AIM:ToinvestigatetheregulationofEaf2proteininmouselenscellsapoptosisinducedbyultraviolet(UV)radiation.METHODS:AneyeofEaf2geneknockoutmiceornormalcontrolmicewasexposedtoUVradiation,andtheotheronewasnon-exposed.AlloflenseswereanalyzedbyTUNELandcaspase3activityassaystodeterminethedifferenceoftheapoptosisinducedbyUVradiation.Inaddition,exposedandnon-exposedlenseswereanalyzedbyquantifiedp53expressionandreal-timereversetranscription-polymerasechainreaction(RT-PCR)ofBax,Bid,Apaf-1,PumaandNoxa,tocompareEaf2geneknockoutmiceandnormalcontrolmice.RESULTS:UVradiationcausedapoptosisoflenscellsinnormalcontrolmiceandEaf2knockoutmice.Activityofcaspase3wassignificantlyhigherinnormalcontrolmicethanEaf2knockoutmice.Expressionofp53proteinwassignificantlyhigherinlensesexposedtoUVradiationthannonexposedlenses,butwassimilarbetweenEaf2geneknockoutmiceandnormalcontrolmiceinthesameUVcondition.AfterexposingtoUVradiation,theanalysisofreal-timeRT-PCRdemonstratedthatmRNAlevelsofPumaandNoxaweresignificantlyhigherinlensesofnormalcontrolmicethanEaf2geneknockoutmice,andthatmRNAlevelsofBax,BidandApaf-1werenotsignificantlydifferentbetweengeneknockoutmiceandnormalcontrolmice.CONCLUSION:Eaf2increaseslenscellsapoptosisinducedbyultravioletradiation.AndEaf2up-regulatesexpressionofthePumaandtheNoxatoactonlenscellsapoptosisafterUVradiation.
