Expression of MicroRNA-29a Regulated by Yes-Associated Protein Modulates the Neurite Outgrowth in N2a Cells.
Expression of MicroRNA-29a Regulated by Yes-Associated Protein Modulates the Neurite Outgrowth in N2a Cells.
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Yes 相关蛋白调控的 MicroRNA-29a 表达可调节 N2a 细胞中的神经突生长。
DOI：
10.1155/2017/5251236
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发表时间：
2017
影响因子：
--
通讯作者：
Liu J
中科院分区：
文献类型：
--
作者：
Tan C;Yu C;Song Z;Zou H;Xu X;Liu J
本研究证实Yes-associated protein （YAP）可增加miR-29a，但相关分子机制尚不清楚。此外，越来越多的证据表明，高水平的miR-29a通过降低PTEN（10号染色体上缺失的磷酸酶和紧张素同源物）来促进神经突的生长。结果表明，YAP质粒转染N2a细胞后，miR-29a表达增加，PTEN表达降低。同时，通过多种方法检测与神经突生长密切相关的GAP-43和NF-200的表达，揭示了神经突生长的进展。当YAP下调时，miR-29a、GAP-43和NF-200的表达呈现与PTEN相反的趋势。用miR-29a mimic和inhibitor处理N2a细胞，我们也发现了相同的结论。对于miR-29a的硅分析，其启动子可能具有YAP的结合位点。基于荧光素酶报告基因实验和染色质免疫沉淀（ChIP）实验，我们证明YAP可以通过靶向miR-29a的启动子来增加miR-29a的表达。综上所述，结果表明YAP通过靶向miR-29a启动子促进神经突生长，可能是一种有效的神经疾病治疗药物。
Yes-associated protein (YAP) is proved to increase miR-29a in the present study, but the relevant molecular mechanism is not clear. Also, growing evidence indicates that the high-level miR-29a promotes the neurite outgrowth by decreasing PTEN (phosphatase and tensin homologue deleted on chromosome 10). Results show that the expression of miR-29a increases but the PTEN decreases during transfecting the N2a cells with the YAP plasmid. Meanwhile, the advancement of neurite outgrowth is presented via using multiple methods to detect the expression of GAP-43 and NF-200, which have a strong association with neurite outgrowth. The expression of miR-29a, GAP-43, and NF-200 shows an opposite tendency compared to the PTEN when YAP is downregulated. By treating N2a cells with miR-29a mimic and inhibitor, we also find the same conclusion. For in silico analysis of miR-29a, its promoter may have a binding site for YAP. Based on a luciferase reporter assay and a chromatin immunoprecipitation (ChIP) experiment, we demonstrate that YAP could increase the expression of miR-29a by targeting the promoter of miR-29a. In conclusion, the results identify that YAP promotes the neurite outgrowth via targeting the promoter of miR-29a, and it may be an effective therapeutic medicine for the neural disease.
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