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抑制miR-15a可促进脑源性神经营养因子(BDNF)的表达,并挽救MeCP2缺陷神经元的树突成熟缺陷。

Inhibition of miR-15a Promotes BDNF Expression and Rescues Dendritic Maturation Deficits in MeCP2-Deficient Neurons.

作者信息

Gao Yu, Su Juan, Guo Weixiang, Polich Eric D, Magyar Daniel P, Xing Yina, Li Hongda, Smrt Richard D, Chang Qiang, Zhao Xinyu

机构信息

Waisman Center, School of Medicine and Public Health, Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA; Department of Neuroscience, School of Medicine and Public Health, Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA.

出版信息

Stem Cells. 2015 May;33(5):1618-29. doi: 10.1002/stem.1950.

Abstract

In both the embryonic and adult brain, a critical step in neurogenesis is neuronal maturation. Deficiency of MeCP2 leads to Rett syndrome, a severe neurodevelopmental disorder. We have previously shown that MeCP2 plays critical roles in the maturation step of new neurons during neurogenesis. MeCP2 is known to regulate the expression of brain-derived neurotrophic factor (BDNF), a potent neurotrophic factor for neuronal maturation. Nevertheless, how MeCP2 regulates BDNF expression and how MeCP2 deficiency leads to reduced BDNF expression remain unclear. Here, we show that MeCP2 regulates the expression of a microRNA, miR-15a. We find that miR-15a plays a significant role in the regulation of neuronal maturation. Overexpression of miR-15a inhibits dendritic morphogenesis in immature neurons. Conversely, a reduction in miR-15a has the opposite effect. We further show that miR-15a regulates expression levels of BDNF, and exogenous BDNF could partially rescue the neuronal maturation deficits resulting from miR-15a overexpression. Finally, inhibition of miR-15a could rescue neuronal maturation deficits in MeCP2-deficient adult-born new neurons. These results demonstrate a novel role for miR-15a in neuronal development and provide a missing link in the regulation of BDNF by MeCP2.

摘要

在胚胎期和成年期大脑中,神经发生的一个关键步骤是神经元成熟。MeCP2的缺乏会导致雷特综合征,这是一种严重的神经发育障碍。我们之前已经表明,MeCP2在神经发生过程中新神经元的成熟步骤中发挥关键作用。已知MeCP2可调节脑源性神经营养因子(BDNF)的表达,BDNF是一种对神经元成熟有强大作用的神经营养因子。然而,MeCP2如何调节BDNF的表达以及MeCP2缺乏如何导致BDNF表达降低仍不清楚。在这里,我们表明MeCP2调节一种微小RNA,即miR-15a的表达。我们发现miR-15a在神经元成熟的调节中发挥重要作用。miR-15a的过表达会抑制未成熟神经元的树突形态发生。相反,miR-15a的减少则有相反的效果。我们进一步表明,miR-15a调节BDNF的表达水平,并且外源性BDNF可以部分挽救由miR-15a过表达导致的神经元成熟缺陷。最后,抑制miR-15a可以挽救MeCP2缺陷的成年新生神经元中的神经元成熟缺陷。这些结果证明了miR-15a在神经元发育中的新作用,并提供了MeCP2对BDNF调节中缺失的环节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc1/4409556/bbf61c3eb3f3/nihms671828f1.jpg

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