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.

简介：AIMTo在氢过氧化物上探索parthenolide的效果(H2在人的透镜的O2)-inducedapoptosis上皮(HLE)apoptoticHLE房间的cells.METHODSThe形态学和数字用光被估计显微镜学和流动cytometry。房间生存能力被山试金测试。另外，相关蛋白质的表示被HLE房间的西方的污点assay.RESULTSApoptosis测量被200导致??丠?????あψ

简介：Mostoftheoculartumorshavepoorprognosis,andtheyremainadifficultproblemintheareaofophthalmology.Withtherapiddevelopmentofmolecularbiologyandimmunologictechniquesandthedeepresearchonoculartumorrelatedgenes,itbecomespossibletodiagnoseandtreatmalignanttumorsfromthemolecularlevel.Thetumornecrosisfactorrelatedapoptosis-inducingligand(TRAIL),amemberofthetumornecrosisfactor(TNF)superfamily,isapromisingcandidate,eitheraloneorincombinationwithestablishedcancertherapies,sinceitcaninitiateapoptosisthroughtheactivationoftheirdeathreceptors.TheabilityofTRAILtoselectivelyinduceapoptosisoftransformed,virus-infectedortumorcellsbutnotnormalcellspromotesthedevelopmentofTRAIL-basedcancertherapy.Here,wewillreviewTRAILanditsreceptors’structure,function,mechanismofactionandapplicationinoculartumorstherapy.

简介：AIMTo评估人的透镜上皮房间apoptosis并且对femtosecond激光在有到N3的N2的帮助奔流外科(FLACS).METHODSSixty奔流病人根据LOCSIII上演的femtosecond激光导致的间充质的转变(EMT)上皮在这研究被注册并且随机把组划分了成三：FLACS1组(由有LenSx的FLACS的奔流外科)，FLACS2组(由有LensAR的FLACS的奔流外科)和用手的组(由phacoemulsification的奔流外科)。在二个FLACS组的病人由LenSx或LensAR激光系统执行了前面的capsulotomy。在用手的组的病人被执行连续曲线的capsulorrhexis(CCC)手工地。恰好在从眼睛移动了以后，前面的囊被修理。在奔流surgery.RESULTSThe囊优势被病理学的染色在用手的capsulotomy在二个FLACS组和光滑的边看不规则和粗糙以后，染色的Hematoxylin-eosine，immunofluorescence染色和即时PCR被执行以便观察人的透镜上皮房间变化。有部分肿、破坏的原子核的房间配置的不规则在二个FLACS组被观察。Femtosecond激光能比手工地执行的CCC在人的透镜上皮房间导致显著地更高的房间apoptosis(P<0.05)。透镜上皮房间apoptosis根据皮尔森关联分析与femtosecond激光持续时间被相关。在二个FLACS组的减少的N-cadherin表示，alpha-SMA和FSP-1水平证明房间EMT.CONCLUSIONFemtosecond激光的抑制可以影响在剥的中央透镜囊下面的透镜上皮房间的apoptosis和EMT。

简介：AIMTo在透镜调查Aquaporin-1(AQP-1)的角色上皮的房间(LEC)和它的潜在的目标基因。AQP-1明确地在眼睛的LEC被表示并且为透镜动态平衡和透明性维护是重要的。此处，在LEC的AQP-1表示被调查在奔流formation.METHODSLECs与它的潜在的角色联合在房间幸存上评估它的影响是有带AQP-1的lentivirus的transfected小介入RNA(siRNA)。实时聚合酶链反应(PCR)并且西方的弄污被进行从不同的组在LEC检测AQP-1表示。同时，房间数kit-8(CCK-8)试金和流动cytometry被执行测量LEC增长和apoptosis，respectively.RESULTSAQP-1表示显著地在LEC被减少，两个都在mRNA和蛋白质铺平(P<；0.05)，在siRNA处理以后。减少的房间生存能力被CCK-8试金与siRNA干扰在LEC检测，与控制房间相比(P<；0.05)。apoptosis率显著地在siRNA干扰以后在房间增加了(P<；0.05).CONCLUSIONThe减少了在规定下面的房间生存能力追随者AQP-1大部分由于它LEC的apoptosis的正式就职。AQP-1减小可能在LEC导致生理的功能的变化，它可能与奔流的出现和发展被联系。

简介：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.

简介：AIM:Tocomparethetrabecularmeshwork(TM)andirisapoptosisoftreatedanduntreatedprimaryopenangleglaucoma(POAG)patients.METHODS:Eighttreatment-naive,newlydiagnosed(group1)and11medlcaiytreated(group2)patientswithPOAGwereincludedinthestudy.Eachpatientunderwentalimbus-basedtrabeculectomy.TheTMandperipheralirisspecimensweredissectedoutandweresnap-frozeninliquidnitrogenandstoredat-80tuntiltheywereassayed.ApoptosisineachgroupwasassesedbyTUNELmethod.RESULTS:Themeanpatientagewas60.6±5.8years(53-68years)vs58.9±8.9years(47-70years)ingroup1andgroup2(P=0.859).Themeantreatmenttimeingroup2was22.2±7.3months(12-34months).ApoptoticindexesinTMandirisweresignificantlyhigherinPOAGpatientsusingmedication(group2)comparedtotreatment-naivePOAGpatients(group1)(P=0.004,0.015;respectively).CONCLUSION:LongtermadministrationoftopicalantiglaucomamedicationscausesadditionaltoxiceffectsonTM.