Search results for "Metalloproteinase 9"

showing 10 items of 74 documents

Gelatinases and their tissue inhibitors in a group of subjects with metabolic syndrome.

2013

Aim To evaluate matrix metalloproteases (MMP)-2 and MMP-9 and tissue inhibitor of metalloproteases (TIMP)-1 and TIMP-2 in a group of subjects with metabolic syndrome (MS) subdivided according to the presence or absence of diabetes mellitus. Methods We examined in 90 subjects (51 men and 39 women) with MS, defined following the International Diabetes Federation criteria, and subsequently subdivided into diabetic subjects (22 men and 11 women) and nondiabetic subjects s (29 men and 28 women), the plasma concentrations of MMP-2 and MMP-9 and of TIMP-1 and TIMP-2 using specific enzyme-linked immunosorbent assay kits. Results We found a significant increase in plasma concentrations of MMP-2, MMP…

MaleGelatinasesmedicine.medical_specialtyMatrix metalloproteinase insulin resistanceMatrix metalloproteinaseBiologyMatrix Metalloproteinase InhibitorsGeneral Biochemistry Genetics and Molecular BiologyDiabetes mellitusInternal medicinemedicineMatrix metalloproteasesHumansInternational diabetes federationMetabolic SyndromeMetalloproteinaseTissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1General MedicineMiddle Agedmedicine.diseaseEndocrinologyMatrix Metalloproteinase 9GelatinasesPlasma concentrationMatrix Metalloproteinase 2FemaleMetabolic syndromeBiomarkersJournal of investigative medicine : the official publication of the American Federation for Clinical Research
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Non-invasive markers of airway inflammation and remodeling in childhood asthma

2009

To evaluate the relationship between pro-inflammatory and pro-remodeling mediators and severity and control of asthma in children, the levels of IL-8, MMP-9, TIMP-1 in induced sputum supernatants, the number of sputum eosinophils, as well as FeNO, were investigated in 35 asthmatic children, 12 with intermittent (IA) and 23 with moderate asthma (MA), and 9 controls (C). The patients with asthma were followed for 1 yr and sputum was obtained twice during the follow-up. Biomarker levels were correlated with the number of exacerbations. We found that IL-8, MMP-9, TIMP-1 and the numbers of eosinophils in induced sputum, as well as FeNO, were increased in children with IA and MA in comparison to …

MaleHumans; Disease Progression; Asthma; Child; Leukocyte Count; Eosinophils; Bronchitis; Follow-Up Studies; Sputum; Interleukin-8; Adolescent; Tissue Inhibitor of Metalloproteinase-1; Matrix Metalloproteinase 9; Biological Markers; Female; MaleAdolescentImmunologyInflammationDiseaseEosinophilBronchitiFollow-Up StudieLeukocyte CountImmunology and AllergyMedicineHumansNONINVASIVE MARKERS INFLAMMATION REMODELING CHILDHOOD ASTHMAProspective cohort studyBronchitisChildAsthmaChildhood asthmaTissue Inhibitor of Metalloproteinase-1business.industryInterleukin-8Airway inflammationSputumrespiratory systemmedicine.diseaseAsthmarespiratory tract diseasesEosinophilsMatrix Metalloproteinase 9Pediatrics Perinatology and Child HealthImmunologyBiological MarkerDisease ProgressionSputumBiomarker (medicine)Femalemedicine.symptombusinessBiomarkersHumanFollow-Up Studies
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Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers

2011

Abstract Mast cells (MC) are c-Kit–expressing cells, best known for their primary involvement in allergic reactions, but recently reappraised as important players in either cancer promotion or inhibition. Here, we assessed the role of MCs in prostate tumor development. In prostate tumors from both tumor-prone transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and human patients, MCs are specifically enriched and degranulated in areas of well-differentiated (WD) adenocarcinoma but not around poorly differentiated (PD) foci that coexist in the same tumors. We derived novel TRAMP tumor cell lines, representative of WD and PD variants, and through pharmacologic stabilization or geneti…

MaleOncologyCancer Researchmedicine.medical_specialtyEpithelial-Mesenchymal TransitionMice TransgenicAdenocarcinomaBiologymedicine.disease_causeCell DegranulationMiceProstate cancerProstateCell Line TumorInternal medicineTumor MicroenvironmentmedicineMast CellAnimalsHumansMast CellsReceptors Tumor Necrosis Factor Member 25Tumor microenvironmentAdenocarcinoma; Animals; Carcinoma Neuroendocrine; Cell Degranulation; Cell Line Tumor; Disease Progression; Epithelial-Mesenchymal Transition; Humans; Male; Mast Cells; Matrix Metalloproteinase 9; Mice; Mice Inbred C57BL; Mice Transgenic; Prostatic Neoplasms; Proto-Oncogene Proteins c-kit; Receptors Tumor Necrosis Factor Member 25; Tumor Microenvironment; Cancer Research; OncologyAnimalProstatic NeoplasmsCancermedicine.diseasehumanitiesCarcinoma NeuroendocrineMice Inbred C57BLProto-Oncogene Proteins c-kitmedicine.anatomical_structureMatrix Metalloproteinase 9OncologyTumor progressionProstatic NeoplasmDisease ProgressionAdenocarcinomaCarcinogenesisHumanTramp
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Associations of rs3918242 and rs2285053 MMP-9 and MMP-2 polymorphisms with the risk, severity, and short- and long-term complications of degenerative…

2016

Abstract Background Degenerative forms of mitral valve diseases (MVDs) are very complex pathologies. Thus, it is difficult to make generalizations about the disease pathways or genetic risk factors contributing to these diseases. However, a key role of metalloproteinases (MMPs) in their pathophysiology is emerging. Thus, we performed for the first time a perspective study to assess eventual associations of some functional single nucleotide polymorphisms (SNPs) in MMP-2 and MMP-9 genes with the MVD risk, symptom severity, and short- and long-term (4.8 years) complications. Materials and methods For this purpose, 90 patients and two control groups were genotyped for rs3918242, rs243865, and r…

MalePathologyHeart Valve DiseasesDisease030204 cardiovascular system & hematologyMatrix metalloproteinasers3918242 rs243865 rs2285053 MMP-2 and MMP-9 gene SNPDegenerative forms of mitral valve diseases; Management and outcome; Metalloproteinases; rs3918242 rs243865 rs2285053 MMP-2 and MMP-9 gene SNPs; Aged; Cohort Studies; Female; Genetic Predisposition to Disease; Genotype; Heart Valve Diseases; Humans; Male; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Middle Aged; Mitral Valve; Prospective Studies; Risk Factors; Polymorphism Single Nucleotide0403 veterinary scienceCohort Studies0302 clinical mediciners2285053 MMP-2 and MMP-9 gene SNPsRisk FactorsGenotypeManagement and outcomeNatriuretic peptideProspective StudiesProspective cohort studyMVDSMetalloproteinaseDegenerative forms of mitral valve diseases04 agricultural and veterinary sciencesGeneral MedicineSingle NucleotideMiddle AgedMetalloproteinasesPathophysiologyMatrix Metalloproteinase 9Matrix Metalloproteinase 2Mitral ValveFemalers3918242Cardiology and Cardiovascular MedicineDegenerative forms of mitral valve diseasemedicine.medical_specialtyGenotype040301 veterinary sciencesmedicine.drug_class2734Single-nucleotide polymorphismDegenerative forms of mitral valve diseases; Management and outcome; Metalloproteinases; rs3918242 rs243865 rs2285053 MMP-2 and MMP-9 gene SNPs; Cardiology and Cardiovascular Medicine; 2734Polymorphism Single NucleotidePathology and Forensic Medicine03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to Diseasers243865PolymorphismAgedbusiness.industrySettore MED/23 - Chirurgia Cardiacabusiness
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A polymorphism in the cyclooxygenase 2 gene as an inherited protective factor against myocardial infarction and stroke

2004

CONTEXT: Myocardial infarction (MI) and ischemic stroke are thought to be caused by matrix digestion by metalloproteinases (MMPs) leading to rupture of atherosclerotic plaques. Production of macrophage MMP-2 and MMP-9 is induced by cyclooxygenase 2 (COX-2) and prostaglandin E(2) synthesis. Although COX-2 expression may be genetically determined, the relation between COX-2 polymorphisms and the risk of MI and stroke is unclear. OBJECTIVE: To investigate the relationship between the -765G-->C polymorphism of the COX-2 gene and clinically evident plaque rupture. DESIGN, SETTING, AND PARTICIPANTS: Prospective, matched case-control study conducted between March 2002 and October 2003 among 864 pa…

MalePathologySettore MED/09 - Medicina InternaArteriosclerosisCarotid StenosiMyocardial InfarctionInfarctionProstacyclinGastroenterologyCohort StudiesCerebrovascular AccidentrteriosclerosiRisk FactorsGenotypeMedicineCarotid StenosisProspective StudiesMyocardial infarctionMembrane ProteinStrokebiologyGeneral MedicineMiddle AgedIsoenzymesStrokePhenotypeMatrix Metalloproteinase 9Matrix Metalloproteinase 2FemaleHumanmedicine.drugmedicine.medical_specialtyGenotypeArteriosclerosiInternal medicineDiabetes mellitusHumansPolymorphism Geneticbusiness.industryC-reactive proteinProstaglandin-Endoperoxide SynthaseMembrane Proteinsmedicine.diseaseEpoprostenolIsoenzymeProspective StudieAtheromaCyclooxygenase 2Prostaglandin-Endoperoxide Synthasesbiology.proteinCohort Studiebusiness
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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
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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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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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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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