preliminaryresearchontheeffectsandmechanismsofmir-144overexpressionlentivirustothepathologyprocessesofsynovialtissueinarthritismouse…

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1、201403056miR-144过表达慢病毒对关节炎模型小鼠滑膜组织病理进程的影响及机制的初步研究闫演飞，康菲，杨波，苗莹，董世武（400038重庆，第三军医大学生物医学工程系生物医学材料学教研室）[摘要]目的探讨miR-144过表达慢病毒对于关节炎模型小鼠滑膜组织病理进程的作用及其可能的机制。方法将Ⅱ型胶原乳剂注射至BALB/c小鼠尾根部皮下构建由Ⅱ型胶原诱导的关节炎(collagen-inducedarthritis，CIA)小鼠模型，再以miRNA-144高表达慢病毒进行尾静脉注射，然后对模型小鼠滑膜组织进行免疫组化检测Cadherin

2、-11和TNF-α的表达和分布，并用HE染色检测滑膜组织的病理变化特点。结果模型小鼠滑膜组织表现出与类风湿性关节炎病理学进程相似的特点，miRNA-144高表达慢病毒处理较生理盐水和空载慢病毒处理组模型小鼠的滑膜组织的炎症反应明显减轻，且TNF-α表达较生理盐水和空载体慢病毒处理组显著下调（P<0.05），进一步检测Cadherin-11的表达亦显著降低（P<0.05）。结论机体中miRNA-144增加可减弱或抑制关节炎模型小鼠中滑膜组织的炎症反应，并下调其TNF-α的表达，且这一作用可能是miRNA-144抑制滑膜细胞中Cadherin-1

3、1的效应。[关键词]微小RNA-144；类风湿性关节炎；钙粘蛋白11；肿瘤坏死因子-α，Ⅱ型胶原[中图法分类号][文献标志码]APreliminaryresearchontheeffectsandmechanismsofmiR-144overexpressionlentivirustothepathologyprocessesofsynovialtissueinarthritismousemodelYanYanfei,KangFei,YangBo,MiaoYing,DongShiwu（DepartmentofBiomedicalMateria

4、lsScience,SchoolofBiomedicalEngineering,ThirdMilitaryMedicalUniversity,Chongqing,400038,China）[Abstract]ObjectiveToexploretheroleofmiR-144-overexpressedlentivirusinthepathologicalprocessofsynovialtissueinarthritismousemodelanditspossiblemechanism.MethodsTypeIIcollagen-induc

5、edarthritis(CIA)mousemodelswereobtainedbyinjectingtheemulsionoftypeIIcollagenintosubcutaneoustailbaseofBALB/cmice.ThenmiRNA-144overexpressionlentiviruswasinjectedintothetailvein.Theexpressionanddistributionofcadherin-11andTNF-αinthesynovialtissueofmodelmiceweredetectedthrou

6、ghimmunofluorescencestainingandthepathologicalcharacteristicswerestudiedwithHEstaining.ResultsThemousemodelexhibitedsimilarcharacteristicsasthepathologicalprocessesofsynovialtissueinrheumatoidarthritis.Comparedwithsalineanddummyvectorlentivirus-treatedgroups,theinflammation

7、ofthesynovialtissuewassignificantlyreducedinthemiRNA-144overexpressionlentivirus-treatedgroup,whoseTNF-αexpressionandcadherin-11proteinexpressionwerealsosignificantlylower(P<0.05,P<0.05).ConclusionTheincreaseofmiRNA-144contentreducestheinflammationofsynovialtissueintheCIAmo

8、usemodels,anddown-regulatestheexpressionofTNF-αwhichmayresultfrommiRNA-144-induced