Search results for " metalloproteinases"

showing 10 items of 77 documents

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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Urokinase Plasminogen Activator and Gelatinases Are Associated with Membrane Vesicles Shed by Human HT1080 Fibrosarcoma Cells

1997

Membrane vesicles are shed by tumor cells both in vivo and in vitro. Although their functions are not well understood, it has been proposed that they may play multiple roles in tumor progression. We characterized membrane vesicles from human HT1080 fibrosarcoma cell cultures for the presence of proteinases involved in tumor invasion. By gelatin zymography and Western blotting, these vesicles showed major bands corresponding to the zymogen and active forms of gelatinase B (MMP-9) and gelatinase A (MMP-2) and to the MMP-9. tissue inhibitor of metalloproteinase 1 complex. Both gelatinases appeared to be associated with the vesicle membrane. HT1080 cell vesicles also showed a strong, plasminoge…

GelatinasesMacromolecular SubstancesFibrosarcomaBlotting WesternCellGelatinase ABiologyBiochemistryTumor Cells CulturedmedicineHumansCollagenasesFibrinolysinMolecular BiologyGlycoproteinsUrokinaseEnzyme PrecursorsVesicleMetalloendopeptidasesTissue Inhibitor of MetalloproteinasesCell BiologyTissue inhibitor of metalloproteinaseUrokinase-Type Plasminogen ActivatorMolecular biologyExtracellular MatrixUrokinase receptorBloodmedicine.anatomical_structureMatrix Metalloproteinase 9GelatinasesMatrix Metalloproteinase 2HT1080medicine.drugJournal of Biological Chemistry
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Role of the Netrin-like Domain of Procollagen C-Proteinase Enhancer-1 in the Control of Metalloproteinase Activity

2010

The netrin-like (NTR) domain is a feature of several extracellular proteins, most notably the N-terminal domain of tissue inhibitors of metalloproteinases (TIMPs), where it functions as a strong inhibitor of matrix metalloproteinases and some other members of the metzincin superfamily. The presence of a C-terminal NTR domain in procollagen C-proteinase enhancers (PCPEs), proteins that stimulate the activity of astacin-like tolloid proteinases, raises the possibility that this might also have inhibitory activity. Here we show that both long and short forms of the PCPE-1 NTR domain, the latter beginning at the N-terminal cysteine known to be critical for TIMP activity, show no inhibition, at …

Glycobiology and Extracellular MatricesMatrix metalloproteinaseBiochemistryBONE MORPHOGENETIC PROTEIN-1AdamalysinFIBRILLAR PROCOLLAGENSTolloid ProteinaseExtracellular Matrix Proteins0303 health sciencesADAMTSFRIZZLED-RELATED PROTEINS030302 biochemistry & molecular biologyTissue Inhibitor of Metalloproteinases11 Medical And Health SciencesALPHA-CONVERTING-ENZYMEI PROCOLLAGENADAM ProteinsExtracellular MatrixPLASMINOGEN ACTIVATIONBiochemistryCollagen03 Chemical SciencesLife Sciences & BiomedicineProcollagenBiochemistry & Molecular BiologyTERMINAL DOMAINTolloid-Like MetalloproteinasesADAMTSBiologyBone morphogenetic protein 1Cell Line03 medical and health sciencesDisintegrinHumansHUMAN TISSUE INHIBITORMatrix MetalloproteinaseMolecular BiologyGlycoproteins030304 developmental biologyThrombospondinScience & TechnologyHeparinADAMCell Biology06 Biological SciencesMATRIX-METALLOPROTEINASESProtein Structure TertiaryADAM ProteinsProcollagen peptidaseSULFATED GLYCOSAMINOGLYCANSEnzymologybiology.proteinJournal of Biological Chemistry
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Mutant p53 gain of function can be at the root of dedifferentiation of human osteosarcoma MG63 cells into 3AB-OS cancer stem cells

2014

Osteosarcoma is a highly metastatic tumor affecting adolescents, for which there is no second-line chemotherapy. As suggested for most tumors, its capability to overgrow is probably driven by cancer stem cells (CSCs), and finding new targets to kill CSCs may be critical for improving patient survival. TP53 is the most frequently mutated tumor suppressor gene in cancers and mutant p53 protein (mutp53) can acquire gain of function (GOF) strongly contributing to malignancy. Studies thus far have not shown p53-GOF in osteosarcoma. Here, we investigated TP53 gene status/role in 3AB-OS cells-a highly aggressive CSC line previously selected from human osteosarcoma MG63 cells-to evaluate its involv…

HistologyTumor suppressor genePhysiologyEndocrinology Diabetes and MetabolismApoptosisIn situ hybridizationBiologyTNF-Related Apoptosis-Inducing LigandCell MovementCancer stem cellCell Line TumorSettore BIO/10 - BiochimicaBiomarkers TumormedicineHumansNeoplasm Invasiveness3AB-OS cells CSCs Cancer cell dedifferentiation Cancer stem cells FISH Fluorescent in situ hybridization GOF Gain of function Human osteosarcoma MMPs Matrix metalloproteinases Mutant p53 Mutant p53 gain of function Mutp53 OS OsteosarcomaClonogenic assayTumor Stem Cell AssayCell ProliferationMembrane Potential MitochondrialOsteosarcomaCancerReceptors Death DomainCell DedifferentiationCell cyclemedicine.diseaseMolecular biologyAmino Acid SubstitutionProto-Oncogene Proteins c-bcl-2Gene Knockdown TechniquesMutationNeoplastic Stem CellsCancer researchOsteosarcomaEctopic expressionTumor Suppressor Protein p53Bone
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Intramuscular Extracellular Matrix: Complex Environment of Muscle Cells

2002

KOVANEN, V. Intramuscular extracellular matrix: Complex environment of muscle cells. Exerc. Sport Sci. Rev., Vol. 30, No. 1, pp 20–25, 2002. Different collagen types among other extracellular matrix molecules, remodeling of the extracellular matrix with the aid of matrix metalloproteinases, and inte

IntegrinsChemistryFibrillar CollagensPhysical Therapy Sports Therapy and RehabilitationNon-Fibrillar CollagensExtracellular matrix moleculesMatrix metalloproteinaseBasement MembraneMatrix MetalloproteinasesExtracellular MatrixCell biologyExtracellular matrixHumansMyocyteOrthopedics and Sports MedicineMuscle SkeletalExercise and Sport Sciences Reviews
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Endothelial cell-matrix interactions.

2002

Dynamic interactions between endothelial cells and components of their surrounding extracellular matrix are necessary for the invasion, migration, and survival of endothelial cells during angiogenesis. These interactions are mediated by matrix receptors that initiate intracellular signaling cascades in response to binding to specific extracellular matrix molecules. The interactions between endothelial cells and their environment are also modulated by enzymes that degrade different matrix components and thus enable endothelial invasion. Recent reports on gene targeting in mice have confirmed the role of two classes of matrix receptors, integrins and cell surface heparan sulfate proteoglycans…

IntegrinsHistologybiologyNeovascularization PathologicAngiogenesisIntegrinProteolytic enzymesNeovascularization PhysiologicMatrix (biology)Matrix metalloproteinaseMatrix MetalloproteinasesCell biologyExtracellular MatrixExtracellular matrixEndothelial stem cellFibronectinMedical Laboratory TechnologyMicebiology.proteinAnimalsHumansEndothelium VascularAnatomyInstrumentationHeparan Sulfate ProteoglycansMicroscopy research and technique
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Collagenolytic proteinases in keratoconus.

2006

To study the proteolytic phenomena contributing to the pathogenesis of keratoconus, corneal enzymes with potential to cleave fibrillar collagen were studied.Immunohistochemical labeling was undertaken of conventional and novel mammalian collagenases (MMP-1, -2, -8, -13, and -14) of the matrix metalloproteinase (MMP) family and other collagenolytic proteinases of the serine (human trypsin-2) and cysteine (cathepsin K) endoproteinase families. The results were analyzed using a semiquantitative scoring system.Labeling of MMP-8 was moderate in healthy controls, but weak in keratoconus. Moderate MMP-2 and weak MMP-14 expressions were similar in controls and keratoconus. MMP-1 was slightly overex…

KeratoconusPathologymedicine.medical_specialtygenetic structuresCathepsin KMatrix metalloproteinaseKeratoconusPathogenesisCorneaImmunoenzyme TechniquesCorneamedicineCathepsin KHumansTrypsinCollagenaseschemistry.chemical_classificationmedicine.diseaseCathepsinseye diseasesMatrix MetalloproteinasesOphthalmologyEnzymemedicine.anatomical_structurechemistryCollagenaseTrypsinogenImmunohistochemistrysense organsKeratoplasty Penetratingmedicine.drugCornea
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Genetic variation in the TLL1 gene is not associated with fibrosis in patients with metabolic associated fatty liver disease.

2020

Metabolic associated fatty liver disease (MAFLD) is the most prevalent liver disease in Western nations, with high heritability. A recent study of Japanese patients with the disease suggested that TLL1 rs17047200 is associated with fibrosis; whether a similar association is observed in Caucasian patients with MAFLD is unknown. We investigated the association of the TLL1 rs17047200 polymorphism with liver fibrosis in a cohort of Caucasian patients with MAFLD (n = 728). We also investigated whether TLL1 expression is altered during liver injury in humans, in murine models of fibrosis, and in in-vitro. While TLL1 expression is upregulated in the liver of humans with MAFLD and in mice, the rs17…

Liver CirrhosisMaleSteatosisGene ExpressionDiseasePathology and Laboratory MedicineInbred C57BLGastroenterologyPathogenesisCytopathologyCohort StudiesLiver diseaseMice0302 clinical medicineFibrosisMedicine and Health SciencesLiver injury0303 health sciencesMultidisciplinaryLiver DiseasesQFatty liverRTLL1Single NucleotideMiddle Aged3. Good healthUp-RegulationAdult; Animals; Cohort Studies; Fatty Liver; Female; Genetic Variation; Humans; Liver Cirrhosis; Male; Mice; Mice Inbred C57BL; Middle Aged; Tolloid-Like Metalloproteinases; Up-Regulation; Polymorphism Single NucleotideMedicineLiver Fibrosis030211 gastroenterology & hepatologyFemaleAnatomyResearch ArticleAdultmedicine.medical_specialtyHistologyTolloid-Like MetalloproteinasesSettore MED/12 - GASTROENTEROLOGIAScienceGastroenterology and HepatologyPolymorphism Single Nucleotide03 medical and health sciencesInternal medicinemedicineGeneticsAnimalsHumansPolymorphism030304 developmental biologyNutritionbusiness.industryAdult Animals Cohort Studies Fatty Liver Female Genetic Variation Humans Liver Cirrhosis Male Mice Mice Inbred C57BL Middle Aged Tolloid-Like Metalloproteinases Up-Regulation Polymorphism Single NucleotideBiology and Life SciencesGenetic Variationmedicine.diseaseFibrosisDietFatty LiverMice Inbred C57BLn/aAnatomical PathologySteatosisbusinessDevelopmental Biology
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Manganese overload affects p38 MAPK phosphorylation and metalloproteinase activity during sea urchin embryonic development.

2014

Abstract In the marine environment, manganese represents a potential emerging contaminant, resulting from an increased production of manganese-containing compounds. In earlier reports we found that the exposure of Paracentrotus lividus sea urchin embryos to manganese produced phenotypes with no skeleton. In addition, manganese interfered with calcium uptake, perturbed extracellular signal-regulated kinase (ERK) signaling, affected the expression of skeletogenic genes, and caused an increase of the hsc70 and hsc60 protein levels. Here, we extended our studies focusing on the temporal activation of the p38 mitogen-activated protein kinase (p38 MAPK) and the proteolytic activity of metalloprot…

MAPK/ERK pathwayEmbryo NonmammalianAquatic ScienceBiologyMatrix metalloproteinaseOceanographyp38 Mitogen-Activated Protein KinasesParacentrotus lividusbiology.animalECM ERK Embryo-toxicity Immunoblotting MAPK MMPs Marine organisms' calcification Mn SDS-PAGE Zymography extracellular matrix extracellular signal-regulated kinase manganese metalloproteinases mitogen-activated protein kinase p38 MAPK sodium dodecyl sulfate-polyacrylamide gel electrophoresisAnimalsSettore BIO/06 - Anatomia Comparata E CitologiaPhosphorylationProtein kinase ASea urchinManganeseKinaseGeneral Medicinebiology.organism_classificationPollutionMatrix MetalloproteinasesBiochemistryMitogen-activated protein kinasebiology.proteinParacentrotusPhosphorylationWater Pollutants ChemicalMarine environmental research
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PHENOTYPIC PROFILING OF THYROID CARCINOMA CELL LINES AND DIFFERENTIAL SECRETION OF MATRIX METALLOPROTEINASES

2011

MATRIX METALLOPROTEINASES
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