简介:Curativetherapyforspinalcordinjury(SCI)remainselusive,howeveridentifyingoptionsfortailoredtreatmentstrategiesisinfullswing.Likeinthebraintherearedistinctregionsintheadultspinalcordthatharborneuralprogenitorcells(NPCs)(Horneretal.,2000).Thisoffersthepossibilityofrecruitingthesecellsinreparativeapproachestosupportendogenousspinalcordregenerativecapacities.Hereby,one
简介:Age-relatedmaculardegeneration(AMD)causesirreversiblelossofcentralvisionforwhichthereisnoeffectivetreatment.IncipientpathologyisthoughttooccurintheretinaformanyyearsbeforeAMDmanifestsfrommidlifeonwardstoaffectalargeproportionoftheelderly.Althoughgeneticaswellasnon-genetic/environmentalrisksarerecognized,itscomplexaetiologymakesitdifficulttoidentifysusceptibility,orindeedwhattypeofAMDdevelopsorhowquicklyitprogressesindifferentindividuals.HerewesummarizetheliteraturedescribinghowtheAlzheimer's-linkedamyloidbeta(Aβ)groupofmisfoldingproteinsaccumulateintheretina.ThediscoveryofthiskeydriverofAlzheimer'sdiseaseinthesenescentretinawasunexpectedandsurprising,enablinganaltogetherdifferentperspectiveofAMD.WearguethatAβfundamentallydiffersfromothersubstanceswhichaccumulateintheageingretina,anddiscussourlatestfindingsfromamousemodelinwhichphysiologicalamountsofAβweresubretinally-injectedtorecapitulatesalientfeaturesofearlyAMDwithinashortperiod.OurdiscoveriesaswellasthoseofotherssuggestthepatternofAβaccumulationandpathologyindonoraged/AMDtissuesarecloselyreproducedinmice,includinglate-stageAMDphenotypes,whichmakesthemhighlyattractivetostudydynamicaspectsofAβ-mediatedretinopathy.Furthermore,wediscussourfindingsrevealinghowAβbehavesatsingle-cellresolution,andconsiderthelong-termimplicationsforneuroretinalfunction.WeproposeAβasakeyelementinswitchingtoadiseasedretinalphenotype,whichisnowbeingusedasabiomarkerforlatestageAMD.
简介:Inthepresentstudy,weconstructedalentivirus,FIV-CMV-GFP-miR-7-3,containingthemicroRNA-7-3geneandthegreenfluorescentproteingene,andusedittotransfecthumangliomaU251cells.Fluorescencemicroscopyshowedthat80%ofU251cellsexpressedgreenfluorescence.Real-timereversetranscriptionPCRshowedthatmicroRNA-7-3RNAexpressioninU251cellswassignificantlyincreased.ProliferationwasslowedintransfectedU251cells,andmostcellswereintheG1phaseofthecellcycle.Inaddition,theexpressionoftheserine/threonineproteinkinase2wasdecreased.ResultssuggestedthattransfectionwithalentiviruscarryingmicroRNA-7-3caneffectivelysuppressepidermalgrowthfactorreceptorpathwayactivityinU251cells,arrestcellcycletransitionfromG1phasetoSphaseandinhibitgliomacellgrowth.