miR-26a promotes neurite outgrowth by repressing PTEN expression
miR-26a promotes neurite outgrowth by repressing PTEN expression
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DOI：
10.3892/mmr.2013.1534
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发表时间：
2013-08-01
影响因子：
3.4
通讯作者：
Sun, Hanxiao
中科院分区：
文献类型：
--
作者：
Li, Baoguo;Sun, Hanxiao
大量研究表明microRNAs（miRNAs）在神经元发育中起重要作用。作为改变某些mRNA表达的关键调节因子，miR-26 a已被证明在中枢神经系统（CNS）中发挥作用。在本研究中，研究了miR-26 a在神经元发育中的功能。假设miR-26 a的过表达显著增强突触可塑性并调节神经元形态发生。miR-26 a显著增加神经突起的数量和分布。此外，抑制miR-26 a功能减弱了神经元的生长。此外，磷酸酶和张力蛋白同源物（PTEN）通过荧光素酶报告基因测定被鉴定为该过程中miR-26 a的直接靶标。神经突起的生长受到PTEN过表达的持续抑制。因此，我们的研究表明，miR-26 a通过抑制PTEN表达促进神经突起生长，表明miR-26 a在神经元发育和形态发生中是重要的。miR-26 a有可能成为阿尔茨海默病（AD）患者的治疗靶点。
A multitude of studies have reported that microRNAs (miRNAs) are important in neuronal development. As a key regulator altering the expression of certain mRNAs, miR-26a has been demonstrated to play a role in the central nervous system (CNS). In the current study, the function of miR-26a in neuronal development was investigated. The overexpression of miR-26a was hypothesized to significantly enhance synaptic plasticity and regulate neuronal morphogenesis. The number and distribution of neurites was markedly increased by miR-26a. In addition, inhibition of miR-26a function attenuated neuronal outgrowth. Furthermore, phosphatase and tensin homolog (PTEN) was identified as a direct target of miR-26a in this process via a luciferase reporter assay. The growth of neurites was consistently suppressed by PTEN overexpression. Therefore, our study demonstrated that miR-26a promoted neurite outgrowth via the suppression of PTEN expression, indicating that miR-26a is important in neuronal development and morphogenesis. miR-26a has the potential to serve as a therapeutic target for patients with Alzheimer's disease (AD).