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?胞质和核定位a-突触核蛋白过表达对人神经母细胞瘤细胞的影响*

DOI: 10.13232/j.cnki.jnju.2013.013, PP. 109-115

Keywords: α-突角虫核蛋白,胞质定位,核定位

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Abstract:

?探讨α一突触核蛋白在人神经母细胞瘤(sh-sy5y)细胞中定位过表达的影响.研究应用plvu-snca-nes(nls)-2aegfp重组慢病毒载体感染sh-sy5y细胞,通过观察绿色荧光蛋白(eg-fp)检测目的基因在细胞中的表达情况.形态观察与mtt检测相结合,分析胞质和核定位α-突角虫核蛋白过表达对sh-sy5y细胞增殖的影响,同时测定鱼藤酮、h2o2对胞质和核定位a突角虫核蛋白过表达sh-sy5y细胞活性的影响.mitotrackcr染色法测定胞质和核定位a突角虫核蛋白过表达的sh-sy5y细胞中线粒体数目的变化.结果发现,α一突触核蛋白胞质定位过表达使得sh-sy5y细胞培养96h时活性显著增强,24h,48h,96h时细胞中线粒体的数目显著增加,增长比率分别为91.18%,41.15%,50.21%;a一突触核蛋白核定位过表达的sh-sy5y细胞相对正常细胞表现出较低的细胞活性,在培养48h,72h后细胞存活率显著下降.400nmol/l鱼藤酮损伤24h后,α-突触核蛋白核定位过表达的sh-sy5y细胞活性显著高于正常细胞角藤酮损伤组.50-800?mol/lh2o2处理条件下,α一突触核蛋白的定位过表达对sh-sy5y细胞活性的影响并不显著.研究结果表明α一突触核蛋白胞质定位过表达表现出一定的神经保护作用,α一突触核蛋白核定位过表达也能使sh-sy5y细胞的活性发生改变.

References

[1]  dingz,dinghq,xiel,etal.lnercasedsuscep-tiblitytoh2o2insh-sy5ycellsaffectedbythe
[2]  deseaseofthioredoxin.journalofnanjinguni-versity(naturalsciences),2006,42(5):470一478.(丁镇,丁红群,谢丽等.角藤酮诱导sh
[3]  feanymb,benderww.adrosophilamodelofparkinson’sdisease.nature,2000,404(6776):349~398.
[4]  zhaodl,wangk,crsynucleinandparkinson’sdisease.chinesemedicinalbiotechnology,2010,5
[5]  (004);300-304.(赵大龙,王坷.crsynuclein与帕金森病.中国医药生物技术,2010,5(004);300~304)
[6]  takahashim,kanukah,fujiwarah,etal.phospho-rylationof[alpha]-synucleincharacteristicofsynuclei-
[7]  nopathylesionsisrecapitulatedin[alpha]-synucleintransgenicdrosophila.neuroscienceletters,2003,336(3):155一158.
[8]  mcleanp,ribichs,llvmanb.subcellularlocali-zationofa-synucleininprimaryneuronal
[9]  cultures:effectofmissensemutations.advancesinresearchonneurodegeneration,2000,7:53.
[10]  marotceauxl,campanellij,schellerr.synuclein;aneuron-specificproteinlocalizedto
[11]  xumf,qianjj,gaoj,etal.constructionofα-sy-nucleinnuclearlocalitztionandnuclearexportgene
[12]  zhuy,duanc,lul,etal.[alpha]-synucleinoverexpressionimpairsmitochondrialfunctionby
[13]  associatingwithadenylatetranslocator.thein-ternationaljournalofbiochemistry&-cellbiolo-gy,2011,43c5):732一741.
[14]  pariharms,parihara,fujitam,etal.alphasynucleinoverexpressionandaggregationexacer-batesimpairmentofmitochondrialfunctionsbyaugmentingoxidativestressinhumanneuroblas-tomacells.theinternationaljournalofbiochem-
[15]  banerjeek,sinham,phamcll,etal.[alpha]-synucleininducedmembranedepolarizationandlossofphosphorylationcapacityofisolatedratbrainmi-tochondria;implicationsinparkinson’sdisease.feesletters,2010,581(8):1571一1576.
[16]  choongcj,sayyh.neuroprotectionofα-synu-cleinunderacuteandchronicrotenoneandmaneb
[17]  treatmentisabolishedbyitsfamilialparkinson’sdiseasemutationsa30p,a53tande46k.neuro-toxicology,2011,32(6):857一863.
[18]  dadakhujaevs,nohhs,jungej,etal.autophagyprotectstherotenone-inducedcelldeathin[alpha]一sy
[19]  nucleinoverexpressingsh-sy5ycells.neuroscienceletters,2010,472(1):47一52.
[20]  liuyy,zhaohy,zhaocl,etal.overexpres-sionofα-synucleininsh-sy5ycellspartiallyprotectedagainstoxidativestressinducedbyro-tenone.actaphysiologicasinica,2006,58(05):421-428.(刘延英,赵焕英,赵春礼等.sh-sy5y细胞a突角虫核蛋白的过表达可部分抵抗鱼藤酮诱导的氧化应激.生理学报,2006,58(05);421一428).
[21]  一by5y细胞对过氧化氢损伤易感性增高与硫氧还蛋白下调有关.南京大学学报(自然科学),2006,42(5):470一480).
[22]  spillantinimg,schmidtml,virginiamyl,etal.asynucleininlewybodies.nature,1997,388(6645).839一840.
[23]  hatcherjm,pennellkd,millergw.parkinson’sdiseaseandpesticides:atoxicological
[24]  perspective.trendsinpharmacologicalsciences,2008,29(6):322一329.
[25]  masliahe,rockensteine,veinbergsl,etal.do-paminergiclossandinclusionbodyformationinα-synucleinmice;implicationsforncurodegenerativedisorders.science,2000,287(5456):1265.
[26]  thenucleusandpresynapticnerveterminal.thejournalofneuroscience,1988,8(8):2804.
[27]  cooksonmr.thebiochemistryofparkinson’sdisease.annualreviewofbiochemistry,2005,74:29一52.
[28]  recombinantlentivirusvector.journalofjiangsuu-niversity(medcineedition),2011,21(2):139一142.
[29]  (徐敏芳,钱进军,高静等.胞质定位和核定位突触核蛋白慢病毒表达载体的构建.江苏大学学报(医学版),2011,21(2):139一142.
[30]  kontopoulose,parvinjn,feanymb,alpha-sy-nucleinactsinthenucleustoinhihithistone
[31]  acetylationandpromoteneurotoxicity.humanmoleculargenetics,2006,15(20):3012一3023.
[32]  nugentsme,mothersillce,seymourc,etal.in-creasedmitochondrialmassincellswithfunctionally
[33]  compromisedmitochondriaafterexposuretobothdirectyradiationandbystanderfactors.radiationre-search,2007,168(1):134一142.
[34]  xias,laterraj.hepatocytegrowthfactorincreasesmitochondrialmassinglioblastomacells.
[35]  biochemicalandbiophysicalresearchcommunicanons,2006,345(4):1358一1364.
[36]  istry&-cellbiology,2009,41(10):2015一2024.

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