2022
Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2
Rodriguez CM, Bechek SC, Jones GL, Nakayama L, Akiyama T, Kim G, Solow-Cordero DE, Strittmatter SM, Gitler AD. Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2. Cell Reports 2022, 41: 111505. PMID: 36288715, PMCID: PMC9664481, DOI: 10.1016/j.celrep.2022.111505.Peer-Reviewed Original ResearchConceptsAmyotrophic lateral sclerosisSpinocerebellar ataxia type 2Nogo receptorAtaxin-2 levelsNovel therapeutic targetNeurodegenerative disease amyotrophic lateral sclerosisGene-based therapeutic strategiesDisease amyotrophic lateral sclerosisNerve injuryAtaxin-2Axonal regenerationAxonal regrowthLateral sclerosisTherapeutic strategiesHuman neuronsKnockout miceTherapeutic targetPotential treatmentType 2Protein levelsPotent modifierProtein ataxin-2Additional strategiesMiceRNA screen
2018
Diltiazem Promotes Regenerative Axon Growth
Huebner EA, Budel S, Jiang Z, Omura T, Ho TS, Barrett L, Merkel JS, Pereira LM, Andrews NA, Wang X, Singh B, Kapur K, Costigan M, Strittmatter SM, Woolf CJ. Diltiazem Promotes Regenerative Axon Growth. Molecular Neurobiology 2018, 56: 3948-3957. PMID: 30232777, PMCID: PMC6424671, DOI: 10.1007/s12035-018-1349-5.Peer-Reviewed Original ResearchConceptsL-type calcium channel blockerDorsal root gangliaCentral nervous systemChondroitin sulfate proteoglycanAxon regenerationMouse dorsal root gangliaAdult central nervous systemHuman sensory neuronsCalcium channel blockersSpinal cord injuryRat cortical culturesCord injuryAxonal regrowthRoot gangliaCortical culturesChannel blockersRegenerative propensityRegenerative axon growthSensory neuronsNervous systemPharmacological enhancersAxon growthPermanent lossSulfate proteoglycanAxotomyFunctional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration
Sekine Y, Lin-Moore A, Chenette DM, Wang X, Jiang Z, Cafferty WB, Hammarlund M, Strittmatter SM. Functional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration. Cell Reports 2018, 23: 415-428. PMID: 29642001, PMCID: PMC5937716, DOI: 10.1016/j.celrep.2018.03.058.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsCentral Nervous SystemFemaleGene Regulatory NetworksGenomeMiceMice, Inbred C57BLMice, KnockoutNerve RegenerationOptic NerveRab GTP-Binding ProteinsRecovery of FunctionRetinal Ganglion CellsRNA InterferenceRNA, Small InterferingSpinal Cord InjuriesSuppressor of Cytokine Signaling ProteinsConceptsAxonal regenerationCentral nervous system axonal regenerationRetinal ganglion cell axon regenerationGreater motor functionOptic nerve crushCerebral cortical neuronsSpinal cord traumaNeurological recoveryCord traumaNerve crushCNS injuryAxonal regrowthCortical neuronsMotor functionAxon regenerationReceptor bindingComprehensive functional screenAdult mammalsInjuryMultiple pathwaysExpression profilesIdentifies pathwaysSignificant overlapPathwayFunction screen
2016
Inhibition of Poly-ADP-Ribosylation Fails to Increase Axonal Regeneration or Improve Functional Recovery after Adult Mammalian CNS Injury
Wang X, Sekine Y, Byrne AB, Cafferty WB, Hammarlund M, Strittmatter SM. Inhibition of Poly-ADP-Ribosylation Fails to Increase Axonal Regeneration or Improve Functional Recovery after Adult Mammalian CNS Injury. ENeuro 2016, 3: eneuro.0270-16.2016. PMID: 28032120, PMCID: PMC5187389, DOI: 10.1523/eneuro.0270-16.2016.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsBenzimidazolesCells, CulturedCerebral CortexDisease Models, AnimalFemaleIsoenzymesMaleMice, 129 StrainMice, Inbred C57BLMice, TransgenicMotor ActivityNerve RegenerationOptic Nerve InjuriesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsRecovery of FunctionSpinal Cord InjuriesThoracic VertebraeConceptsOptic nerve crush injuryNerve crush injuryThoracic spinal cordAxonal regenerationSpinal cordDorsal hemisectionCrush injuryFunctional recoveryPARP inhibitorsMotor function recoveryRecovery of functionPoly (ADP-ribose) polymeraseClinical PARP inhibitorsNeurological recoveryShort hairpin RNACNS traumaCNS injuryFunction recoveryAxonal regrowthSystemic administrationPharmacodynamic actionAxon regenerationTraumatic damageTherapeutic efficacyNeurological trauma
2011
Membrane-type Matrix Metalloproteinase-3 Regulates Neuronal Responsiveness to Myelin through Nogo-66 Receptor 1 Cleavage*
Ferraro GB, Morrison CJ, Overall CM, Strittmatter SM, Fournier AE. Membrane-type Matrix Metalloproteinase-3 Regulates Neuronal Responsiveness to Myelin through Nogo-66 Receptor 1 Cleavage*. Journal Of Biological Chemistry 2011, 286: 31418-31424. PMID: 21768085, PMCID: PMC3173120, DOI: 10.1074/jbc.m111.249169.Peer-Reviewed Original ResearchConceptsMatrix metalloproteinase-3Primary neuronsMetalloproteinase-3Neuronal responsesSH-SY5Y neuroblastoma cellsMetalloproteinase-dependent mannerNeuronal responsivenessAxonal regrowthCortical neuronsNeuronal knockdownNgR1Receptor 1Neuroblastoma cellsNeuronsCell surfaceMT3-MMPMyelinSpecific metalloproteinasesGlycosylphosphatidylinositol-anchored receptorInhibitorsPhysiological consequencesCleavage fragmentsCleavage-resistant formMetalloproteinasesReceptors
2010
MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma
Cafferty WB, Duffy P, Huebner E, Strittmatter SM. MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma. Journal Of Neuroscience 2010, 30: 6825-6837. PMID: 20484625, PMCID: PMC2883258, DOI: 10.1523/jneurosci.6239-09.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBiotinCells, CulturedDextransDisease Models, AnimalFemaleFunctional LateralityGanglia, SpinalGPI-Linked ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMutationMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve Tissue ProteinsNeuronsNogo ProteinsPyramidal TractsReceptors, Cell SurfaceReceptors, SerotoninRecovery of FunctionSpinal Cord InjuriesConceptsAxonal growthSpinal Cord Injury StudyMutant miceGreater axonal growthGreater behavioral recoverySpinal cord traumaWild-type miceAxonal growth inhibitionHeterozygous mutant miceDeficient myelinNeurological recoveryCNS damageTriple-mutant miceBehavioral recoveryCord traumaFunctional recoveryNeurological functionMyelin inhibitorsAxonal regrowthReceptor mechanismsInjury studiesMyelin inhibitionDecoy receptorOptimal chanceMice
2003
Targeting the Nogo Receptor to Treat Central Nervous System Injuries
Lee DH, Strittmatter SM, Sah DW. Targeting the Nogo Receptor to Treat Central Nervous System Injuries. Nature Reviews Drug Discovery 2003, 2: 872-879. PMID: 14668808, DOI: 10.1038/nrd1228.Peer-Reviewed Original ResearchConceptsCentral nervous systemAxonal regrowthNogo receptorCentral nervous system injuryNovel drug discovery strategyCNS myelinNervous system injurySpinal cord injuryTraumatic head injuryLarge unmet needOligodendrocyte myelin glycoproteinAxonal damageSystem injuryCNS injuryCord injuryAxonal regenerationHead injuryCNS neuronsGrowth cone collapseSuch injuriesAxon regrowthNervous systemUnmet needDrug discovery strategiesInjuryThe Nogo-66 receptor: focusing myelin inhibition of axon regeneration
McGee AW, Strittmatter SM. The Nogo-66 receptor: focusing myelin inhibition of axon regeneration. Trends In Neurosciences 2003, 26: 193-198. PMID: 12689770, DOI: 10.1016/s0166-2236(03)00062-6.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAnimalsAxonsCells, CulturedGPI-Linked ProteinsHumansIn Vitro TechniquesMiceMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve RegenerationNeural InhibitionNeuronal PlasticityNogo ProteinsNogo Receptor 1RatsReceptor, Nerve Growth FactorReceptors, Cell SurfaceReceptors, Nerve Growth FactorSignal TransductionConceptsNogo-66 receptorMembrane protein NogoSpinal cord injuryFunctional recoveryCord injuryAxonal regrowthSecond messenger pathwaysProtein NogoAdult CNSAxon regenerationMyelin inhibitionAxonal outgrowthAdditional studiesCNS myelinMyelinNeurite elongationPhysiological roleReceptorsMolecular determinantsInhibitorsInhibitionNGRCurrent understanding