Axotomy-Induced miR-21 Promotes Axon Growth in Adult Dorsal Root Ganglion Neurons 英文参考文献.docVIP

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Axotomy-Induced miR-21 Promotes Axon Growth in Adult Dorsal Root Ganglion Neurons 英文参考文献.doc

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Axotomy-Induced miR-21 Promotes Axon Growth in Adult Dorsal Root Ganglion Neurons 英文参考文献

Axotomy-InducedmiR-21PromotesAxonGrowthin AdultDorsalRootGanglionNeurons IainT.Strickland1,LouiseRichards1,FionaE.Holmes1,2,DavidWynick1,2,JamesB.Uney1 ,Liang-Fong Wong1* 1SchoolofClinicalSciences,UniversityofBristol,Bristol,UnitedKingdom,2SchoolofPhysiologyandPharmacology,UniversityofBristol,Bristol,UnitedKingdom Abstract Followinginjury,dorsalrootganglion(DRG)neuronsundergotranscriptionalchangessoastoadoptphenotypicchanges thatpromotecellsurvivalandaxonalregeneration.Hereweusedamicroarrayapproachtoprofilechangesinapopulation ofsmallnoncodingRNAsknownasmicroRNAs(miRNAs)intheL4andL5DRGfollowingsciaticnervetransection.Results showed that 20 miRNA transcripts displayed a significant change in expression levels, with 8 miRNAs transcripts being alteredbymorethan1.5-fold.UsingquantitativereversetranscriptionPCR,wedemonstratedthatoneofthesemiRNAs, miR-21,wasupregulatedby7-foldintheDRGat7dayspost-axotomy.IndissociatedadultratDRGneuronslentiviralvector- mediated overexpression of miR-21 promoted neurite outgrowth on a reduced laminin substrate. miR-21 directly downregulated expression of Sprouty2 protein, as confirmed by Western blot analysis and 39 untranslated region (UTR) luciferaseassays.OurdatashowthatmiR-21isanaxotomy-inducedmiRNAthatenhancesaxongrowth,andsuggestthat miRNAsareimportantplayersinregulatinggrowthpathwaysfollowingperipheralnerveinjury. Citation:StricklandIT,RichardsL,HolmesFE,WynickD,UneyJB,etal.(2011)Axotomy-InducedmiR-21PromotesAxonGrowthinAdultDorsalRootGanglion Neurons.PLoSONE6(8):e23423.doi:10.1371/journal.pone.0023423 Editor:StephenD.Ginsberg,NathanKlineInstituteandNewYorkUniversity,UnitedStatesofAmerica ReceivedMay12,2011;AcceptedJuly17,2011;PublishedAugust10,2011 Copyright: ? 2011 Strickland et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:Thisworkwassupportedby