European Brain Research Institute (EBRI) "Rita Levi-Montalcini", Viale Regina Elena, 295, 00161 Rome, Italy.
CNR, Institute of Molecular Biology and Pathology (IBPM), P.le Aldo Moro, 5, 00185 Rome, Italy.
Cells. 2021 Feb 16;10(2):405. doi: 10.3390/cells10020405.
In the brain, the neurotrophin Nerve growth factor (NGF) regulates not only neuronal survival and differentiation, but also glial and microglial functions and neuroinflammation. NGF is known to regulate oligodendrogenesis, reducing myelination in the central nervous system (CNS). In this study, we found that NGF controls oligodendrogenesis by modulating the levels of miR-219a-5p, a well-known positive regulator of oligodendrocyte differentiation. We exploited an NGF-deprivation mouse model, the AD11 mice, in which the postnatal expression of an anti-NGF antibody leads to NGF neutralization and progressive neurodegeneration. Notably, we found that these mice also display increased myelination. A microRNA profiling of AD11 brain samples and qRT-PCR analyses revealed that NGF deprivation leads to an increase of miR-219a-5p levels in hippocampus and cortex and a corresponding down-regulation of its predicted targets. Neurospheres isolated from the hippocampus of AD11 mice give rise to more oligodendrocytes and this process is dependent on miR-219a-5p, as shown by decoy-mediated inhibition of this microRNA. Moreover, treatment of AD11 neurospheres with NGF inhibits miR-219a-5p up-regulation and, consequently, oligodendrocyte differentiation, while anti-NGF treatment of wild type (WT) oligodendrocyte progenitors increases miR-219a-5p expression and the number of mature cells. Overall, this study indicates that NGF inhibits oligodendrogenesis and myelination by down-regulating miR-219a-5p levels, suggesting a novel molecular circuitry that can be exploited for the discovery of new effectors for remyelination in human demyelinating diseases, such as Multiple Sclerosis.
在大脑中,神经营养因子神经生长因子(NGF)不仅调节神经元的存活和分化,还调节神经胶质细胞和小胶质细胞的功能和神经炎症。已知 NGF 调节少突胶质细胞的分化,减少中枢神经系统(CNS)的髓鞘形成。在这项研究中,我们发现 NGF 通过调节 miR-219a-5p 的水平来控制少突胶质细胞的分化,miR-219a-5p 是少突胶质细胞分化的一个众所周知的正调节剂。我们利用了一种 NGF 剥夺的小鼠模型,即 AD11 小鼠,在这种小鼠模型中,抗 NGF 抗体的产后表达导致 NGF 中和和进行性神经退行性变。值得注意的是,我们发现这些小鼠也表现出髓鞘形成增加。AD11 脑样本的 microRNA 分析和 qRT-PCR 分析显示,NGF 剥夺导致海马体和皮质中 miR-219a-5p 水平升高,以及其预测靶标的相应下调。AD11 小鼠海马体分离的神经球产生更多的少突胶质细胞,这个过程依赖于 miR-219a-5p,因为用诱饵介导的这种 microRNA 的抑制可以证明这一点。此外,NGF 处理 AD11 神经球可抑制 miR-219a-5p 的上调,从而抑制少突胶质细胞的分化,而抗 NGF 处理野生型(WT)少突胶质细胞祖细胞可增加 miR-219a-5p 的表达和成熟细胞的数量。总的来说,这项研究表明,NGF 通过下调 miR-219a-5p 水平来抑制少突胶质细胞的分化和髓鞘形成,提示一种新的分子电路,可用于发现人类脱髓鞘疾病(如多发性硬化症)中的髓鞘再生新效应器。