Search results for "Proteinase"

showing 10 items of 407 documents

Aprotinin inhibits leukocyte–endothelial cell interactions after hemorrhage and reperfusion

2003

Background. The serine protease inhibitor aprotinin has been successfully used to reduce blood loss in patients undergoing cardiac operations. We studied aprotinin for its ability to modulate leukocyte– endothelial cell interactions after ischemia and reperfusion. Methods. The effects of aprotinin on leukocyte– endothelial cell interactions were observed by intravital microscopy in the rat mesenteric microcirculation and immunohistochemical analysis. The inflammatory cascade (leukocyte rolling, firm adherence, and transmigration) was studied after thrombin stimulation and after hemorrhage and reperfusion. Results. Intravenous bolus administration of aprotinin treatment (20,000 U/kg) signifi…

MalePulmonary and Respiratory MedicineSerine Proteinase InhibitorsEndotheliumHemorrhageInflammationLeukocyte RollingCell CommunicationPharmacologyMicrocirculationRats Sprague-DawleyAprotininThrombinLeukocytesmedicineAnimalsMesenteryAprotininbusiness.industryMicrocirculationThrombinImmunohistochemistryRatsEndothelial stem cellP-Selectinmedicine.anatomical_structureReperfusionImmunologySurgeryEndothelium Vascularmedicine.symptomCardiology and Cardiovascular Medicinebusinesshormones hormone substitutes and hormone antagonistsIntravital microscopymedicine.drugThe Annals of Thoracic Surgery
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Two‐dimensional analysis of myocardial protein expression following myocardial ischemia and reperfusion in rabbits

2002

Myocardial ischemia and reperfusion injury (MI/R) can be related to leukocyte activation with subsequent release of cytokines and oxygen derived free radicals. Activation of the complement system has been implicated in the pathogenesis of myocardial ischemia and reperfusion injury. Inflammatory injury will subsequently result in cellular activation and protein synthesis. In the present study we analyzed the myocardial protein expression and its pattern following myocardial ischemia and reperfusion, with and without complement inhibition with the synthetic serine protease inhibitor Futhan/nafamstat mesilate (FUT-175) known to inhibit classical and alternative complement pathway in a rabbit m…

MaleSerine Proteinase InhibitorsNecrosisProteomeNeutrophilsMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryPharmacologyGuanidinesBiochemistrySuperoxide dismutaseNecrosisRandom AllocationComplement inhibitormedicineAnimalsElectrophoresis Gel Two-DimensionalCreatine KinaseMolecular BiologybiologySuperoxide DismutaseChemistryGene Expression ProfilingMyocardiumHemodynamicsProteinsalpha-Crystallin B Chainmedicine.diseaseBenzamidinesComplement systemBiochemistrybiology.proteinAlternative complement pathwayCreatine kinaseRabbitsmedicine.symptomReperfusion injuryPROTEOMICS
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Expression of MMP-2 and MMP-9 in odontogenic myxoma in a child: report of a clinical case

2011

Odontogenic myxoma (OM) is a benign, locally invasive, non-metastasizing neoplasm of the jaw bones. Despite the benign nature of these lesions, there is a high rate of recurrence and the current recommended therapy, depending on the size and behaviour of the lesion, can vary from curettage with peripheral ostectomy, segmental resection up to radical resections for more aggressive lesions. OM is a rare tumour which occurs predominantly in the third decade of life and it is rare in children. Matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases responsible for the degradation and remodelling of extracellular matrix, they are known to be involved in the progression and …

MaleSettore BIO/17 - IstologiaPathologymedicine.medical_specialtymedicine.medical_treatmentOdontogenic TumorsBiologyInferior alveolar nerveMatrix metalloproteinaseOdontogenic myxomaLesionExtracellular matrixSettore MED/28 - Malattie OdontostomatologichemedicineHumansChildGeneral DentistryDNA PrimersBase SequenceReverse Transcriptase Polymerase Chain Reactionmedicine.diseaseCurettageMatrix Metalloproteinase 9ImmunohistochemistryMatrix Metalloproteinase 2medicine.symptomSegmental resectionMyxomaOdontogenic myxoma Child MMP-2 MMP-9 it
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MMP-2, MMP-9, and iNOS Expression in Human Dental Pulp Subjected to Orthodontic Traction

2009

Abstract Objective: To test the hypothesis that some metalloproteinases (MMP-2, MMP-9) and inducible nitric oxide synthetase (iNOS) enzymes in dental pulp samples do not vary when subjected to orthodontic treatment. Materials and Methods: Human dental pulps were taken from male and female patients (N=10; age 10–14 years). A straight wire technique was used with nickel-titanium or steel archwires. The increase of pressure applied on teeth was gradual. Five patients were subjected to premolar extractions after 14 months of treatment and one after 24 months. Samples were Bouin-fixed, paraffin-embedded, and afterwards processed for immunohistochemistry using anti-MMP-2, anti-MMP-9, and anti-iNO…

MaleSettore BIO/17 - IstologiaTime FactorsNitric oxide synthetaseAdolescentTooth Movement TechniquesNitric Oxide Synthase Type IIDentistryOrthodonticsMalocclusion Angle Class IIMatrix metalloproteinaseNickelFemale patientOrthodontic WiresPressurePremolarHumansMedicineBicuspidChildTitaniumOdontoblastsMMP-2Orthodontic wirebusiness.industrymedicine.diseaseImmunohistochemistryBiomechanical PhenomenaDental pulpiNOSmedicine.anatomical_structureMatrix Metalloproteinase 9SteelMatrix Metalloproteinase 2ImmunohistochemistryFemaleStress MechanicalTreatment timeMalocclusionMMP-9businessImmunohistochemistry Dental pulp MMP-2 MMP-9 iNOS.Dental AlloysFollow-Up StudiesThe Angle Orthodontist
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Heme oxygenase-1 regulates the progression of K/BxN serum transfer arthritis.

2012

Background Heme oxygenase-1 (HO-1) is induced in many cell types as a defense mechanism against stress. We have investigated the possible role of endogenous HO-1 in the effector phase of arthritis using the K/BxN serum transfer model of arthritis in HO-1 heterozygous and homozygous knock-out mice. Methodology/Principal Findings Arthritis was induced in C57/Black-6 xFVB (HO-1+/+, HO-1+/− and HO-1−/−) mice by intraperitoneal injection of 150 µl serum from arthritic K/BxN mice at days 0 and 2. Blood was collected and animals were sacrificed at day 10. Histological analysis was performed in ankle sections. The levels of inflammatory mediators were measured in serum and paw homogenates by enzyme…

MaleTime FactorsAnatomy and PhysiologyMouseNon-Clinical MedicineArthritislcsh:MedicineEndogenyBiochemistryAntioxidantsMicechemistry.chemical_compoundDrug Discoverylcsh:ScienceMusculoskeletal SystemHemeRegulation of gene expressionMultidisciplinaryEffectorSystems BiologyAnimal ModelsEnzymesDisease ProgressionMedicineMatrix Metalloproteinase 3Inflammation Mediatorsmedicine.symptomResearch ArticleCell typeOsteocalcinRheumatoid ArthritisInflammationModel OrganismsRheumatologymedicineAnimalsBiologyBlood CellsRANK Ligandlcsh:Rmedicine.diseaseArthritis ExperimentalMolecular biologyMice Inbred C57BLHeme oxygenaseDisease Models AnimalGene Expression RegulationchemistryImmunologylcsh:QAnkle JointHeme Oxygenase-1PLoS ONE
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Effects of small interfering RNAs targeting fascin on human esophageal squamous cell carcinoma cell lines

2010

Abstract Background Fascin induces membrane protrusions and cell motility. Fascin overexpression was associated with poor prognosis, and its downregulation reduces cell motility and invasiveness in esophageal squamous cell carcinoma (ESCC). Using a stable knockdown cell line, we revealed the effect of fascin on cell growth, cell adhesion and tumor formation. Methods We examined whether fascin is a potential target in ESCC using in vitro and in vivo studies utilizing a specific siRNA. We established a stable transfectant with downregulated fascin from KYSE170 cell line. Results The fascin downregulated cell lines showed a slower growth pattern by 40.3% (p In vivo, the tumor size was signific…

MaleTime FactorsHistologyEsophageal NeoplasmsMice NudeApoptosismacromolecular substancesCysteine Proteinase InhibitorsBiologyTransfectionAmino Acid Chloromethyl KetonesPathology and Forensic MedicineExtracellular matrixMiceDownregulation and upregulationCell Line TumorCell Adhesionlcsh:PathologyAnimalsHumansRNA Small InterferingCell adhesionCell ProliferationFascinMice Inbred BALB CCell growthResearchMicrofilament ProteinsGeneral MedicineTransfectionCaspase InhibitorsXenograft Model Antitumor AssaysTumor BurdenCell biologyCell cultureApoptosisCaspasesCarcinoma Squamous Cellbiology.proteinRNA InterferenceCollagenCarrier Proteinslcsh:RB1-214Diagnostic Pathology
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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Anemia during treatment with peginterferon Alfa-2b/ribavirin and boceprevir: Analysis from the serine protease inhibitor therapy 2 (SPRINT-2) trial

2013

International audience; Boceprevir (BOC) added to peginterferon alfa-2b (PegIFN) and ribavirin (RBV) significantly increases sustained virologic response (SVR) rates over PegIFN/RBV alone in previously untreated adults with chronic hepatitis C genotype 1. We evaluate the relationship of incident anemia with triple therapy. A total of 1,097 patients received a 4-week lead-in of PegIFN/RBV followed by: (1) placebo plus PegIFN/RBV for 44 weeks (PR48); (2) BOC plus PegIFN/RBV using response-guided therapy (BOC/RGT); and (3) BOC plus PegIFN/RBV for 44 weeks (BOC/PR48). The management of anemia (hemoglobin [Hb]<10 g/dL) included RBV dose reduction and/or erythropoietin (EPO) use. A total of 1,080…

Male[SDV]Life Sciences [q-bio]MedizinGastroenterologyPolyethylene GlycolsPlaceboschemistry.chemical_compoundHemoglobins0302 clinical medicinehemic and lymphatic diseasesMedicine030212 general & internal medicineChronicSettore MED/12 - GastroenterologiaInterferon-alpha; Serine Proteinase Inhibitors; Proline; Recombinant Proteins; Hematinics; Humans; Ribavirin; Anemia; Antiviral Agents; Drug Therapy Combination; Erythropoietin; Hemoglobins; Adult; Treatment Outcome; Placebos; Polyethylene Glycols; Hepatitis C Chronic; Female; MaleAnemiaHepatitis CHepatitis CRecombinant Proteins3. Good health[SDV] Life Sciences [q-bio]Treatment OutcomeCombinationPeginterferon alfa-2b030211 gastroenterology & hepatologyDrug Therapy CombinationFemalemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsProlineAnemiaInterferon alpha-2PlaceboAntiviral Agentsprotease inhibitor03 medical and health sciencesDrug TherapyInternal medicineBoceprevirRibavirinHumansAdverse effectErythropoietinHepatologybusiness.industryRibavirinInterferon-alphaHepatitis C Chronicmedicine.diseaseSurgerychemistryErythropoietinHematinicsbusiness
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Matrix metalloproteinase-12 cleaved fragment of titin as a predictor of functional capacity in patients with heart failure and preserved ejection fra…

2020

Serum levels of matrix metalloproteinase-12 cleaved fragment of titin (TIM), a novel circulatory biomarker specific for cardiac titin degradation, has emerged as a potential biomarker in cardiovascular diseases. In this work, we aimed to evaluate the association between TIM and maximal functional capacity assessed by the percentage of predicted peak exercise oxygen uptake (pp-peakVO2) in patients with heart failure and preserved ejection fraction (HFpEF). Design. In this post-hoc study, we included 46 stable symptomatic (New York Heart Association II-III) HFpEF patients enrolled in the TRAINING-HF study (NCT02638961). pp-peak-VO2 was calculated from baseline values. Baseline circulating lev…

Maleanimal structuresfunctional capacity030204 cardiovascular system & hematologyMatrix (biology)Matrix metalloproteinase03 medical and health sciences0302 clinical medicineMatrix Metalloproteinase 12HumansMedicineConnectin030212 general & internal medicineExerciseAgedAged 80 and overHeart FailureEjection fractionbiologybusiness.industryStroke Volumetitin degradationmusculoskeletal systemmedicine.diseaseMolecular biologyheartfailure with preservedejection fractionHeart failureembryonic structuresCirculatory systemcardiovascular systembiology.proteinBiomarker (medicine)FemaleTitinCardiology and Cardiovascular MedicinebusinessHeart failure with preserved ejection fractiontissuesBiomarkers
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