2023
TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury
Shafit-Zagardo B, Sidoli S, Goldman J, DuBois J, Corboy J, Strittmatter S, Guzik H, Edema U, Arackal A, Botbol Y, Merheb E, Nagra R, Graff S. TMEM106B Puncta Is Increased in Multiple Sclerosis Plaques, and Reduced Protein in Mice Results in Delayed Lipid Clearance Following CNS Injury. Cells 2023, 12: 1734. PMID: 37443768, PMCID: PMC10340176, DOI: 10.3390/cells12131734.Peer-Reviewed Original ResearchConceptsAxonal damageMultiple sclerosisRelapsing-remitting multiple sclerosisHypomorphic miceExperimental autoimmune encephalomyelitisRelapsing-remitting MSNormal-appearing white matterMultiple sclerosis plaquesWhite matter plaquesNon-neurologic controlsWild-type miceBrains of individualsLipid droplet accumulationAutoimmune encephalomyelitisMyelin oligodendrocyteCNS injuryLipid clearanceSpinal cordNeuronal integrityTransmembrane protein 106BWhite matterAlzheimer's diseaseMice resultsDroplet accumulationPlaquesNogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model
Ye S, Theotokis P, Lee J, Kim M, Nheu D, Ellen O, Bedford T, Ramanujam P, Wright D, McDonald S, Alrehaili A, Bakhuraysah M, Kang J, Siatskas C, Tremblay C, Curtis D, Grigoriadis N, Monif M, Strittmatter S, Petratos S. Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model. Brain Communications 2023, 5: fcad108. PMID: 37091588, PMCID: PMC10116608, DOI: 10.1093/braincomms/fcad108.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisHaematopoietic stem cellsFc fusion proteinMultiple sclerosisAnimal modelsExperimental autoimmune encephalomyelitis lesionsCNS-infiltrating macrophagesStem cellsMultiple sclerosis modelInflammatory cell infiltrateNogo receptor 1Spinal cord injuryContext of neuroinflammationRecipient female miceImmune cell lineagesHigh-affinity receptorDisease-specific mannerDifferentiated phagocytesNeurological recoveryExtensive demyelinationAxonal damageCell infiltrateCNS lesionsNeurological decline
2021
Optic nerve regeneration screen identifies multiple genes restricting adult neural repair
Lindborg JA, Tran NM, Chenette DM, DeLuca K, Foli Y, Kannan R, Sekine Y, Wang X, Wollan M, Kim IJ, Sanes JR, Strittmatter SM. Optic nerve regeneration screen identifies multiple genes restricting adult neural repair. Cell Reports 2021, 34: 108777. PMID: 33657370, PMCID: PMC8009559, DOI: 10.1016/j.celrep.2021.108777.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsCRISPR-Cas SystemsDependovirusFemaleGene EditingGene Expression RegulationGenetic Association StudiesHEK293 CellsHumansInterleukinsMaleMAP Kinase Kinase KinasesMice, Inbred C57BLMice, TransgenicNerve RegenerationNeurogenesisOptic NerveOptic Nerve InjuriesRetinal Ganglion CellsSignal TransductionSTAT3 Transcription FactorConceptsOptic nerve crushRetinal ganglion cellsRegeneration-associated genesShort hairpin RNAIL-22Neural repairCentral nervous system traumaNeurological deficits persistNervous system traumaNerve crushAxonal damageAxonal regenerationGanglion cellsSystem traumaInflammatory responseCNS regenerationDeficits persistAxonal growthHairpin RNAConcurrent activationTranscription 3Cell-autonomous factorsKinase pathwaySignal transducerRepair
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 strategiesInjury
2002
Small Proline-Rich Repeat Protein 1A Is Expressed by Axotomized Neurons and Promotes Axonal Outgrowth
Bonilla IE, Tanabe K, Strittmatter SM. Small Proline-Rich Repeat Protein 1A Is Expressed by Axotomized Neurons and Promotes Axonal Outgrowth. Journal Of Neuroscience 2002, 22: 1303-1315. PMID: 11850458, PMCID: PMC6757578, DOI: 10.1523/jneurosci.22-04-01303.2002.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAxonsAxotomyCell DifferentiationCell Surface ExtensionsCornified Envelope Proline-Rich ProteinsCOS CellsGanglia, SpinalMaleMembrane ProteinsMiceMice, Inbred C57BLNerve CrushNerve RegenerationNeuronsOligonucleotide Array Sequence AnalysisProtein BiosynthesisProteinsRNA, MessengerS100 ProteinsSciatic NerveSciatic NeuropathySpinal Cord InjuriesTransfectionConceptsSmall proline-rich repeat protein 1AProtein 1AAxonal outgrowthMembrane rufflesP21/WAFDifferentiation genesCDNA microarrayNerve regenerationF-actinEpithelial differentiation genesPeripheral axonal damageSciatic nerve regenerationSuccessful nerve regenerationAbility of neuronsSPRR1AGenesUninjured neuronsAxotomized neuronsRange of substratesAxonal damageSensory neuronsOutgrowthNeuronsRufflesAxons