Search results for "Matrix Metalloproteinase"

showing 10 items of 212 documents

Intramural neovascularization and haemorrhages are major long‐term effects of intravascularγ‐radiation after stenting

2003

Structural changes that might influence the structural integrity of the vessel in response to intravascular brachytherapy (IVB) and stenting were examined, focus being on the importance of neovascularization in rabbit stented arteries. Stents were implanted in the infrarenal aortas of rabbits, immediately followed by gamma IVB or a sham radiation procedure, and the arteries harvested at 6 months. Labelling for von Willebrand factor showed an increase in adventitial and medial neovascularization in irradiated versus control arteries group (5.04+/-0.89 versus 1.51+/-0.23 mm(-2), respectively; p=0.004). Moreover, intramedial haemorrhages (free hemosiderin deposition) and inflammation (macropha…

MalePathologymedicine.medical_specialtyBrachytherapyHemorrhageInflammationMatrix metalloproteinaseCoronary RestenosisNeovascularizationHemosiderin DepositionVon Willebrand factorReference ValuesmedicineAnimalsRadiology Nuclear Medicine and imagingAorta AbdominalVascular Diseasesγ radiationNeovascularization PathologicRadiological and Ultrasound Technologybiologybusiness.industryStructural integrityIntravascular brachytherapyGamma RaysMetalloproteasesbiology.proteinStentsCollagenRabbitsmedicine.symptombusinessInternational Journal of Radiation Biology
researchProduct

TIMP expression in toxic and cholestatic liver injury in rat.

1997

Abstract Background/Aims: Hepatic fibrosis is a dynamic pathological process with a net accumulation of extracellular matrix proteins. Recent evidence suggests that besides their increased synthesis, inhibition of matrix degradation plays a significant role. ECM degradation occurs via metalloproteinases which are inhibited in situ by specific tissue inhibitors of metalloproteinases (TIMPs). The aim of our studies was to determine the expression of TIMPs during toxic liver injury and cholestatic liver injury leading to fibrosis. Methods: We examined the expression of TIMP-1, -2 and -3 in two different rat models for liver injury (intraperitoneal CCl 4 injection and bile duct ligation) by Nor…

MalePathologymedicine.medical_specialtyIn situ hybridizationCholestasis IntrahepaticMatrix metalloproteinaseBiologyRats Sprague-DawleyCholestasisFibrosisInternal medicinemedicineAnimalsNorthern blotIn Situ HybridizationLiver injuryTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1HepatologyCarbon Tetrachloride PoisoningAcute-phase proteinTissue Inhibitor of Metalloproteinasesmedicine.diseaseRatsEndocrinologyLiverChemical and Drug Induced Liver InjuryHepatic fibrosisJournal of hepatology
researchProduct

Matrix metalloproteinases production in malignant pleural effusions after talc pleurodesis

2003

SUMMARY In this study we have evaluated the modifications of matrix metalloproteinases (MMPs) in malignant pleural fluids taken from patients suffering from lung cancer and treated with intrapleural talc instillation to induce pleurodesis. Furthermore, we have analysed the variations of some inflammatory mediators (C-reactive protein, α-1 antitrypsin) and of a protein (plasminogen) involved in MMP activation. In all patients the clinical improvement after talc pleurodesis was followed by a reduction in MMP-1, TIMP-1, C-reactive protein, α-1 antitrypsin and plasminogen activity. Furthermore, MMP-9 levels were variable; in fact, in some patients they were high at the beginning of treatment, i…

MalePathologymedicine.medical_specialtyPleural effusionmedicine.medical_treatmentImmunologyMatrix metalloproteinaseTalcStatistics NonparametricClinical StudiesHumansImmunology and AllergyMedicineLung cancerPleurodesisAgedTissue Inhibitor of Metalloproteinase-1business.industryTalc pleurodesisA proteinPlasminogenMiddle Agedmedicine.diseaseMatrix MetalloproteinasesPleural Effusion MalignantC-Reactive ProteinMatrix Metalloproteinase 9Talcalpha 1-AntitrypsinImmunologyPleural fluidFemaleMatrix Metalloproteinase 1businessPleurodesismedicine.drugClinical and Experimental Immunology
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Study of the Correlations among Some Parameters of the Oxidative Status, Gelatinases, and Their Inhibitors in a Group of Subjects with Metabolic Synd…

2014

Our aim was to examine some parameters of oxidative status, gelatinases, and their inhibitors and to evaluate their interrelationships in subjects with metabolic syndrome (MS). We enrolled 65 MS subjects, subdivided according to the presence or not of diabetes mellitus. We examined lipid peroxidation (expressed as thiobarbituric acid reacting substances, TBARS), protein oxidation (expressed as carbonyl groups), nitric oxide metabolites (NOx), total antioxidant status (TAS), MMP-2, MMP-9, TIMP-1, and TIMP-2. We found that MS subjects, diabetics and nondiabetics, showed an increase in TBARS, PC, and NOx. A significant decrease in TAS was observed only in nondiabetic MS subjects in comparison …

Malemedicine.medical_specialtyGelatinasesSettore MED/09 - Medicina InternaArticle SubjectThiobarbituric acidImmunologymedicine.disease_causeProtein oxidationNitric OxideThiobarbituric Acid Reactive SubstancesAntioxidantsLipid peroxidationchemistry.chemical_compoundOxidative Status Gelatinases Metabolic SyndromeInternal medicineDiabetes mellitusmedicineTBARSlcsh:PathologyHumansMetabolic SyndromeTissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1business.industryCell BiologyMiddle Agedmedicine.diseaseEndocrinologychemistryBiochemistryMatrix Metalloproteinase 9GelatinasesMatrix Metalloproteinase 2FemaleLipid PeroxidationMetabolic syndromebusinessOxidative stresslcsh:RB1-214Research ArticleMediators of Inflammation
researchProduct