Search results for "Matrix Metalloproteinase 3"

showing 10 items of 14 documents

Propeptide glycosylation and galectin‐3 binding decrease proteolytic activation of human proMMP‐9/progelatinase B

2019

Matrix metalloproteinases (MMPs) are secreted as proenzymes, containing propeptides that interact with the catalytic zinc, thereby controlling MMP activation. The MMP‐9 propeptide is unique in the MMP family because of its post‐translational modification with an N‐linked oligosaccharide. ProMMP‐9 activation by MMP‐3 occurs stepwise by cleavage of the propeptide in an aminoterminal (pro‐AT) and carboxyterminal (pro‐CT) peptide. We chemically synthesized aglycosyl pro‐AT and pro‐CT and purified recombinant glycosylated pro‐ATS f−9. First, we report new cleavage sites in the MMP‐9 propeptide by MMP‐3 and neutrophil elastase. Additionally, we demonstrated with the use of western blot analysis a…

0301 basic medicinePNGase FN-linked glycosylationGlycosylationGlycosylationmatrix metalloproteinase‐9Galectin 3GalectinsProteolysisgalectin‐3Biochemistry03 medical and health scienceschemistry.chemical_compoundCongenital Disorders of Glycosylation0302 clinical medicineN-linked glycosylationmatrix metalloproteinase-9galectin-3medicineHumansZymographyAmino Acid SequenceProtein precursorMolecular BiologyN‐linked glycosylationEnzyme Precursorspropeptidemedicine.diagnostic_testbiologyBlood ProteinsOriginal ArticlesCell BiologyTrypsinEnzyme Activation030104 developmental biologyMatrix Metalloproteinase 9chemistryBiochemistryGelatinasesCase-Control Studiesproteolytic activation030220 oncology & carcinogenesisNeutrophil elastaseProteolysisbiology.proteinMatrix Metalloproteinase 3Original ArticleLeukocyte Elastasemedicine.drug
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Molecular interactions between human cartilaginous endplates and nucleus pulposus cells: a preliminary investigation.

2014

Study Design. Conditioned media (CM) of cartilaginous endplates (CEPs) of intervertebral discs were analyzed in a bioassay with regard to their influence on matrix turnover and inflammatory factors on nucleus pulposus (NP) cells of the same patient. CEP tissue underwent further histological and ultrastructural analysis. Objective. To identify possible interactions between the CEP and the disc via molecular factors that may influence disc matrix degradation and to determine degenerative changes of CEP tissue. Summary of Background Data. Impaired endplate perme-ability due to degeneration and calcification is considered to be a key contributor to disc degeneration. An upregulation of metallop…

AdultMalePathologymedicine.medical_specialtyCellIntervertebral Disc DegenerationMatrix metalloproteinaseMatrix (biology)Proinflammatory cytokineDownregulation and upregulationMatrix Metalloproteinase 13MedicineHumansOrthopedics and Sports MedicineAggrecansIntervertebral DiscAggrecanCells CulturedAgedbusiness.industryInterleukin-6Interleukin-8Middle AgedCell biologyTissue Degenerationmedicine.anatomical_structureCartilageTumor necrosis factor alphaFemaleMatrix Metalloproteinase 3Neurology (clinical)businessSpine
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Partial restoration of pre-transformation levels of lysyl oxidase and transin mRNAs in phenotypic ras revertants.

1995

Neoplastic transformation mediated by ras oncogenes is associated with deregulated expression of genes encoding, for example, various proteases, lysyl oxidase, and smooth-muscle α-actin. To define the role of these genes in the initiation or maintenance of the ras-transformed state, we compared their steady-state mRNA levels in two different sets of preneoplastic fibroblast lines, ras-transformed clones, and phenotypic revertants derived from them. Compared with the preneoplastic fibroblasts, the ras-transformed derivatives exhibited elevated levels of cathepsin L (major excreted protein), transin (stromelysin I, matrix metalloproteinase–3), and collagenase I (matrix metalloproteinase–1) mR…

Cancer ResearchTranscription GeneticCathepsin LBlotting WesternGene ExpressionLysyl oxidaseCell LineCathepsin LProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-mycDownregulation and upregulationEndopeptidasesmedicineAnimalsNeoplastic transformationCollagenasesRNA MessengerFibroblastMolecular BiologyGeneMessenger RNAbiologyMetalloendopeptidasesPhenotypeMolecular biologyCathepsinsNeoplasm ProteinsRatsCysteine Endopeptidasesmedicine.anatomical_structureCell Transformation NeoplasticGenes rasPhenotypebiology.proteinMatrix Metalloproteinase 3Matrix Metalloproteinase 1Precancerous ConditionsMolecular carcinogenesis
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Genetic abrogation of the fibronectin-α5β1 integrin interaction in articular cartilage aggravates osteoarthritis in mice.

2018

The balance between synthesis and degradation of the cartilage extracellular matrix is severely altered in osteoarthritis, where degradation predominates. One reason for this imbalance is believed to be due to the ligation of the α5β1 integrin, the classic fibronectin (FN) receptor, with soluble FN fragments instead of insoluble FN fibrils, which induces matrix metalloproteinase (MMP) expression. Our objective was to determine whether the lack of α5β1-FN binding influences cartilage morphogenesis in vivo and whether non-ligated α5β1 protects or aggravates the course of osteoarthritis in mice. We engineered mice (Col2a-Cre;Fn1RGE/fl), whose chondrocytes express an α5β1 binding-deficient FN, …

Cartilage ArticularMale0301 basic medicineIntegrinsKnee JointGlycobiologylcsh:MedicineCartilage morphogenesisOsteoarthritisMatrix metalloproteinaseBiochemistryExtracellular matrixMice0302 clinical medicineAnimal CellsMedicine and Health Scienceslcsh:ScienceConnective Tissue CellsStainingMultidisciplinarybiologyChemistryExtracellular MatrixCell biologymedicine.anatomical_structureConnective TissueProteoglycansMatrix Metalloproteinase 3AnatomyCellular Structures and OrganellesCellular TypesResearch ArticleIntegrin alpha5beta1Signal TransductionIntegrinMice TransgenicResearch and Analysis Methods03 medical and health sciencesChondrocytesPhysical Conditioning AnimalMatrix Metalloproteinase 13OsteoarthritisCell AdhesionmedicineAnimalsHumansRegenerationCytoplasmic Staining030203 arthritis & rheumatologyCartilagelcsh:RBiology and Life SciencesProteinsCell Biologymedicine.diseaseFibronectinsFibronectinDisease Models AnimalBiological TissueCartilage030104 developmental biologyProteoglycanSpecimen Preparation and Treatmentbiology.proteinSafranin Staininglcsh:QCollagensArticular CartilagePLoS ONE
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Analysis of early biochemical markers and regulation by tin protoporphyrin IX in a model of spontaneous osteoarthritis

2011

Abstract Age-related changes in joint tissues lead to osteoarthritis (OA). Detection of early changes in OA patients may help to initiate treatments before the establishment of irreversible joint destruction. STR/ort mice develop with age a severe degenerative joint disease that resembles human OA thus allowing the investigation of biochemical markers as well as new treatments in an accelerated time frame. We have analyzed the changes in serum levels of different mediators during the early phases of idiopathic OA in STR/ort mice. Serum levels of matrix metalloproteinase-3 (MMP-3) but not those of tumor necrosis factor-α, interleukin(IL)-1β, IL-17 or prostaglandin E 2 correlated with histopa…

MaleAgingmedicine.medical_specialtyPathologyMetalloporphyrinsmedicine.medical_treatmentDrug Evaluation PreclinicalProtoporphyrinsMice Inbred StrainsOsteoarthritisMatrix metalloproteinaseBiochemistryMiceEndocrinologyInternal medicineOsteoarthritisGeneticsmedicineAnimalsEnzyme InhibitorsMolecular BiologyBiochemical markersbusiness.industryInterleukinCell BiologyClinical Enzyme TestsTin protoporphyrin IXmedicine.diseaseArthritis ExperimentalEarly DiagnosisEndocrinologyHeme Oxygenase (Decyclizing)Disease ProgressionBiomarker (medicine)Matrix Metalloproteinase 3Tumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersProstaglandin EExperimental Gerontology
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Conditioned Media from Adipose-Tissue-Derived Mesenchymal Stem Cells Downregulate Degradative Mediators Induced by Interleukin-1β in Osteoarthritic C…

2013

Osteoarthritis (OA) is the most frequent joint disorder and an important cause of disability. Recent studies have shown the potential of adipose-tissue-derived mesenchymal stem cells (AD-MSC) for cartilage repair. We have investigated whether conditioned medium from AD-MSC (CM) may regulate in OA chondrocytes a number of key mediators involved in cartilage degeneration. CM enhanced type II collagen expression in OA chondrocytes while decreasing matrix metalloproteinase (MMP) activity in cell supernatants as well as the levels of MMP-3 and MMP-13 proteins and mRNA in OA chondrocytes stimulated with interleukin- (IL-) 1β. In addition, CM increased IL-10 levels and counteracted the stimulating…

MaleArticle Subjectmedicine.medical_treatmentImmunologyInterleukin-1betaType II collagenAdipose tissueDown-RegulationNitric OxideChondrocytesMatrix Metalloproteinase 13Osteoarthritislcsh:PathologymedicineHumansProstaglandin E2Interleukin 6Collagen Type IICells CulturedAgedbiologyChemistryInterleukin-6Tumor Necrosis Factor-alphaMesenchymal stem cellNF-kappa BInterleukinMesenchymal Stem CellsCell BiologyMiddle AgedCell biologyAdipose TissueCulture Media ConditionedImmunologybiology.proteinTumor necrosis factor alphaFemaleMatrix Metalloproteinase 3Inflammation Mediatorslcsh:RB1-214Prostaglandin Emedicine.drugResearch Article
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes

2010

Introduction High mobility group box 1 (HMGB1) is released by necrotic cells or secreted in response to inflammatory stimuli. Extracellular HMGB1 may act as a pro-inflammatory cytokine in rheumatoid arthritis. We have recently reported that HMGB1 is released by osteoarthritic synoviocytes after activation with interleukin-1beta (IL-1β) The present study investigated the role of HMGB1 in synovial inflammation in osteoarthritis (OA). Methods HMGB1 was determined in human synovium using immunohistochemistry, comparing normal to OA. OA synoviocytes were incubated with HMGB1 at 15 or 25 ng/ml in the absence or presence of IL-1β (10 ng/ml). Gene expression was analyzed by quantitative PCR and pro…

MaleChemokineMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaImmunologyInflammationchemical and pharmacologic phenomenaCCL2HMGB1p38 Mitogen-Activated Protein KinasesRheumatologySynovitisMatrix Metalloproteinase 13HumansMedicineImmunology and AllergyRNA MessengerHMGB1 ProteinExtracellular Signal-Regulated MAP KinasesCells CulturedAgedbiologybusiness.industrySynovial MembraneNF-kappa BOsteoarthritis Kneemedicine.diseaseImmunohistochemistryMolecular biologyCCL20Cytokinemedicine.anatomical_structurebiology.proteinFemaleMatrix Metalloproteinase 3Matrix Metalloproteinase 1Synovial membranemedicine.symptombusinessProto-Oncogene Proteins c-aktResearch ArticleArthritis Research & Therapy
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Cordycepin protects against cerebral ischemia/reperfusion injury in vivo and in vitro.

2011

Cordycepin, (3'-deoxyadenosine), a bioactive compound of Cordyceps militaris, has been shown to exhibit many pharmacological actions, such as anti-inflammatory, antioxidative and anticancer activities. Little is known about the neuroprotective action of cordycepin as well as its molecular mechanisms. In this study, cordycepin was investigated for its neuroprotective potential in mice with ischemia following 15 min of the bilateral common carotid artery occlusion and 4h of reperfusion. The effect of cordycepin was also studied in mice brain slices treated with oxygen-glucose deprivation (OGD) injury. Our results showed that cordycepin was able to prevent postischemic neuronal degeneration an…

MaleExcitatory Amino AcidsIschemiaCell CountPharmacologyNeuroprotectionHippocampusBrain IschemiaSuperoxide dismutaseBrain ischemiachemistry.chemical_compoundMiceIn vivoMalondialdehydemedicineAnimalsPharmacologyNeuronsbiologyCordycepinDeoxyadenosinesbusiness.industrySuperoxide DismutaseGlutamate receptormedicine.diseaseOxygenGlucoseBiochemistrychemistryReperfusion Injurybiology.proteinMatrix Metalloproteinase 3businessReperfusion injuryPropidiumEuropean journal of pharmacology
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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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