2008
TNF-&agr; Induces MMP2 Gelatinase Activity and MT1-MMP Expression in an In Vitro Model of Nucleus Pulposus Tissue Degeneration
Séguin CA, Pilliar RM, Madri JA, Kandel RA. TNF-&agr; Induces MMP2 Gelatinase Activity and MT1-MMP Expression in an In Vitro Model of Nucleus Pulposus Tissue Degeneration. Spine 2008, 33: 356-365. PMID: 18277865, DOI: 10.1097/brs.0b013e3181642a5e.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleElectrophoretic Mobility Shift AssayExtracellular Signal-Regulated MAP KinasesGene ExpressionImmunoblottingIn Vitro TechniquesIntervertebral DiscLuciferasesMatrix Metalloproteinase 14Matrix Metalloproteinase 2Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaUp-RegulationConceptsMMP-2 gelatinase activityERK MAPK pathwayTranscriptional activationMT1-MMPElectrophoretic mobility shift assaysMT1-MMP promoterMMP-2 geneMobility shift assaysSignal transduction mechanismsProtein levelsERK 1/2 activationNP tissuesTranscription factorsShift assaysMT1-MMP expressionReporter constructsTNF-alpha inductionERK MAPKGelatinase activityLuciferase constructEgr-1TNF-alpha treatmentMMP-2 activationSP-1Transduction mechanismsDifferential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells
Kim JI, Cordova AC, Hirayama Y, Madri JA, Sumpio BE. Differential Effects of Shear Stress and Cyclic Strain on Sp1 Phosphorylation by Protein Kinase Cζ Modulates Membrane Type 1–Matrix Metalloproteinase in Endothelial Cells. Endothelium 2008, 15: 33-42. PMID: 18568943, PMCID: PMC2644408, DOI: 10.1080/10623320802092260.Peer-Reviewed Original ResearchConceptsSp1 phosphorylationMT1-MMP expressionPromoter sitesPKCzeta inhibitorProtein kinase CzetaAffinity of Sp1Egr-1 bindingProtein kinase CζExtracellular matrix remodelingEndothelial cell migrationSp1Cell migrationPhosphorylationMatrix remodelingProtein expressionCyclic strainExpressionMembrane typeEndothelial cellsKey roleCzetaInhibitorsCζMetalloproteinaseAffinity
2004
MMP‐2 null mice exhibit an early onset and severe experimental autoimmune encephalomyelitis due to an increase in MMP‐9 expression and activity
Esparza J, Kruse M, Lee J, Michaud M, Madri JA. MMP‐2 null mice exhibit an early onset and severe experimental autoimmune encephalomyelitis due to an increase in MMP‐9 expression and activity. The FASEB Journal 2004, 18: 1682-1691. PMID: 15522913, DOI: 10.1096/fj.04-2445com.Peer-Reviewed Original ResearchMeSH KeywordsAge of OnsetAnimalsBasement MembraneBlood-Brain BarrierBrainCD3 ComplexCell MovementEncephalomyelitis, Autoimmune, ExperimentalEnzyme ActivationGene Expression Regulation, EnzymologicMatrix Metalloproteinase 14Matrix Metalloproteinase 2Matrix Metalloproteinase 9Matrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesMiceMice, KnockoutT-Lymphocyte SubsetsT-LymphocytesConceptsMMP-2 KO miceExperimental autoimmune encephalomyelitisMMP-9 expressionAutoimmune encephalomyelitisEarly onsetWT miceKO miceMMP-9Bone marrowSevere experimental autoimmune encephalomyelitisMMP-2 null miceSimilar early onsetWT bone marrowClinical disease scoresMMP-2-deficient miceKO bone marrowMatrix metalloproteinase-2MT1-MMP expressionEndothelial cell monolayersSevere diseaseDisease scoreMetalloproteinase-2Collagen type IVMMP-2Matrix metalloproteinase
1999
Egr-1 Mediates Extracellular Matrix-driven Transcription of Membrane Type 1 Matrix Metalloproteinase in Endothelium*
Haas T, Stitelman D, Davis S, Apte S, Madri J. Egr-1 Mediates Extracellular Matrix-driven Transcription of Membrane Type 1 Matrix Metalloproteinase in Endothelium*. Journal Of Biological Chemistry 1999, 274: 22679-22685. PMID: 10428849, DOI: 10.1074/jbc.274.32.22679.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCloning, MolecularDNA-Binding ProteinsEarly Growth Response Protein 1Endothelium, VascularExtracellular MatrixGene Expression Regulation, EnzymologicHalf-LifeImmediate-Early ProteinsMatrix Metalloproteinase 14Matrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesMiceMolecular Sequence DataNeovascularization, PhysiologicProtein BindingRatsRNA, MessengerSp1 Transcription FactorTranscription FactorsTranscription, GeneticUp-RegulationConceptsMembrane type 1 matrix metalloproteinaseEgr-1MT1-MMPTranscription factor Egr-1Number of proteinsExtracellular matrix environmentEnhanced transcriptional activityEndothelial cellsTranscriptional activityPromoter correlatesIncreased transcriptionCellular invasionInvasive phenotypeMatrix metalloproteinaseTranscriptionMatrix environmentMatrix metalloproteinase activityMetalloproteinase activityCellsMatrix metalloproteinasesInvasionIncrease productionAngiogenesisMetalloproteinaseProtein
1998
The interrelationship of alpha4 integrin and matrix metalloproteinase-2 in the pathogenesis of experimental autoimmune encephalomyelitis.
Graesser D, Mahooti S, Haas T, Davis S, Clark R, Madri J. The interrelationship of alpha4 integrin and matrix metalloproteinase-2 in the pathogenesis of experimental autoimmune encephalomyelitis. Laboratory Investigation 1998, 78: 1445-58. PMID: 9840619.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDCell AdhesionCell MembraneCell MovementCells, CulturedClone CellsEncephalomyelitis, Autoimmune, ExperimentalEndothelium, VascularGelatinasesIntegrin alpha4Matrix Metalloproteinase 14Matrix Metalloproteinase 2Matrix Metalloproteinases, Membrane-AssociatedMetalloendopeptidasesMiceMice, Inbred StrainsProtease InhibitorsTissue Inhibitor of Metalloproteinase-2T-LymphocytesTransfectionConceptsExperimental autoimmune encephalomyelitisT cell clonesRecombinant vascular cell adhesion molecule-1Autoreactive T cell clonesAlpha4 integrinsMMP-2EAE inductionAutoimmune encephalomyelitisMyelin basic protein-reactive T cell clonesDisease processMatrix metalloproteinaseVascular cell adhesion molecule-1Cell adhesion molecule-1Human multiple sclerosisSusceptible mouse strainsAdhesion molecule-1T cell transmigrationMatrix metalloproteinase-2Microvascular endothelial cellsAlpha4 integrin expressionExpression of alpha4Adoptive transferMultiple sclerosisMouse modelEndothelial cell layer