miR30a大多发性硬化症及EAE中的作用和机制对策

更新时间:2023-06-10 02:39:07 阅读: 评论:0

Abstracts
Multiplesclerosisisaprototypicautoimmunedemyelinationdiseaseofcentralnervoussystem.Becauseoflimitedunderstandingofthepathogenesisofmultiplesclerosisandalackofsensitivebiomarkers,accordingtothepresentcriteria,theearlydiagnosisand
爬黄山treatmentofmultiplesclerosisstilldependsonrepeatedoccurrenceofthedisease.MSpathogenesisisverycomplicated.Currently,itisthoughtthatdiseaseismediatedbypathogenicTcellresponsesagainstmyelinantigens,followedbyabroaderneurodegenerativeprocess.Amongthem,CD4+Tcell-mediatedautoimmunityhaslongbeenacceptedasoneofthemostimportantaspectsofmultiplesclerosispathogenesis,
theearlyinitiationofdisease.ThcellscalldifferentiateintodifferentTespeciallyfor
人像摄影技巧helpercellsdependinguponthecytokineenvironment,includingThl,"lh2,Thl7a11d
门山cellscanspecificallysecretIL-17Treg.Thl7cellsareanewsubsetofThelpercells,Thl7
andplayacriticalroleinthepathogenesisofmultiplesclerosis.RecentstudieshaveshownthatthenumberofThl7cellsinperipheralbloodofMSpatientsWassignificantlyhigherthanthatinhealthycontrols.Furthermore,theexpressionlevelofIL一23receptorandRORc(CriticalcytokinereceptorsandtranscriptionfactorsregulatingThl7differentiation)werealsomuchhigherthanthatofhealthycontrols.InMSanimalmodelEAE(ExperimentalAllergic/A
utoirnmuneEncephalomyelitis),itWasfoundthatantibodies
EAE,Moreover,micelackingneutralizingIL一17coulddelaynervedysfunctioninducedby程相
of11117cellsorwithlessThl7cellswerelesssensitivetoEAE.Therefore,regulatingThl7differentiationandIL-17secretionarethemostimportantkeypointsinEAEtreatment.ItisworthnotingthatwehavealreadygotacertaindegreeofunderstandingofthemechanismunderlyingThl7polarizationatcytokines,receptors,signalingpathwaysandtranscriptionfactorlevel.However,theroleofepigeneticmodificationinrnll7differentiationandEAEisstillunclear.
SmallRNA(microRNA,miRNA)-mediatedpost-transc
riptionalgeneregulationisoneoftheimportantmechanismofepigenetiemodification.microRNAisaclassof
foundineukaryotes.AccordingtOthereports,microRNAisendogenousnon—codingRNA
humandiseasesandpotentiallyserveasgooddiagnosticcriticallyinvolvedinarangeof
markers,prognosticmarkersortherapeutictargets.IfthemiRNAisperfectlyornearlycomplementarytoitstarget,itcallspecificallycleavethetargetmRNA.Endogenously
·4.
miRNAsareusuallyimperfectlycomplementarytotheirtargetgene(s)andexpressed1990年属相
紫花地丁的功效与作用
modulatestheeffectongeneexpressionviatranslationalrepression.Inthepresentstudy,weusedtheonlinemiRNAtarget-predictionsoftwareandfound106microRNAsmight
studiesshownthattheexpressionlevelofoneofregulateThl7differentiation.Previous
thepredictedmicroRNA,miR-30awasdownregulatedinseveralautoimmunediseaseslesions.However,theroleofmiR-30ainThl7differentiationandMSpathogenesishasnotbeenreported.
Ourstudywasdesignedtoexplore:1.theexpressionpatternofmiR-30ainperipheralbloodmononuclearcellsfromMSpatientsandEAEmice;2.thetherapeuticeffectofmiR-30ainEAEand3.thepossibleregulatingmechanismofmiR-30aonThl7differentiation.
手绘风景ElucidationtherolesofmiR-30ainMS/EAEwilldeepentheknowledgeofhowthisnoncodingRNA-mediatedmechanismcontributestothepathogenesisofmultiplesclerosisandhelptoidentifynewtherapeuticmoleculartargets,alsoprovideanewmolecularmechanismforepigenetieregulationofThl7cellsdifferentiation.Inthisstudy,firstly,wecollectedtheperipheralbloodofMSpatientsduringrelapseandremissionperiod,isolatedperipheralbloodmononuclearcellsandanalyzedtherelativeexpressionlevelofmiR·30a.Then,weanalyzeathecorrelationbetweenrelativeexpressionofmiR-30aandrelativeexpressionofIFN吖、IL-4、TGF-13andIL-17inperipheralbloodmononuclearcellscollectedfromEAEmice.Furthermore,wemadeastableanimalmodelofMSbyinjectiingmyelinassociatedglycoproteinfragmentintravenouslytoinduceCNSdemyelination.Toin
vestigatewhethermanipulationofmiR-30acallinfluencethedevelopmentofEAE,WedeliveredmiR-30arecombinantlentivirustomicebyintravenousinjectionthroughthetailvein.Finally,weconstructedSOCSIandIIⅡ43’.UTRwildtypeplasmidandmutantplasmid,usedual—luciferasereportsystemtodetectcombinationofmiR-30aand3q3TRoftargetgenesSOCS1andIRF4.Theresultsareasfollows:
1)WecollectedEDTAanticoagulatedbloodfromeightMSpatientsandfourhealthycontrols.Wethenusedlymphocyteseparationdensitygradient
methodtogetperipheralbloodmononuclearcellsandfurthereentrifugation
usedflowcytometrysortingmethodtocollectCD4+Tcells.Cellviability公司年终总结
andpuritywerecheckedandweregreaterthan99%.
-5·

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