miR-124 Represses ROCK1 Expression to Promote Neurite Elongation Through Activation of the PI3K/Akt Signal Pathway
miR-124 Represses ROCK1 Expression to Promote Neurite Elongation Through Activation of the PI3K/Akt Signal Pathway
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DOI：
10.1007/s12031-013-0190-6
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发表时间：
2014-01-01
影响因子：
3.1
通讯作者：
Wang, Xuemin
中科院分区：
文献类型：
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作者：
Gu, Xi;Meng, Siying;Wang, Xuemin
最近的研究表明，miR-124，最丰富和最保守的脑特异性microRNA（miRNA），在促进神经元分化过程中的轴突生长和延伸的重要作用。这种miRNA的靶基因和执行这种作用的机制仍不清楚。在这项研究中，我们确定了ROCK 1，一种小的GT3 Rho激酶，作为miR-124调节神经突延伸的直接靶点。miR-124显著抑制M17细胞中ROCK 1的表达。抑制ROCK 1促进神经突伸长，并且ROCK 1的过表达强烈抑制miR-124在M17细胞中的神经突伸长促进作用。我们确定Akt作为一种新的ROCK 1下游效应子在调节神经突生长和伸长中发挥作用。
Recent studies have demonstrated an important role for miR-124, the most abundant and well-conserved brain-specific microRNA(miRNA), in promoting neurite outgrowth and elongation during neuronal differentiation. This miRNA's target genes and the mechanisms that execute this role remain unclear. In this study, we identified ROCK1, a small GTPase Rho kinase, as a direct target of miR-124 for regulating neurite elongation. miR-124 significantly inhibited ROCK1 expression in M17 cells. Inhibiting ROCK1 promoted neurite elongation, and the overexpression of ROCK1 strongly repressed the neurite elongation-enhancing effect of miR-124 in M17 cells. We determined that Akt functions as a novel ROCK1 downstream effector in regulating neurite outgrowth and elongation.