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1、ChapterC8CORONAVIRUS-INDUCEDDEMYELINATIONANDSPONTANEOUSREMYELINATIONGrowthfactorexpressionandfunctionReginaC.Armstrong1'2,JeffreyM.Redwine2'3,andDonnaJ.Messersmith1'41DepartmentofAnatomy,Physiology,andGenetics,and2PrograminNeuroscience,UniformedServicesUnive
2、rsityoftheHealthSciences,4301JonesBridgeRd.,Bethesda,MD20814-4799;rarmstrong@usuhs.mil3Currentaffiliation:NeuromeInc.,LaJolla,CA920374Currentaffiliation:NationalCenterforBiotechnologyInformation,Bethesda,MD20894Abstract:MHV-A59coronavirusinfectionproducesatr
3、ansientepisodeofdemyelinationthatisfollowedbyspontaneousremyelination.ThisparadigmprovidesacomplexlesionenvironmenttoexaminecellularandmolecularmechanismsinvolvedinsuccessfulCNSremyelination.Ourworkinthismodelhasfocusedontherolesofplatelet-derivedgrowthfacto
4、randfibroblastgrowthfactor2inregulatingoligodendrocyteprogenitorresponsesrequiredforremyelination.Keywords:platelet-derivedgrowthfactor,fibroblastgrowthfactor,estrouscycle,gender,demyelinatingdisease,remyelination,coronavirus,cuprizone.INTRODUCTIONInsufficie
5、ntremyelinationresultsinprolongedneurologicalimpairmentindemyelinatingdiseasestates,suchasmultiplesclerosis.Acriticaldeterminantofremyelinationisregulationofoligodendrocytelineageresponses.Survivingand/ornewlygeneratedoligodendrocytelineagecellsmustberecruit
6、edtoappropriatesiteswithindemyelinatedtissuesandinducedtodifferentiateandformmyelin.Eachoftheseoligodendrocytelineagecellresponsesappearstoberegulatedbysignalswithinthelesionenvironment,suchasgrowthfactors,cytokines,andcell-cellinteractions.Thepathologyofmul
7、tiplesclerosis(MS)lesionsisheterogeneousbetweenpatients,withatleastfourfundamentallydifferentpatternsof794ChapterC8demyelination(12).Therefore,analysisofexperimentalmodelsofdemyelinationwithdistinctmechanismsofpathogenesisiswarranted.Inaddition,differentexpe
8、rimentalmodelshaveadvantagesforexaminingspecificaspectswithinthecourseofdemyelinatingdiseases.ThemousemodelofmurinehepatitisstrainA59(MHV-A59)coronavirusinfectionservesasarelevantmodelforanalyzi
