Search results for "Proteinase"

showing 10 items of 407 documents

Human leukocyte elastase counteracts matrix metalloproteinase-7 induced apoptosis resistance of tumor cells.

2008

Matrix metalloproteinase-7 (MMP-7/Matrilysin) is a component of the tumor microenvironment associated with malignant progression. Its expression in tumors protects tumor cells from CD95-mediated apoptosis and the cytotoxic activity of tumor specific CD8(+) T cells. In the present study, we show that human leukocyte elastase (HLE) secreted by polymorphonuclear leukocytes cleaves MMP-7 resulting in loss of enzymatic activity. The anti-apoptotic effect of MMP-7 is reduced in the presence of HLE for CD95-, doxorubicin- and CTL-mediated apoptosis. Our data indicates that HLE may be a natural inactivator of MMP-7 which can counteract MMP-7-induced apoptosis resistance.

Cancer ResearchTumor microenvironmentbiologyChemistryNeutrophilsApoptosisMatrix metalloproteinaseFas receptorCell biologyOncologyApoptosisDoxorubicinNeutrophil elastaseMatrix Metalloproteinase 7NeoplasmsCancer researchbiology.proteinCytotoxic T cellHumanssense organsMatrilysinLeukocyte ElastaseCD8Cells CulturedT-Lymphocytes CytotoxicCancer letters
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Procollagen C-Proteinase Enhancer 1 (PCPE-1) is a marker of myocardial fibrosis and impaired cardiac function in a murine model of pressure overload

2021

Abstract(1)AimsProcollagen C-proteinase enhancer 1 (PCPE-1) is an extracellular matrix protein and a major regulator of fibrillar collagen biosynthesis. Previous work has shown that its abundance is often increased in the context of tissue repair and fibrosis. The present study was designed to evaluate its potential as a biomarker of myocardial interstitial fibrosis (MIF), a well-established pathogenic pathway leading to heart failure.(2)Methods and ResultsCardiac fibrosis was induced in rats using an optimized model of chronic pressure overload triggered by angiotensin II and Nω-nitro-L-arginine methyl ester (L-NAME). All treated animals suffered from heart hypertrophy and the increase in …

Cardiac function curvemedicine.medical_specialtyCardiac fibrosis[SDV]Life Sciences [q-bio]Diastoleheart failure030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineFibrosisInternal medicinemedicine030304 developmental biologyPressure overload0303 health sciencesCardiac fibrosiscirculating biomarkerbusiness.industrycollagen biosynthesismedicine.diseaseProcollagen C-proteinase enhancer 1 (PCPE-1)Angiotensin IIEndocrinologyHeart failureMyocardial fibrosisPET-MR imagingbusiness
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Adipose Stromal Vascular Fraction Improves Cardiac Function in Chronic Myocardial Infarction Through Differentiation and Paracrine Activity

2012

Fresh adipose-derived cells have been shown to be effective in the treatment of acute myocardial infarction (MI), but their role in the chronic setting is unknown. We sought to determine the long-term effect of the adipose derived-stromal vascular fraction (SVF) cell transplantation in a rat model of chronic MI. MI was induced in 82 rats by permanent coronary artery ligation and 5 weeks later rats were allocated to receive an intramyocardial injection of 107 GFP-expressing fresh SVF cells or culture media as control. Heart function and tissue metabolism were determined by echocardiography and 18F-FDG-microPET, respectively, and histological studies were performed for up to 3 months after t…

Cardiac function curvemedicine.medical_specialtymedicine.medical_treatmentHeart VentriclesBiomedical EngineeringMyocardial Infarctionlcsh:MedicineAdipose tissue030204 cardiovascular system & hematologyRevascularizationRats Sprague-Dawley03 medical and health sciences0302 clinical medicineFibrosisInternal medicineParacrine CommunicationmedicineAdipocytesMyocardial RevascularizationAnimalsMyocardial infarctionAngiogenic ProteinsVentricular remodeling030304 developmental biology0303 health sciencesTransplantationTissue Inhibitor of Metalloproteinase-1Ventricular Remodelingbusiness.industrylcsh:RCell DifferentiationTissue Inhibitor of MetalloproteinasesCell BiologyStromal vascular fractionmedicine.diseaseRatsTransplantationDisease Models AnimalPhenotypeEchocardiographyPositron-Emission TomographyChronic DiseaseCardiologyCytokinesFemaleStromal CellsbusinessCell Transplantation
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Leukocyte subtypes, gelatinases, and their tissue inhibitors in a group of subjects with asymptomatic carotid atherosclerosis

2022

In a cohort of subjects with asymptomatic carotid atherosclerosis (ACA), we have evaluated the neutrophil and lymphocyte count and their ratio (NLR), the gelatinases (MMP-2 and MMP-9) and their tissue inhibitors (TIMP-1 and TIMP-2). At baseline, no difference was observed between ACA subjects and subject control group regarding neutrophil and lymphocyte count while was evident in ACA subjects a significant increase in MMP-2, MMP-9 and TIMP-2 associated to a significant decrease in TIMP-1. Dividing the ACA according to the number of cardiovascular risk factors (CRFs) we have observed an increase in lymphocyte count in the subgroup with 3–5 CRFs. Evaluating the leukocyte subtypes according to…

Carotid Artery Diseasescardiovascular risk factorslymphocytesTissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1PhysiologyHematologyTIMP-2Asymptomatic carotid atherosclerosisTIMP-1Matrix Metalloproteinase 9neutrophilsinsulin resistancePhysiology (medical)LeukocytesHumansMatrix Metalloproteinase 2Cardiology and Cardiovascular MedicinegelatinasesBiomarkersResearch ArticleClinical Hemorheology and Microcirculation
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Fetuin-A and Cystatin C Are Endogenous Inhibitors of Human Meprin Metalloproteases

2010

Meprin α and β, zinc metalloproteinases, play significant roles in inflammation, including inflammatory bowel disease (IBD), possibly by activating cytokines, like interleukin 1β, interleukin 18, or tumor growth factor α. Although a number of potential activators for meprins are known, no endogenous inhibitors have been identified. In this work, we analyzed the inhibitory potential of human plasma and identified bovine fetuin-A as an endogenous meprin inhibitor with a K(i) (inhibition constant) of 4.2 × 10(-5) M for meprin α and a K(i) of 1.1 × 10(-6) M meprin β. This correlated with data obtained for a fetuin-A homologue from carp (nephrosin inhibitor) that revealed a potent meprin α and β…

Carpsalpha-2-HS-GlycoproteinMolecular Sequence DataMatrix metalloproteinaseBiochemistryPlasma03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCystatin C030304 developmental biology0303 health sciencesMetalloproteinasebiology030302 biochemistry & molecular biologyProteolytic enzymesMetalloendopeptidasesBlood ProteinsTrypsinFetuinProtease inhibitor (biology)3. Good healthBiochemistryCystatin Cbiology.proteinCattleCystatinSequence Alignmentmedicine.drugBiochemistry
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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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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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Ensemble-based ADME-Tox profiling and virtual screening for the discovery of new inhibitors of the Leishmania mexicana cysteine protease CPB2.8ΔCTE

2018

Abstract: In an effort to identify novel molecular warheads able to inhibit Leishmania mexicana cysteine protease CPB2.8CTE, fused benzo[b]thiophenes and ,'-triketones emerged as covalent inhibitors binding the active site cysteine residue. Enzymatic screening showed a moderate-to-excellent activity (12%-90% inhibition of the target enzyme at 20m). The most promising compounds were selected for further profiling including in vitro cell-based assays and docking studies. Computational data suggest that benzo[b]thiophenes act immediately as non-covalent inhibitors and then as irreversible covalent inhibitors, whereas a reversible covalent mechanism emerged for the 1,3,3'-triketones with a Y-to…

Cell SurvivalLeishmania mexicanaProtozoan ProteinsADME-Tox; Benzo[b]thiophenes; Cysteine protease; Leishmaniasis; TriketonesThiophenesCysteine Proteinase Inhibitors010402 general chemistry01 natural sciencesBiochemistryLeishmania mexicanaCysteine Proteinase InhibitorsCell LineInhibitory Concentration 50Structure-Activity RelationshipCysteine ProteasesCatalytic DomainDrug DiscoveryHumansStructure–activity relationshipcysteine proteaseBinding siteADME-Tox; benzo[b]thiophenes; cysteine protease; leishmaniasis; triketones; Biochemistry; Molecular MedicineBiologyleishmaniasisPharmacologychemistry.chemical_classificationVirtual screeningBinding Sitesbiology010405 organic chemistryPharmacology. TherapyOrganic Chemistrytriketonesbiology.organism_classificationCysteine protease0104 chemical sciencesMolecular Docking SimulationChemistryEnzymeBiochemistrychemistryDocking (molecular)ADME-ToxMolecular Medicinebenzo[b]thiophenes
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