Search results for "Tissue Inhibitor of Metalloproteinase-3"

showing 5 items of 5 documents

Quantitative Proteomics Reveals Changes Induced by TIMP-3 on Cell Membrane Composition and Novel Metalloprotease Substrates

2021

Ectodomain shedding is a key mechanism of several biological processes, including cell-communication. Disintegrin and metalloproteinases (ADAMs), together with the membrane-type matrix metalloproteinases, play a pivotal role in shedding transmembrane proteins. Aberrant shedding is associated to several pathological conditions, including arthritis. Tissue inhibitor of metalloproteases 3 (TIMP-3), an endogenous inhibitor of ADAMs and matrix metalloproteases (MMPs), has been proven to be beneficial in such diseases. Thus, strategies to increase TIMP-3 bioavailability in the tissue have been sought for development of therapeutics. Nevertheless, high levels of TIMP-3 may lead to mechanism-based …

0301 basic medicineProteomicsADAM15ProteomeCellMatrix metalloproteinaseMass SpectrometryCell membranelcsh:Chemistryanalysis [Proteome]lcsh:QH301-705.5proteomicSpectroscopybiologyChemistrytissue inhibitor of metalloproteases 3 (TIMP-3)General MedicineTransmembrane proteinComputer Science ApplicationsCell biologymedicine.anatomical_structureEctodomainddc:540TIMP3 protein humanmetalloproteinaseectodomain sheddingmetabolism [Tissue Inhibitor of Metalloproteinase-3]Quantitative proteomicsADAM15 protein humanchemistry [Cell Membrane]Catalysismetabolism [Cell Membrane]ArticlemetalloproteinasesInorganic Chemistry03 medical and health sciencestissue inhibitor of metalloproteases 3 (TIMP-3).medicineDisintegrinHumansPhysical and Theoretical ChemistryMolecular BiologyTissue Inhibitor of Metalloproteinase-3030102 biochemistry & molecular biologyOrganic ChemistryCell MembraneMembrane Proteinsmetabolism [Proteome]ADAM Proteins030104 developmental biologyHEK293 Cellslcsh:Biology (General)lcsh:QD1-999metabolism [ADAM Proteins]biology.proteinmetabolism [Membrane Proteins]International Journal of Molecular Sciences
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Inhibition of Histone Deacetylase Activity in Human Endometrial Stromal Cells Promotes Extracellular Matrix Remodelling and Limits Embryo Invasion

2011

Invasion of the trophoblast into the maternal decidua is regulated by both the trophoectoderm and the endometrial stroma, and entails the action of tissue remodeling enzymes. Trophoblast invasion requires the action of metalloproteinases (MMPs) to degrade extracellular matrix (ECM) proteins and in turn, decidual cells express tissue inhibitors of MMPs (TIMPs). The balance between these promoting and restraining factors is a key event for the successful outcome of pregnancy. Gene expression is post-transcriptionally regulated by histone deacetylases (HDACs) that unpacks condensed chromatin activating gene expression. In this study we analyze the effect of histone acetylation on the expressio…

Anatomy and PhysiologyGene ExpressionHydroxamic AcidsEndometriumEndocrinologyPregnancyMolecular Cell BiologyCells Culturedreproductive and urinary physiologyRegulation of gene expressionMultidisciplinarybiologyQRObstetrics and GynecologyExtracellular MatrixChromatinCell biologyHistonemedicine.anatomical_structureMatrix Metalloproteinase 9embryonic structuresMatrix Metalloproteinase 2MedicineFemaleHistone deacetylase activityResearch Articlemedicine.drugAdultStromal cellScienceDown-RegulationGene Expression Regulation EnzymologicYoung AdultmedicineHumansEmbryo ImplantationBiologyTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-1Reproductive SystemTrophoblastUrokinase-Type Plasminogen ActivatorMolecular biologyHistone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinStromal CellsDevelopmental Biology
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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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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
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Microvesicles shed by oligodendroglioma cells and rheumatoid synovial fibroblasts contain aggrecanase activity

2012

Membrane microvesicle shedding is an active process and occurs in viable cells with no signs of apoptosis or necrosis. We report here that microvesicles shed by oligodendroglioma cells contain an ‘aggrecanase’ activity, cleaving aggrecan at sites previously identified as targets for adamalysin metalloproteinases with disintegrin and thrombospondin domains (ADAMTSs). Degradation was inhibited by EDTA, the metalloproteinase inhibitor GM6001 and by tissue inhibitor of metalloproteinases (TIMP)-3, but not by TIMP-1 or TIMP-2. This inhibitor profile indicates that the shed microvesicles contain aggrecanolytic ADAMTS(s) or related TIMP-3-sensitive metalloproteinase(s). The oligodendroglioma cells…

OligodendrogliomaMembrane vesicleRA rheumatoid arthritisADAMTSMatrix metalloproteinaseCell Physiological PhenomenaAdamalysin03 medical and health sciences0302 clinical medicineSettore BIO/10 - BiochimicaEndopeptidasesHumansAggrecansADAM adamalysinADAMTS a disintegrin and metalloproteinase with thrombospondin motifsMolecular BiologyMetalloproteinase030304 developmental biologyAggrecanaseTissue Inhibitor of Metalloproteinase-3MEF mouse embryonic fibroblasts0303 health sciencesMetalloproteinaseChemistryBrief ReportMVs microvesiclesADAMTSMicrovesicleCytoplasmic VesiclesDipeptidesFibroblastsMolecular biologyRecombinant ProteinsMicrovesiclesECM extracellular matrixMembrane vesiclesCell biologyEnzyme ActivationMMP matrix metalloproteinaseADAM ProteinsADAMTS4030220 oncology & carcinogenesisProteolysisADAMTS5 ProteinRheumatic FeverTIMP tissue inhibitor of metalloproteinaseAggrecan
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