Search results for "Plasmin"

showing 10 items of 176 documents

The Altered Expression of microRNA408 Influences the Arabidopsis Response to Iron Deficiency

2019

MicroRNAs contribute to the adaptation of plants to varying environmental conditions by affecting systemic mineral nutrient homeostasis. Copper and iron deficiencies antagonistically control the expression of Arabidopsis thaliana microRNA408 (miR408), which post-transcriptionally regulates laccase-like multicopper oxidase family members LAC3, LAC12, and LAC13. In this work, we used miR408 T-DNA insertion mutants (408-KO1 and 408-KO2) and a previously characterized transgenic line overexpressing miR408 (35S:408-14) to explore how miR408 influences copper- and iron-dependent metabolism. We observed that the altered expression of miR408 diminished plant performance and the activation of the ir…

0106 biological sciences0301 basic medicineTransgeneArabidopsisligninhydrogen peroxidePlant Sciencelcsh:Plant cultureMulticopper oxidase01 natural sciencesLignin03 medical and health sciencesiron deficiencyMicroRNA408ArabidopsisArabidopsis thalianalcsh:SB1-1110Iron deficiency (plant disorder)Original ResearchLaccasebiologyChemistryIron deficiencybiology.organism_classificationVascular bundleHydrogen peroxideCell biologymicroRNA408030104 developmental biologybiology.proteinCeruloplasmin010606 plant biology & botany
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Analysis of cold activation of the contact system in hereditary angioedema with normal C1 inhibitor.

2021

Hereditary angioedema (HAE) attacks are caused by excessive activation of the contact system. Understanding how the contact system is activated in HAE, especially in patients with normal C1 inhibitor (HAEnCI), is essential to effectively treat this disease. Contact system activation involves the cleavage of several proteins including Factor XII (FXII), high molecular weight kininogen (HK), prekallikrein, sgp120 (ITIH4) and C1 inhibitor (C1-INH) before the subsequent generation of bradykinin that mediates HAE. In this study, we evaluated the fragmentation and enzymatic activity of contact system proteins in HAEnCI plasma samples before and after contact system activation induced by incubatio…

0301 basic medicineAdultMalemedicine.medical_specialtyHigh-molecular-weight kininogenImmunologyProteinase Inhibitory Proteins SecretoryBradykininBradykininC1-inhibitorHereditary Angioedema Type III03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicinemedicineHumansFragmentation (cell biology)Molecular BiologyBlood CoagulationFactor XIIbiologyKininogensPrekallikreinPrekallikreinEstrogensPlasminogenKallikreinMiddle Agedmedicine.diseaseCold Temperature030104 developmental biologyEndocrinologychemistryHereditary angioedemaFactor XIIbiology.proteinFemaleKallikreinsComplement C1 Inhibitor Protein030215 immunologyMolecular immunology
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New insights in the neurological phenotype of aceruloplasminemia in Caucasian patients

2017

Abstract Introduction The diagnosis aceruloplasminemia is usually made in patients with advanced neurological manifestations of the disease. In these patients prognosis is poor, disabilities are severe and patients often die young. The aim of our study was to facilitate recognition of aceruloplasminemia at a disease stage at which treatment can positively influence outcome. Currently, the neurological phenotype of aceruloplasminemia has been mainly described in Japanese patients. This ‘classical’ phenotype consists of cerebellar ataxia, hyperkinetic movement disorders and cognitive decline. In this study we describe the spectrum of neurological disease in Caucasian patients. Methods Data on…

0301 basic medicineAdultMalemedicine.medical_specialtyPediatricsAtaxiaMovement disordersBiologyWhite People03 medical and health sciencesNeurological manifestation0302 clinical medicinePhenotypic variabilitymedicineAceruloplasminemiaHumansCognitive declineAceruloplasminemiaPsychiatryDystoniaCerebellar ataxiaParkinsonismCeruloplasminChoreaNeurodegenerative DiseasesMiddle Agedmedicine.diseaseIron Metabolism DisordersPedigree030104 developmental biologyPsychiatric changesPhenotypeNeurologyFemaleNeurology (clinical)Geriatrics and Gerontologymedicine.symptomNervous System DiseasesSettore M-EDF/01 - Metodi E Didattiche Delle Attivita' Motorie030217 neurology & neurosurgeryFollow-Up Studies
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Numerous Fasciola plasminogen-binding proteins may underlie blood-brain barrier leakage and explain neurological disorder complexity and heterogeneit…

2019

15 páginas, 5 figuras y 1 tabla

0301 basic medicineAntifibrinolyticContact systemmedicine.drug_classmedicine.medical_treatment030231 tropical medicineBradykininInflammationNeurological disorderFibrinolysis systemProteomic and mass spectrometry analysesBlood–brain barrierFasciola excretome/secretomeProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood-brain barrier leakageFibrinolysismedicineIndicators and preventionAcute and chronic phasesPlasminogen-binding proteinsFasciolabiologyHuman fascioliasis030108 mycology & parasitologymedicine.diseasebiology.organism_classificationInfectious Diseasesmedicine.anatomical_structurechemistryImmunologyAnimal Science and ZoologyParasitologymedicine.symptomNeurological disordersResearch Article
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Annexin A2-Mediated Plasminogen Activation in Endothelial Cells Contributes to the Proangiogenic Effect of Adenosine A2A Receptors

2021

Adenosine A2A receptor mediates the promotion of wound healing and revascularization of injured tissue, in healthy and animals with impaired wound healing, through a mechanism depending upon tissue plasminogen activator (tPA), a component of the fibrinolytic system. In order to evaluate the contribution of plasmin generation in the proangiogenic effect of adenosine A2A receptor activation, we determined the expression and secretion of t-PA, urokinase plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) and annexin A2 by human dermal microvascular endothelial cells stimulated by the selective agonist CGS-21680. The plasmin generation was assayed through an enzymatic assay a…

0301 basic medicineFarmacologiaAngiogenesisPlasminmedicine.medical_treatmentVasodilatadorsAdenosine A2A receptorRM1-950030204 cardiovascular system & hematologyTissue plasminogen activatormicrovascular endothelial cells03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFibrinolysismedicinePharmacology (medical)urokinase plasminogen activatorPharmacologytissue plasminogen activatorChemistryBrief Research Reportannexin A2adenosine receptorsCell biology030104 developmental biologyPlasminogen activator inhibitor-1plasminogen activator inhibitor-1Therapeutics. PharmacologyPlasminogen activatorProteïnesAnnexin A2medicine.drug
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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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Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures.

2020

The Alzheimer disease-associated multifunctional low-density lipoprotein receptor-related protein-1 is expressed in the brain. Recent studies uncovered a role of this receptor for the appropriate functioning of neural stem cells, oligodendrocytes, and neurons. The constitutive knock-out (KO) of the receptor is embryonically lethal. To unravel the receptors' role in the developing brain we generated a mouse mutant by specifically targeting radial glia stem cells of the dorsal telencephalon. The low-density lipoprotein receptor-related protein-1 lineage-restricted KO female and male mice, in contrast to available models, developed a severe neurological phenotype with generalized seizures duri…

0301 basic medicineMaleEpendymoglial CellsBiology03 medical and health sciencesCellular and Molecular NeuroscienceEpilepsyMice0302 clinical medicineProsencephalonSeizuresmedicineAnimalsReceptors LipoproteinLipoprotein receptor-related proteinmedicine.diseaseNeural stem cellLipoproteins LDL030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTissue Plasminogen ActivatorForebrainFemaleSynaptic signalingStem cellPostsynaptic densityNeuroscience030217 neurology & neurosurgeryAstrocyteGliaREFERENCES
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Intravenous thrombolysis for suspected ischemic stroke with seizure at onset

2019

Objective Seizure at onset (SaO) has been considered a relative contraindication for intravenous thrombolysis (IVT) in patients with acute ischemic stroke, although this appraisal is not evidence based. Here, we investigated the prognostic significance of SaO in patients treated with IVT for suspected ischemic stroke. Methods In this multicenter, IVT-registry-based study we assessed the association between SaO and symptomatic intracranial hemorrhage (sICH, European Cooperative Acute Stroke Study II definition), 3-month mortality, and 3-month functional outcome on the modified Rankin Scale (mRS) using unadjusted and adjusted logistic regression, coarsened exact matching, and inverse probabil…

0301 basic medicineMalemedicine.medical_specialtymedicine.medical_treatmentLogistic regressionGUIDELINESCLASSIFICATION3124 Neurology and psychiatryBrain IschemiaEARLY MANAGEMENT03 medical and health sciences0302 clinical medicineALTEPLASEModified Rankin ScaleSeizuresMIMICSInternal medicineMedicineHumansThrombolytic TherapyPLASMINOGEN-ACTIVATOR610 Medicine & healthStrokeContraindicationPOPULATIONAgedAged 80 and overHEALTH-CARE PROFESSIONALSbusiness.industryConfounding3112 NeurosciencesOdds ratioThrombolysisASSOCIATIONMiddle Agedmedicine.diseasePrognosisConfidence intervalStroke030104 developmental biologyTreatment OutcomeNeurologySAFETYFemaleNeurology (clinical)business030217 neurology & neurosurgery
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Analysis of Plasminogen Genetic Variants in Multiple Sclerosis Patients.

2016

Multiple sclerosis (MS) is a prevalent neurological disease of complex etiology. Here, we describe the characterization of a multi-incident MS family that nominated a rare missense variant (p.G420D) in plasminogen (PLG) as a putative genetic risk factor for MS. Genotyping of PLG p.G420D (rs139071351) in 2160 MS patients, and 886 controls from Canada, identified 10 additional probands, two sporadic patients and one control with the variant. Segregation in families harboring the rs139071351 variant, identified p.G420D in 26 out of 30 family members diagnosed with MS, 14 unaffected parents, and 12 out of 30 family members not diagnosed with disease. Despite considerably reduced penetrance, lin…

0301 basic medicineProbandMaleGene ExpressionQH426-470multiple sclerosis0302 clinical medicineRisk FactorsGenotypeMissense mutationExomegeneticsguidelinesGenetics (clinical)degradationriskGeneticsLinkagedeficiencyMiddle AgedPenetrance3. Good healthPedigreeplasminogenChromosomes Human Pair 6FemalelinkageAdultGenotype610 Medicine & healthInvestigationsBiologysystemPolymorphism Single Nucleotideblood-brain-barrieractivatorMultiple sclerosisAssociation03 medical and health scienceslamininGenetic linkagemedicineGeneticsHumansAmino Acid Sequenceddc:610Molecular BiologyGenotypingAgeddiseaseSequence Homology Amino AcidMultiple sclerosisCase-control studyassociationPlasminogenmedicine.diseasediagnostic-criteria030104 developmental biologyCase-Control StudiesImmunologySequence Alignment030217 neurology & neurosurgery
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Plasmin-Induced Activation of Human Platelets Is Modulated by Thrombospondin-1, Bona Fide Misfolded Proteins and Thiol Isomerases

2020

Inflammatory processes are triggered by the fibrinolytic enzyme plasmin. Tissue-type plasminogen activator, which cleaves plasminogen to plasmin, can be activated by the cross-&beta

0301 basic medicineProtein FoldingPlatelet AggregationPlasmin030204 cardiovascular system & hematologyProtein aggregationFibrinogenThrombospondin 10302 clinical medicinePlateletFibrinolysinprotein misfoldingIsomerasesSpectroscopyChemistryfood and beveragesGeneral Medicinethiol-isomerasesComputer Science ApplicationsCell biologyP-Selectinplateletsmedicine.drugcirculatory and respiratory physiologyBlood PlateletsCatalysisArticleInorganic Chemistry03 medical and health sciencesProtein AggregatesThrombospondin 1medicineHumansPlatelet activationSulfhydryl CompoundsPhysical and Theoretical Chemistrythrombospondin-1Molecular BiologyplasminInflammationOrganic ChemistryfungiFibrinogen bindingFibrinogenPlasminogenPlatelet Activation030104 developmental biologyProtein Conformation beta-StrandPeptidesPlasminogen activatorInternational Journal of Molecular Sciences
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