2016
Axonal branching in lateral olfactory tract is promoted by Nogo signaling
Iketani M, Yokoyama T, Kurihara Y, Strittmatter SM, Goshima Y, Kawahara N, Takei K. Axonal branching in lateral olfactory tract is promoted by Nogo signaling. Scientific Reports 2016, 6: 39586. PMID: 28000762, PMCID: PMC5175167, DOI: 10.1038/srep39586.Peer-Reviewed Original ResearchConceptsLateral olfactory tractCultured OB neuronsOB neuronsCollateral branchesAxonal branchingOlfactory bulbOlfactory tractAxonal bundlesMajor projection neuronsReceptor 1 antagonistKnockdown of NogoCollateral formationProjection neuronsPrimary axonsNogo signalingMitral cellsMiceNeuronsExpression levelsAbnormal increaseTractNogoAntagonistAxons
2015
Gene-Silencing Screen for Mammalian Axon Regeneration Identifies Inpp5f (Sac2) as an Endogenous Suppressor of Repair after Spinal Cord Injury
Zou Y, Stagi M, Wang X, Yigitkanli K, Siegel CS, Nakatsu F, Cafferty WB, Strittmatter SM. Gene-Silencing Screen for Mammalian Axon Regeneration Identifies Inpp5f (Sac2) as an Endogenous Suppressor of Repair after Spinal Cord Injury. Journal Of Neuroscience 2015, 35: 10429-10439. PMID: 26203138, PMCID: PMC4510284, DOI: 10.1523/jneurosci.1718-15.2015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsDisease Models, AnimalGene Knockdown TechniquesImmunohistochemistryInositol Polyphosphate 5-PhosphatasesMiceMice, Inbred C57BLMice, KnockoutNerve RegenerationPhosphoric Monoester HydrolasesRecovery of FunctionReverse Transcriptase Polymerase Chain ReactionSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryEndogenous suppressorAxon regenerationNonoverlapping substrate specificityGenome-wide scaleHigh-throughput functional screensFunctional recoveryAxonal regenerationCNS axon repairSpinal cord injury researchDorsal hemisection injuryMammalian genesPI3K/AKT/mTOR pathwayCNS axon growthAKT/mTOR pathwayLipid phosphataseCorticospinal tract axonsCNS axon regenerationAdult mammalian CNSFunctional screenSubstrate specificityNovel suppressorShRNA resultsINPP5F
2014
Progressive retinal degeneration and accumulation of autofluorescent lipopigments in Progranulin deficient mice
Hafler BP, Klein ZA, Zhou Z, Strittmatter SM. Progressive retinal degeneration and accumulation of autofluorescent lipopigments in Progranulin deficient mice. Brain Research 2014, 1588: 168-174. PMID: 25234724, PMCID: PMC4254024, DOI: 10.1016/j.brainres.2014.09.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedElectroretinographyGranulinsImmunohistochemistryIntercellular Signaling Peptides and ProteinsMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalNeuronal Ceroid-LipofuscinosesOptical ImagingPhotoreceptor Cells, VertebrateProgranulinsRetinal DegenerationRetinal Ganglion CellsConceptsProgranulin-deficient miceNeuronal ceroid lipofuscinosisAdult-onset neuronal ceroid lipofuscinosisDeficient miceRetinal degenerationCeroid lipofuscinosisRetinal ganglion cellsCentral nervous systemAutofluorescent storage materialMotor dysfunctionNeuropathological analysisGanglion cellsVision lossOptic atrophyEarly deathAutofluorescent lipopigmentsClinical observationsNervous systemDegenerative pathologyMiceDegenerationHomozygous mutationAutofluorescent materialPatientsNeuronsDiffusion Tensor Imaging as a Predictor of Locomotor Function after Experimental Spinal Cord Injury and Recovery
Kelley BJ, Harel NY, Kim CY, Papademetris X, Coman D, Wang X, Hasan O, Kaufman A, Globinsky R, Staib LH, Cafferty WB, Hyder F, Strittmatter SM. Diffusion Tensor Imaging as a Predictor of Locomotor Function after Experimental Spinal Cord Injury and Recovery. Journal Of Neurotrauma 2014, 31: 1362-1373. PMID: 24779685, PMCID: PMC4120934, DOI: 10.1089/neu.2013.3238.Peer-Reviewed Original ResearchConceptsSpinal cord injuryDiffusion tensor imagingCord injuryAxonal integrityLocomotor functionExperimental spinal cord injuryTraumatic spinal cord injuryFemale Sprague-Dawley ratsTensor imagingFractional anisotropyFunctional recovery assessmentSpinal cord contusionLimited functional recoveryLong-term disabilityQuantitative diffusion tensor imagingRodent SCI modelsSprague-Dawley ratsSpinal cord morphologyWhite matter pathologyCaudal spinal cordWhite matter integrityInjury epicenterMidthoracic laminectomyCord contusionPrimary outcome
2011
Cartilage Acidic Protein–1B (LOTUS), an Endogenous Nogo Receptor Antagonist for Axon Tract Formation
Sato Y, Iketani M, Kurihara Y, Yamaguchi M, Yamashita N, Nakamura F, Arie Y, Kawasaki T, Hirata T, Abe T, Kiyonari H, Strittmatter SM, Goshima Y, Takei K. Cartilage Acidic Protein–1B (LOTUS), an Endogenous Nogo Receptor Antagonist for Axon Tract Formation. Science 2011, 333: 769-773. PMID: 21817055, PMCID: PMC3244695, DOI: 10.1126/science.1204144.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBinding SitesCalcium-Binding ProteinsCell LineCells, CulturedGPI-Linked ProteinsGrowth ConesHumansImmunohistochemistryLigandsMiceMice, Inbred ICRMyelin ProteinsNogo ProteinsNogo Receptor 1Olfactory PathwaysProsencephalonProtein BindingReceptors, Cell SurfaceSignal TransductionConceptsTract formationNogo receptor 1Axon growth inhibitorsProtein 1BEndogenous antagonismAxon tract formationReceptor antagonistGrowth cone collapseAxonal projectionsCircuitry formationNeural circuitry formationMouse brainReceptor 1LOT formationNeural regenerationNgR1Key moleculesCone collapseMiceFluorophore-assisted light inactivationGrowth inhibitorAntagonistBrainMyelinNogo
2010
Nogo Receptor Deletion and Multimodal Exercise Improve Distinct Aspects of Recovery in Cervical Spinal Cord Injury
Harel NY, Song KH, Tang X, Strittmatter SM. Nogo Receptor Deletion and Multimodal Exercise Improve Distinct Aspects of Recovery in Cervical Spinal Cord Injury. Journal Of Neurotrauma 2010, 27: 2055-2066. PMID: 20809785, PMCID: PMC2978056, DOI: 10.1089/neu.2010.1491.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalExercise TherapyFemaleGene DeletionGenotypeGPI-Linked ProteinsHand StrengthImmunohistochemistryMaleMiceMice, Inbred C57BLMyelin ProteinsNeuronal PlasticityNogo Receptor 1Physical Conditioning, AnimalPostural BalanceReceptors, Cell SurfaceReproducibility of ResultsSerotoninSpinal CordSpinal Cord InjuriesWalkingConceptsSpinal cord injuryCord injuryCervical spinal cord injuryIncomplete spinal cord injuryCervical spinal injurySignificant histological differencesMultimodal exerciseExercise trainingLateral hemisectionReceptor deletionSpinal injuryLesion modelMouse modelAdult miceLesion sizeGene deletionHistological differencesNeural plasticityMild deficitsHistological analysisTraining regimenInjuryPhysical interventionsC3-C4MiceAnti-PrPC monoclonal antibody infusion as a novel treatment for cognitive deficits in an alzheimer's disease model mouse
Chung E, Ji Y, Sun Y, Kascsak RJ, Kascsak RB, Mehta PD, Strittmatter SM, Wisniewski T. Anti-PrPC monoclonal antibody infusion as a novel treatment for cognitive deficits in an alzheimer's disease model mouse. BMC Neuroscience 2010, 11: 130. PMID: 20946660, PMCID: PMC2964735, DOI: 10.1186/1471-2202-11-130.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalBlotting, WesternCerebral CortexCognition DisordersEnzyme-Linked Immunosorbent AssayHippocampusHumansImage Processing, Computer-AssistedImmunohistochemistryMemory, Short-TermMiceMice, TransgenicPrPC ProteinsPsychomotor PerformanceSynapsesSynaptophysinConceptsAPP/PS1 Tg miceAPP/PS1 transgenic miceAPP/PS1 TgPS1 transgenic miceDisease model miceTransgenic miceCognitive deficitsTg miceAβ oligomersBehavioral testingVehicle solutionAlzheimer's disease model miceDentate gyrus molecular layerAPP/PS1 groupWild-type control groupConformational neurodegenerative disordersMonoclonal antibody infusionAD transgenic miceAmyloid plaque burdenAβ oligomer levelsDays/weekNovel therapeutic approachesMurine hippocampal slicesShort-term treatmentAnti-PrP antibodies
2009
Inosine Alters Gene Expression and Axonal Projections in Neurons Contralateral to a Cortical Infarct and Improves Skilled Use of the Impaired Limb
Zai L, Ferrari C, Subbaiah S, Havton LA, Coppola G, Strittmatter S, Irwin N, Geschwind D, Benowitz LI. Inosine Alters Gene Expression and Axonal Projections in Neurons Contralateral to a Cortical Infarct and Improves Skilled Use of the Impaired Limb. Journal Of Neuroscience 2009, 29: 8187-8197. PMID: 19553458, PMCID: PMC2856695, DOI: 10.1523/jneurosci.0414-09.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBrain InfarctionCerebral CortexComplement C1qComplement C3Disease Models, AnimalExtremitiesFunctional LateralityGene Expression RegulationHeat-Shock ProteinsImmunohistochemistryInjections, IntraventricularInosineNeuronsOligonucleotide Array Sequence AnalysisProteasome Endopeptidase ComplexRatsRats, Sprague-DawleyRecovery of FunctionRNA, MessengerTreatment OutcomeUbiquitinationConceptsUndamaged neuronsSpinal cordSynaptic bouton-like structuresImpaired limbAlters gene expressionCorticospinal tract axonsSpecific cortical areasBouton-like structuresCortical infarctsCorticospinal neuronsDenervated sideUnaffected hemisphereAxon collateralsSensorimotor cortexBrain damageBrain injuryInjury modelLaser capture microdissectionAxonal projectionsGene expressionCortical areasDenervated halfComplement cascadeNeuronsAxon growth
2006
Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat
Marklund N, Fulp CT, Shimizu S, Puri R, McMillan A, Strittmatter SM, McIntosh TK. Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat. Experimental Neurology 2006, 197: 70-83. PMID: 16321384, PMCID: PMC2849132, DOI: 10.1016/j.expneurol.2005.08.029.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternBrainBrain InjuriesCell CountCornified Envelope Proline-Rich ProteinsDensitometryFunctional LateralityGPI-Linked ProteinsHippocampusImmunohistochemistryMaleMembrane ProteinsMicrotubule-Associated ProteinsMyelin ProteinsNogo ProteinsNogo Receptor 1OligodendrogliaRatsRats, Sprague-DawleyReceptors, Cell SurfaceThalamusConceptsTraumatic brain injurySmall proline-rich repeat protein 1ANogo-66 receptorBrain injuryIpsilateral cortexReticular thalamusNeuN cellsLateral fluid percussion brain injuryTraumatic central nervous system injuryFluid percussion brain injuryAxonal outgrowthCentral nervous system injuryIpsilateral external capsuleOligodendrocyte marker RIPNeuN-positive cellsNeuronal marker NeuNExpression of NogoNervous system injuryWhite matter tractsImportant brain regionsNgR expressionPoor regenerative capacitySPRR1A expressionWestern blot analysisSystem injury
2004
Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury
Kim JE, Liu BP, Park JH, Strittmatter SM. Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury. Neuron 2004, 44: 439-451. PMID: 15504325, DOI: 10.1016/j.neuron.2004.10.015.Peer-Reviewed Original ResearchMeSH Keywords5,7-DihydroxytryptamineAnimalsAxonsBehavior, AnimalBlotting, NorthernBlotting, SouthernBrainCell CountCells, CulturedCloning, MolecularCornified Envelope Proline-Rich ProteinsDesipramineDisease Models, AnimalEvoked Potentials, MotorFemaleGanglia, SpinalGlial Fibrillary Acidic ProteinGlucoseGPI-Linked ProteinsGrowth ConesImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutMotor ActivityMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinNerve RegenerationNeuronsNogo ProteinsNogo Receptor 1Phospholipid EthersProteinsPyramidal TractsReceptors, Cell SurfaceRecovery of FunctionSerotoninSerotonin AgentsSpinal CordSpinal Cord InjuriesTime FactorsConceptsAdult CNSNogo-66Spinal cord injuryAdult mammalian CNSNogo-66 receptorDorsal hemisectionDRG neuronsFunctional recoveryRubrospinal fibersCord injuryMyelin inhibitorsComplete transectionCorticospinal fibersMotor functionSpinal cordMotor impairmentAxon regenerationMammalian CNSAxonal growthAxonal outgrowthCNS myelinMiceInhibitory proteinInjuryGrowth conesNeonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity
Weiss J, Takizawa B, McGee A, Stewart WB, Zhang H, Ment L, Schwartz M, Strittmatter S. Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity. Experimental Neurology 2004, 189: 141-149. PMID: 15296844, DOI: 10.1016/j.expneurol.2004.05.018.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornAxonsBehavior, AnimalBiotinCentral Nervous SystemDextransDisease Models, AnimalExploratory BehaviorHumansHypoxia, BrainImmunoblottingImmunohistochemistryInfant, NewbornInfant, PrematureMiceMice, Inbred C57BLMyelin Basic ProteinMyelin ProteinsMyelin-Associated GlycoproteinNogo ProteinsOligodendrogliaReceptors, Cell SurfaceTime FactorsConceptsChronic sublethal hypoxiaPeriventricular leukomalaciaMyelin associated glycoproteinCorticospinal tractWhite matterLow birth weight infantsCerebral white matter volumeBirth weight infantsLow birth weightAnterograde axonal tracingPeriventricular white matterPremature human infantsCNS white matterWhite matter volumeHypoxia-induced reductionWeight infantsAxonal sproutingCerebral ventriculomegalyCorticofugal fibersLocomotor hyperactivityNeonatal hypoxiaPersistent abnormalitiesMotor cortexBirth weightHuman prematurityRGM and its receptor neogenin regulate neuronal survival
Matsunaga E, Tauszig-Delamasure S, Monnier PP, Mueller BK, Strittmatter SM, Mehlen P, Chédotal A. RGM and its receptor neogenin regulate neuronal survival. Nature Cell Biology 2004, 6: 749-755. PMID: 15258591, DOI: 10.1038/ncb1157.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAvian ProteinsCaspasesCell SurvivalCells, CulturedChick EmbryoChickensDown-RegulationEnzyme ActivationGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsImmunohistochemistryIn Situ HybridizationLuminescent ProteinsMembrane ProteinsMutagenesis, Site-DirectedNeuronsRatsRNA, Small InterferingConceptsRepulsive guidance moleculeNeural tubePro-apoptotic activityAxon guidance proteinCytoplasmic domainImmortalized neuronal cellsGene transfer technologyDependence receptorsCell deathGuidance proteinsNeuronal cellsNeogenin receptorGuidance moleculesNeuronal survivalRetinal axonsChick embryosNeogeninReceptor neogeninExpressionCaspasesReceptorsTransfer technologyEmbryosProteinApoptosis
1989
Localization of angiotensin converting enzyme in the ciliary epithelium of the rat eye.
Strittmatter SM, Braas KM, Snyder SH. Localization of angiotensin converting enzyme in the ciliary epithelium of the rat eye. Investigative Ophthalmology & Visual Science 1989, 30: 2209-14. PMID: 2551838.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoradiographyBinding SitesCaptoprilCiliary BodyEpitheliumImmunohistochemistryPeptidyl-Dipeptidase ARatsScleraTissue DistributionConceptsCiliary epitheliumRat eyesLocalization of angiotensinAnti-ACE antibodiesAqueous humor productionACE immunoreactivityACE inhibitorsPotent ACE inhibitorPosterior chamberChoroid plexusImmunocytochemical stainingMonoclonal antibodiesChoroidal epitheliumVentricular surfaceEpitheliumAngiotensinHumor productionEyesMajor siteACEAntibodiesLow levelsHigh levelsPlexusImmunoreactivity