简介：AIM:Toexploretheeffectsandmechanismofvascularendothelialcadherin(VE-cadherin)onexperimentalcornealneovascularization(CRNV).·METHODS:MousecorneaswereburnedwithsodiumhydroxidetobuildaCRNVmodel.Theburnedcorneaswerelocallyadministratedwithanti-mouseVE-cadherinneutralizingantibody.AnnexinVandclusterofdifferentiation31(CD31)doublestainingwasusedtomeasurevascularendothelialcellapoptosiswiththeuseofflowcytometry(FCM).TheproteinexpressionofNADPHoxidase2(Nox2),caspase-3,andproteinkinaseC(PKC)intheburnedcorneaswereexaminedbyWesternblot.Humanretinalendothelialcell(HREC)proliferationwasdetectedusingaCellCountingKit8(CCK-8)assayinvitro.·RESULTS:TheamountofCRNVpeakedtwoweeksafterthealkaliburn.FCMconfirmedthatVE-cadherinneutralizingantibodytreatmentincreasedCD31positivecellapoptosis.WesternblotrevealedthattheintracornealproteinexpressionofNox2andcaspase-3wereup-regulated,whilePKCwasdown-regulatedintheVE-cadherinneutralizingantibodyadministratedgroup.CCK-8assayshowedthatVE-cadherinneutralizingantibodymarkedlyinhibitedHRECproliferation.·CONCLUSION:VE-cadherinexhibitedananti-apoptosiseffectthroughenhancedPKCsignalingandanenhancedcellproliferationpathway.