长链非编码RNA母系印迹基因3(MEG3)通过p53促进缺血缺氧神经细胞损伤  

Long non-coding RNA maternally imprinted gene 3(MEG3) promotes neuronal cell hypoxia-ischemia injury through p53

作　　者：阎红琳 饶洁[1] 胡继昌[1] 袁静萍[1] 

机构地区：[1]武汉大学人民医院病理科,武汉430060

出　　处：《中国组织化学与细胞化学杂志》2016年第4期309-314,共6页Chinese Journal of Histochemistry and Cytochemistry

基　　金：武汉大学自主科研项目(2042016kf0116)

摘　　要：目的通过小鼠神经母细胞瘤细胞(N2a细胞)氧糖剥夺(oxygen glucose deprivation,OGD)研究长链非编码RNA(long non-coding RNA,lncRNA)母系印记基因3(maternally imprinted genes 3,MEG3)在神经细胞缺氧缺血损伤中的作用,并初步探讨其机制。方法采用OGD模型诱导N2a细胞凋亡模拟神经细胞缺血缺氧损伤过程,实时荧光定量PCR检测MEG3的水平;在N2a细胞中过表达MEG3,采用PI染色检测细胞凋亡,Western blot和荧光素酶报告基因检测N2a细胞中过表达MEG3后对p53蛋白表达及转录活性的影响。结果经OGD处理后,N2a细胞MEG3水平较对照组(常氧组)明显增强;在N2a细胞中过表达MEG3能够激活p53转录活性,增强p53蛋白表达,促进细胞凋亡。结论 lncRNA MEG3可能通过p53促进凋亡,加重缺血缺氧造成的神经损伤。Objective To investigate the role of long non-coding RNA （ IncRNA） maternally imprinted gene 3 （MEG3） in hy-poxic-ischemic injury and explore its mechanism by oxygen glucose deprivation （OGD） of mouse neuroblastoma N2a cells. Methods N2a cell apoptosis was induced by OGD to induce neural cell hypoxic-ischemic injury. The expression of MEG3 was measured by quan-titative real-time PCR （qRT-PCR）. Cell apoptosis was measured by propidium iodide （PI） staining in the over-expression of MEG3 N2a cells. The effect of MEG3 on the expression and transcriptional activity of p53 was detected by western blot （WB） and the lucifer- ase reporter gene assay. Results MEG3 expression was significantly up-regulated after OGD treatment compared with the normoxic group. The over-expression of MEG3 in N2a cells was able to activate p53 transcriptional activity, increased the expression of p53 pro-tein, and promoted cell apoptosis. Conclusion LncRNA MEG3 may promote apoptosis through p53 pathway, and aggravate neural cell injury induced by hypoxia-ischemia.

关 键 词：长链非编码RNA 母系印记基因3 氧糖剥夺 凋亡 小鼠神经母细胞瘤细胞 

分 类 号：R338.2[医药卫生—人体生理学]