Search results for "Matrix metalloproteinase"

showing 10 items of 212 documents

Haem oxygenase-1 regulates catabolic and anabolic processes in osteoarthritic chondrocytes

2007

Pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro-inflammatory cytokines such as interleukin-1β (IL-1β) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase-1 (HO-1) is down-regulated by pro-inflammatory cytokines and up-regulated by IL-10 in OA chondrocytes. The aim of this study was to determine whether HO-1 can modify the catabolic effects of IL-1β in OA cartilage and chondrocytes. Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1β in OA …

Cartilage ArticularMaleMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaProtoporphyrinsMatrix metalloproteinaseChondrocytePathology and Forensic MedicineExtracellular matrixChondrocytesmedicineExtracellularHumansInsulin-Like Growth Factor ICollagen Type IICells CulturedAggrecanAgedbiologyChemistryCartilageGrowth factorOsteoarthritis KneeMatrix MetalloproteinasesCell biologymedicine.anatomical_structureProteoglycanImmunologybiology.proteinFemaleProteoglycansHeme Oxygenase-1The Journal of Pathology
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Haem oxygenase-1 induction reverses the actions of interleukin-1β on hypoxia-inducible transcription factors and human chondrocyte metabolism in hypo…

2013

HO-1 (haem oxygenase-1) catalyses the degradation of haem and possesses anti-inflammatory and cytoprotective properties. The role of inflammatory mediators in the pathogenesis of OA (osteoarthritis) is becoming increasingly appreciated. In the present study, we investigated the effects of HO-1 induction in OA and healthy HACs (human articular chondrocytes) in response to inflammatory cytokine IL-1 β (interleukin-1β) under hypoxic conditions. Hypoxia was investigated as it is a more physiological condition of the avascular cartilage. Hypoxic signalling is mediated by HIFs (hypoxia-inducible factors), of which there are two main isoforms, HIF-1α and HIF-2α. Normal and OA chondrocytes were sti…

Cartilage ArticularMaleSmall interfering RNAmedicine.medical_treatmentInterleukin-1betaBiologyMatrix metalloproteinaseChondrocytesOsteoarthritisBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaCollagen Type IITranscription factorAgedTumor Necrosis Factor-alphaCatabolismSOX9 Transcription FactorGeneral MedicineMiddle AgedHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCOPPMatrix MetalloproteinasesCell biologyCytokineBiochemistryFemaleTumor necrosis factor alphamedicine.symptomHeme Oxygenase-1Clinical Science
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Expression of Gelatinases (MMP-2, MMP-9) in human articular cartilage

2013

Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by destruction of the articular cartilage, subchondral bone alterations and synovitis. Matrix metalloproteinases (MMPs) are expressed in joint tissues of patients with osteoarthritis (OA). The objective of this study was to define the steady state levels of two different MMPs to provide more insight into the role of MMPs in cartilage destruction in OA. We investigated the expression of gelatinases through immunohistochemistry Our results show that high levels of MMP-2 and MMP-9 are present in OA and suggest that once these MMPs are fully activated they may contribute to the cartilage destruction in OA.

Cartilage ArticularSettore BIO/17 - IstologiaGelatinasesPathologymedicine.medical_specialtyImmunologyArticular cartilage; Metalloproteinases; Immunohistochemistry; OsteoarthritisArticular cartilageOsteoarthritisMatrix metalloproteinaseArticular cartilageOsteoarthritis HipDownregulation and upregulationSynovitisOsteoarthritisHumansImmunology and AllergyMedicineMetalloproteinasePharmacologybusiness.industryCartilageAnatomyOsteoarthritis Kneemedicine.diseaseImmunohistochemistryUp-Regulationmedicine.anatomical_structureMatrix Metalloproteinase 9Case-Control StudiesMatrix Metalloproteinase 2Immunohistochemistrybusiness
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TIMP-3 facilitates binding of target metalloproteinases to the endocytic receptor LRP-1 and promotes scavenging of MMP-1.

2020

AbstractMatrix metalloproteinases (MMPs) and the related families of disintegrin metalloproteinases (ADAMs) and ADAMs with thrombospondin repeats (ADAMTSs) play a crucial role in extracellular matrix (ECM) turnover and shedding of cell-surface molecules. The proteolytic activity of metalloproteinases is post-translationally regulated by their endogenous inhibitors, known as tissue inhibitors of metalloproteinases (TIMPs). Several MMPs, ADAMTSs and TIMPs have been reported to be endocytosed by the low-density lipoprotein receptor-related protein-1 (LRP-1). Different binding affinities of these proteins for the endocytic receptor correlate with different turnover rates which, together with di…

Cell biologyTIMP-3 LRP-1 MMP-1 extracellular matrix endocytosis metalloproteinases endocytic receptorlcsh:MedicinePlasma protein bindingMatrix metalloproteinaseBiochemistryArticleExtracellular matrixDisintegrinHumanslcsh:ScienceReceptorTissue Inhibitor of Metalloproteinase-3MetalloproteinaseThrombospondinMultidisciplinarybiologyChemistrylcsh:RLigand (biochemistry)EndocytosisMatrix MetalloproteinasesCell biologyKineticsMultiprotein Complexesbiology.proteinlcsh:Qlipids (amino acids peptides and proteins)Matrix Metalloproteinase 1Low Density Lipoprotein Receptor-Related Protein-1Protein BindingScientific reports
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PTHrP [67-86] regulates the expression of stress proteins in breast cancer cells inducing modifications in urokinase-plasminogen activator and MMP-1 …

2003

It was previously reported that a midregion domain of parathyroid hormone-related protein (PTHrP), that is, [67-86]-amide, is able to restrain growth and promote matrigel penetration by the 8701-BC cell line, derived from a biopsy fragment of a primary ductal infiltrating carcinoma of the human breast, and that cell invasion in vitro is drastically impaired by inactivation of urokinase-plasminogen activator (uPa). In this study we started a more detailed investigation of the possible effects on gene expression arising from the interaction between PTHrP [67-86]-amide and 8701-BC breast cancer cells by a combination of conventional-, differential display-and semi-quantitative multiplex-polyme…

CellBreast NeoplasmsBiologyHeat Shock Transcription FactorsDownregulation and upregulationCell Line TumorHeat shock proteinmedicineHumansNeoplasm InvasivenessHSP90 Heat-Shock ProteinsEnzyme InhibitorsHSF1Heat-Shock ProteinsMatrigelActivator (genetics)CarcinomaParathyroid Hormone-Related ProteinCell BiologyOligonucleotides AntisenseUrokinase-Type Plasminogen ActivatorMolecular biologyPeptide FragmentsProtein Structure TertiaryUp-RegulationDNA-Binding ProteinsGene Expression Regulation NeoplasticHeat shock factormedicine.anatomical_structureCell cultureCancer researchFemaleQuercetinMatrix Metalloproteinase 1Transcription FactorsJournal of Cell Science
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Neuronal Activity Drives Localized Blood-Brain-Barrier Transport of Serum Insulin-like Growth Factor-I into the CNS

2010

Upon entry into the central nervous system (CNS), serum insulin-like growth factor-1 (IGF-I) modulates neuronal growth, survival, and excitability. Yet mechanisms that trigger IGF-I entry across the blood-brain barrier remain unclear. We show that neuronal activity elicited by electrical, sensory, or behavioral stimulation increases IGF-I input in activated regions. Entrance of serum IGF-I is triggered by diffusible messengers (i.e., ATP, arachidonic acid derivatives) released during neurovascular coupling. These messengers stimulate matrix metalloproteinase-9, leading to cleavage of the IGF binding protein-3 (IGFBP-3). Cleavage of IGFBP-3 allows the passage of serum IGF-I into the CNS thro…

Central Nervous SystemTime FactorsMicrodialysismedicine.medical_treatmentAction PotentialsStimulationFunctional LateralityBody TemperatureReceptor IGF Type 1chemistry.chemical_compoundNeural PathwaysPremovement neuronal activityDrug InteractionsInsulin-Like Growth Factor IMicroscopy ImmunoelectronReceptorCells CulturedNeuronsGeneral NeuroscienceSysneuro//purl.org/becyt/ford/3.1 [https]Protein TransportMedicina Básicamedicine.anatomical_structureMatrix Metalloproteinase 9Blood-Brain BarrierSIGNALING//purl.org/becyt/ford/3 [https]Arachidonic acidNeurogliaLow Density Lipoprotein Receptor-Related Protein-1CIENCIAS MÉDICAS Y DE LA SALUDNeuroscience(all)Central nervous systemNeurocienciasBiophysicsGlutamic AcidEnzyme-Linked Immunosorbent AssayNerve Tissue ProteinsBiologyBlood–brain barrierMOLNEUROmedicineAnimalsHumansImmunoprecipitationRats WistarAnalysis of VarianceGrowth factorEndothelial CellsTransporterCoculture TechniquesElectric StimulationSignalingRatsMolneurochemistryRegional Blood FlowVibrissaeSYSNEURODigoxigeninExcitatory Amino Acid AntagonistsNeuroscience
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Vascular Microarchitecture of Murine Colitis-Associated Lymphoid Angiogenesis

2009

In permissive tissues, such as the gut and synovium, chronic inflammation can result in the ectopic development of anatomic structures that resemble lymph nodes. These inflammation-induced structures, termed lymphoid neogenesis or tertiary lymphoid organs, may reflect differential stromal responsiveness to the process of lymphoid neogenesis. To investigate the structural reorganization of the microcirculation involved in colonic lymphoid neogenesis, we studied a murine model of dextran sodium sulfate (DSS)-induced colitis. Standard 2-dimensional histology demonstrated both submucosal and intramucosal lymphoid structures in DSS-induced colitis. A spatial frequency analysis of serial histolog…

Colitis LymphocyticPathologymedicine.medical_specialtyHistologyStromal cellLymphoid TissueAngiogenesisBiologyArticleMicrocirculationMicemedicineAnimalsIntestinal MucosaColoring AgentsEcology Evolution Behavior and SystematicsMicrodissectionMicroscopy ConfocalNeovascularization PathologicStaining and LabelingMicrocirculationDextran SulfateHistologyMatrix MetalloproteinasesCapillariesMice Inbred C57BLDisease Models AnimalLymphatic systemRegional Blood FlowCytokinesLymphChemokinesAnatomyIntravital microscopyBiotechnologyThe Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
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Vitamin A deficiency disturbs collagen IV and laminin composition and decreases matrix metalloproteinase concentrations in rat lung. Partial reversib…

2011

Vitamin A is essential for lung development and pulmonary cell differentiation. Its deficiency leads to altered lung structure and function and to basement membrane architecture and composition disturbances. Previously, we showed that lack of retinoids thickens the alveolar basement membrane and increases collagen IV, which are reversed by retinoic acid, the main biologically active vitamin A form. This study analyzed how vitamin A deficiency affects the subunit composition of collagen IV and laminin of lung basement membranes and pulmonary matrix metalloproteinase content, plus the recovering effect of all-trans-retinoic acid. Male weanling pups were fed a retinol-adequate/-deficient diet …

Collagen Type IVMaleVitaminmedicine.medical_specialtyEndocrinology Diabetes and MetabolismClinical BiochemistryRetinoic acidGene ExpressionTretinoinMatrix metalloproteinaseBiochemistryBasement Membranechemistry.chemical_compoundLamininInternal medicineGene expressionmedicineAnimalsRats WistarVitamin ALungMolecular BiologyBasement membraneNutrition and DieteticsLungbiologyVitamin A DeficiencyTissue Inhibitor of Metalloproteinasesmedicine.diseaseMatrix MetalloproteinasesRatsVitamin A deficiencymedicine.anatomical_structureEndocrinologyBiochemistrychemistrybiology.proteinFemaleLamininThe Journal of Nutritional Biochemistry
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Regulation of type IV collagen gene expression and degradation in fast and slow muscles during dexamethasone treatment and exercise.

2003

Glucocorticoids have anti-anabolic effects on many tissues and can cause muscle atrophy. However, their effects on type IV collagen gene expression and degradation in skeletal muscle have not been studied previously. Rats were treated daily with dexamethasone or saline. Half the groups of experimental and control animals were also subjected to daily endurance or uphill running exercise to determine the possible preventive effects of exercise. After an experimental period of 3 or 10 days, the extensor digitorum longus, soleus and tibialis anterior muscles were studied. Dexamethasone treatment for 10 days reduced muscle weight and type IV collagen mRNA abundance in all muscles. Gene expressio…

Collagen Type IVmedicine.medical_specialtyPhysiologyClinical BiochemistryAnti-Inflammatory AgentsRadioimmunoassayMatrix metalloproteinaseDexamethasoneRats Sprague-DawleyType IV collagenPhysiology (medical)Internal medicinePhysical Conditioning AnimalGene expressionmedicineAnimalsRNA MessengerReceptorMuscle SkeletalGlucocorticoidsDexamethasoneRegulation of gene expressionTissue Inhibitor of Metalloproteinase-2ChemistrySkeletal muscleBlotting NorthernMuscle atrophyRatsEndocrinologymedicine.anatomical_structureMuscle Fibers Slow-TwitchGene Expression RegulationMuscle Fibers Fast-TwitchMatrix Metalloproteinase 2Femalemedicine.symptommedicine.drugPflugers Archiv : European journal of physiology
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Roflumilast N-oxide reverses corticosteroid resistance in neutrophils from patients with chronic obstructive pulmonary disease

2013

Background Glucocorticoid functions are markedly impaired in patients with chronic obstructive pulmonary disease (COPD). The phosphodiesterase 4 inhibitor roflumilast N-oxide (RNO) is the active metabolite of roflumilast approved as a treatment to reduce the risk of exacerbations in patients with severe COPD. Objective We sought to characterize the differential effects of RNO versus corticosteroids and their potential additive/synergistic effect in neutrophils from patients with COPD, thus providing scientific rationale for the combination of roflumilast with corticosteroids in the clinic. Methods Peripheral blood neutrophils were isolated from patients with COPD (n = 32), smokers (n = 7), …

CyclopropanesLipopolysaccharidesMaleMAPK/ERK pathwaymedicine.medical_specialtyNeutrophilsPrimary Cell CultureImmunologyDrug ResistanceAminopyridinesGene ExpressionComplex MixturesDexamethasoneHistone DeacetylasesPhosphatidylinositol 3-KinasesPulmonary Disease Chronic ObstructiveGlucocorticoid receptorAdrenal Cortex HormonesInternal medicineTobaccomedicineHumansImmunology and AllergyMacrophage Migration-Inhibitory FactorsDexamethasoneActive metaboliteRoflumilastAgedCOPDbusiness.industryInterleukin-8Drug SynergismMiddle Agedmedicine.diseaseIntramolecular OxidoreductasesEndocrinologyMatrix Metalloproteinase 9BenzamidesMitogen-Activated Protein Kinase PhosphatasesFemaleMacrophage migration inhibitory factorPhosphodiesterase 4 InhibitorsbusinessBiomarkersGlucocorticoidmedicine.drugJournal of Allergy and Clinical Immunology
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