2021
NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates
Boghdadi AG, Spurrier J, Teo L, Li M, Skarica M, Cao B, Kwan WC, Merson TD, Nilsson SK, Sestan N, Strittmatter SM, Bourne JA. NogoA-expressing astrocytes limit peripheral macrophage infiltration after ischemic brain injury in primates. Nature Communications 2021, 12: 6906. PMID: 34824275, PMCID: PMC8617297, DOI: 10.1038/s41467-021-27245-0.Peer-Reviewed Original ResearchConceptsBrain injuryPeripheral macrophage infiltrationIschemic brain injuryAnti-inflammatory responseMajority of astrocytesNeurite outgrowth inhibitory proteinIschemic strokePeripheral macrophagesReactive astrocytesMacrophage infiltrationStroke recoveryAstrocyte clustersMarmoset monkeysVisual cortexAstrocytesNogoASingle-nucleus transcriptomicsInhibitory proteinInjuryStrokeHuman brainInfiltrationCritical rolePrecise functionOligodendrocytes
2012
PlexinA2 limits recovery from corticospinal axotomy by mediating oligodendrocyte-derived Sema6A growth inhibition
Shim SO, Cafferty WB, Schmidt EC, Kim BG, Fujisawa H, Strittmatter SM. PlexinA2 limits recovery from corticospinal axotomy by mediating oligodendrocyte-derived Sema6A growth inhibition. Molecular And Cellular Neuroscience 2012, 50: 193-200. PMID: 22564823, PMCID: PMC3383336, DOI: 10.1016/j.mcn.2012.04.007.Peer-Reviewed Original ResearchConceptsAxonal growthSpinal cordPellet retrieval taskCervical spinal cordWild-type miceContralateral gray matterAxon guidance cuesSevered fibersSprouted fibersAxonal sproutingCorticofugal projectionsFunctional recoveryBehavioral recoveryCNS injuryImpaired forelimbClass 3 semaphorinsCorticospinal fibersCorticospinal tractMedullary pyramidsSynaptic punctaInhibitor receptorsType miceUnilateral pyramidotomyNeuron inhibitionAdult trauma
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
Blockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury
Li S, Liu BP, Budel S, Li M, Ji B, Walus L, Li W, Jirik A, Rabacchi S, Choi E, Worley D, Sah DW, Pepinsky B, Lee D, Relton J, Strittmatter SM. Blockade of Nogo-66, Myelin-Associated Glycoprotein, and Oligodendrocyte Myelin Glycoprotein by Soluble Nogo-66 Receptor Promotes Axonal Sprouting and Recovery after Spinal Injury. Journal Of Neuroscience 2004, 24: 10511-10520. PMID: 15548666, PMCID: PMC6730300, DOI: 10.1523/jneurosci.2828-04.2004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsEvoked Potentials, MotorFemaleGPI-Linked ProteinsInjections, SpinalMotor ActivityMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNogo ProteinsNogo Receptor 1OligodendrogliaPeptide FragmentsRatsRats, Sprague-DawleyReceptors, Cell SurfaceReceptors, PeptideRecombinant Fusion ProteinsSerotoninSolubilitySpinal CordSpinal Cord InjuriesConceptsAxonal sproutingTraumatic spinal cord injurySpinal-injured ratsSpinal cord injuryAdult mammalian CNSNogo-66 receptorOligodendrocyte myelin glycoproteinMyelin associated glycoproteinRaphespinal fibersLocomotor recoveryCord injurySpinal injuryMammalian CNSNgR functionTherapeutic potentialAxonal growthNogo-66Myelin glycoproteinInjuryMyelin proteinsImproved locomotionViral blockadeBlockadeFc proteinSproutingNeonatal 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 prematurity
2002
Localization of Nogo-A and Nogo-66 Receptor Proteins at Sites of Axon–Myelin and Synaptic Contact
Wang X, Chun SJ, Treloar H, Vartanian T, Greer CA, Strittmatter SM. Localization of Nogo-A and Nogo-66 Receptor Proteins at Sites of Axon–Myelin and Synaptic Contact. Journal Of Neuroscience 2002, 22: 5505-5515. PMID: 12097502, PMCID: PMC6758202, DOI: 10.1523/jneurosci.22-13-05505.2002.Peer-Reviewed Original ResearchConceptsAdult CNSLimited axonal regenerationSpinal cord injuryNogo-66 receptorInteraction of NogoAxonal plasticityCord injurySynaptic contactsAxonal regenerationNgR proteinMyelinated fibersPostnatal neuronsLocalization of NogoMyelinated axonsAxonal growthOligodendrocyte surfacePhysiologic roleAxonsNogoProtein expressionNeuronsReceptorsInhibitory proteinInjuryCNS
2000
Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein
GrandPré T, Nakamura F, Vartanian T, Strittmatter S. Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein. Nature 2000, 403: 439-444. PMID: 10667797, DOI: 10.1038/35000226.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAxonsCattleCell DivisionCell LineCentral Nervous SystemChick EmbryoCloning, MolecularConsensus SequenceEscherichia coliGrowth InhibitorsHumansMembrane ProteinsMolecular Sequence DataMyelin ProteinsNerve RegenerationNogo ProteinsOligodendrogliaPC12 CellsRatsRecombinant ProteinsSequence Homology, Amino AcidConceptsCentral nervous systemPeripheral nervous systemCNS white matterAxonal regenerationAxon regenerationNervous systemWhite matterAdult central nervous systemMammalian axon regenerationIN-1 antibodiesReticulon 1Dorsal root ganglion growth conesFunctional recoverySpinal cordSchwann cellsCNS axonsExtracellular domainAxonal extensionNogoAxon extensionGrowth conesOligodendrocytesInhibitory activityReticulon 4Moderate degree