MiRNA-106a参与β-淀粉样蛋白致AD的相关研究
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国家自然科学基金(81170540);江苏省自然科学基金(BK2011846)


The effect of miR-106a on amyloid beta protein-induced Alzheimer’s disease in primary cultured hippocampus neurons and PC 12 cells
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    摘要:

    目的:探讨miR-106a参与老年性痴呆(Alzheimer’s disease,AD)的发生及可能机制。方法:应用β淀粉样蛋白(amyloid beta protein,Aβ)处理小鼠原代海马神经元及大鼠嗜铬细胞系(PC12细胞)建立AD细胞模型,分别采用RT- PCR及Western blot检测AD细胞模型中miR-106a-STAT3-JAK2 mRNA及STAT3-p-STAT3-JAK2蛋白水平的表达情况。结果:miR-106a在2种AD细胞模型中的表达量均明显低于对照组(P < 0.05),同时miR-106a的靶基因STAT3 mRNA和蛋白水平表达量均明显高于对照组(P < 0.05),而JAK2 mRNA和蛋白水平与对照组比较无统计学差异(P > 0.05)。结论:miR-106a负性调节STAT3表达而参与AD的发生。

    Abstract:

    Objective:To study the effect and mechanism of miR-106a on the development of Alzheimer’s disease (AD) induced by amyloid beta protein (Aβ) in primary cultured hippocampus neurons and PC12 cells. Methods:The primary cultured hippocampus neurons and PC12 cells were treated with Aβ. The expression of miR-106a,STAT3 and JAK2 mRNA were detected by RT-PCR,while the expression of STAT3,p-STAT3 and JAK2 protein were evaluated by Western blot. Results:The expression of miR-106a was lower in Aβ-treated primary cultured hippocampus neurons and PC12 cells than that of controls (P < 0.05). In addition,the expression of STAT3 mRNA and protein was higher in Aβ-treated cells than that of controls (P < 0.05),while the expression of JAK2 showed no significant difference whether Aβ-treated was used or not (P > 0.05). Conclusion:This study suggested that miR-106a might contribute to the pathogenesis of AD by negatively regulating the expression of STAT3.

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从 静,王超君,浦丹华,张 敏,谭容容,吴 洁. MiRNA-106a参与β-淀粉样蛋白致AD的相关研究[J].南京医科大学学报(自然科学版),2013,(11):1493-1496, 1507

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  • 收稿日期:2013-05-17
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  • 在线发布日期: 2013-11-25
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