Protein Tyrosine Phosphatase Receptor Type Z Negatively Regulates Oligodendrocyte Differentiation and Myelination 英文参考文献.docVIP

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Protein Tyrosine Phosphatase Receptor Type Z Negatively Regulates Oligodendrocyte Differentiation and Myelination 英文参考文献.doc

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Protein Tyrosine Phosphatase Receptor Type Z Negatively Regulates Oligodendrocyte Differentiation and Myelination 英文参考文献

ProteinTyrosinePhosphataseReceptorTypeZ NegativelyRegulatesOligodendrocyteDifferentiation andMyelination KazuyaKuboyama1.,AkihiroFujikawa1.,MakotoMasumura1,3.,RyokoSuzuki1,MasahitoMatsumoto1, MasaharuNoda1,2 * 1Division of Molecular Neurobiology, National Institute for Basic Biology, Aichi, Japan, 2School of Life Science, The Graduate University for Advanced Studies, 5-1 Higashiyama,Myodaiji-cho,Okazaki,Aichi,Japan,3FacultyofPharmacologyII,AsubioPharmaCo.Ltd.,6-4-3Minatojima-Minamimachi,Chuo-ku,Kobe,Hyogo,Japan Abstract Background:Fyntyrosinekinase-mediateddown-regulationofRhoactivitythroughactivationofp190RhoGAPiscrucialfor oligodendrocyte differentiation and myelination. Therefore, the loss of function of its counterpart protein tyrosine phosphatase(PTP)mayenhancemyelinationduringdevelopmentandremyelinationindemyelinatingdiseases.Totestthis hypothesis, we investigated whether Ptprz, a receptor-like PTP (RPTP) expressed abuntantly in oligodendrocyte lineage cells,isinvolvedinthisprocess,becausewerecentlyrevealedthatp190RhoGAPisaphysiologicalsubstrateforPtprz. Methodology/PrincipalFindings:Wefoundanearlyonsetoftheexpressionofmyelinbasicprotein(MBP),amajorprotein of the myelin sheath, and early initiation of myelination in vivo during development of the Ptprz-deficient mouse, as comparedwiththewild-type.Inaddition,oligodendrocytesappearedearlierinprimaryculturesfromPtprz-deficientmice than wild-type mice. Furthermore, adult Ptprz-deficient mice were less susceptible to experimental autoimmune encephalomyelitis (EAE) induced by active immunization with myelin/oligodendrocyte glycoprotein (MOG) peptide than werewild-typemice.AfterEAEwasinduced,thetyrosinephosphorylationofp190RhoGAPincreasedsignificantly,andthe EAE-inducedlossofMBPwasmarkedlysuppressedinthewhitematterofthespinalcordinPtprz-deficientmice.Here,the numberofT-cellsandmacrophages/microgliainfiltratingintothespinalcorddidnotdifferbetweenthetwogenotypes afterMOGimmunization.Allthesefindingsstronglysupportth