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母系表达基因3(MEG3)是第一个被发现作为肿瘤抑制因子的长链非编码RNA(lncRNA)。近年发现MEG3与神经胶质瘤、亨廷顿病和脑卒中等神经系统疾病的发病有关,可能是神经系统疾病新的生物标志物。MEG3在神经系统疾病中的作用涉及多种机制,包括参与基因调控、促进细胞增殖、抑制细胞凋亡、促进血管生成等。MEG3在神经胶质瘤中表达缺失,主要由于DNA甲基转移酶1介导的MEG3启动子的高甲基化所致,以肿瘤抑制因子的角色发挥抗肿瘤作用。MEG3在亨廷顿病中表达下调,通过表观遗传调控多种基因的表达影响神经元活动,而在缺血性脑卒中中表达上调,可通过直接与p53基因的DBD270-281位点结合而促进p53表达,从而促进神经元凋亡。 [ABSTRACT FROM AUTHOR]

Objective To investigate the role of miR-21 and p53 in hypoxic-ischemic injury of neural cells and to explore its mechanism. Methods The cultured mouse neuroblastoma cell line N2a was randomly divided into the miR-21 (20, 40, 60 nmol/L) transfection group, negative control group, and blank control group by using Lipo2000 liposome transfection method. Ischemia-reperfusion injury model was established by oxygen glucose deprivation and reperfusion. Ap-optotic index was measured by TUNEL staining, the expression of intracellular miR-21 and p53 mRNA was detected by real-time fluorescence quantitative PCR , and the expression of p53 protein was detected by Western blotting. Results Compared with blank control group and negative control group, the relative expression of miR-21 in the transfection group was higher (P<0.05) , and the relative expression of miR-21 was concentration-dependent (P< 0.05). The apoptotic index of miR-21 (60 nmol/L) transfection group was lower than that of negative control group and blank control group (P < 0.05). The expression of p53 in the cells transfected with miR-21 (40, 60 nmol/L) was lower than that in the negative control group and the blank control group (P < 0. 05) , and the higher the concentration, the lower the expression of p53 ( P <0. 05 ). Conclusion Overexpression of miR-21 can protect neurons from hypoxic-ischemic injury, which may be related to its negative regulation of p53 expression in N2a cells. [ABSTRACT FROM AUTHOR]