Regression AnalysisFemaleCardiology and Cardiovascular MedicineBody mass index
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Hereditary angioedema with normal C1-INH withversuswithout specificF12gene mutations

2015

Background Hereditary angioedema with normal C1-INH may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or mutations in genes that are still unknown (HAE-unknown). To assess the differences in transmission and inheritance, clinical features, and laboratory parameters between patients with HAE-FXII and HAE-unknown. Methods Sixty-nine patients with HAE-FXII from 23 unrelated families and 196 patients with HAE-unknown from 65 unrelated families were studied. Results Both HAE-FXII and HAE-unknown are inherited as autosomal-dominant traits with incomplete penetrance. The male to female ratio was 1 : 68 in HAE-FXII and 1 : 6.3 in HAE-unknown. The maternal to pa…

AdultMalemedicine.medical_specialtyDatabases FactualOffspringImmunologyGene mutationSeverity of Illness IndexCohort StudiesYoung Adultchemistry.chemical_compoundAge DistributionInternal medicineHumansImmunology and AllergyMedicineHereditary Angioedema Type IIIAge of OnsetSex DistributionRetrospective Studiesmedicine.diagnostic_testAngioedemabusiness.industryIncidenceAngioedemas HereditaryMiddle AgedPrognosismedicine.diseasePenetranceRecombinant ProteinsPedigreePhenotypeEndocrinologychemistryPlasminogen activator inhibitor-1Factor XIIMutationHereditary angioedemaFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinPartial thromboplastin timeAllergy
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