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-induced arthritis,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-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-11的效应。
Objective To determine the role of miR-144-overexpressed lentivirus process of synovial tissue in arthritis mouse model and its possible mechanism. Methods in the pathological Type 11 collagen- induced arthritis （CIA） mouse models were obtained by injecting the emulsion of type II collagen into subcuta- neous tail base of BALB/c mice. Then miRNA-144 overexpression lentivirus was injected into the tail vein. The expression and distribution of cadherin-11 and TNF-a in the synovial tissue of model mice were detected through immunofluorescence staining and the pathological characteristics were studied with HE staining. Results The mouse model exhibited similar characteristics as the pathological processes of synovial tissue in rheumatoid arthritis. Compared with saline and dummy vector lentivirus-treated groups, the inflammation of the synovial tissue was significantly reduced in the miRNA-144 overexpression lentivirus-treated group, whose TNF-a expression and cadherin-11 protein expression were also significantly lower （ P 〈 0.05, P 〈 0. 05 ）. Conclusion The increase of miRNA-144 content reduces the inflammation of synovial tissue in the CIA mouse models, and down-regulates the expression of TNF-a which may result from miRNA-144-induced cadherin-11 inhibition.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2014年第10期1031-1035,共5页
Journal of Third Military Medical University
基金
国家重点基础研究发展计划(973计划
2011CB964701)
国家科技支撑计划(2012BAI42G01)
国家自然科学基金(81271980)~~
