Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Center for Systems Neuroscience, University of Veterinary Medicine Hannover, 30559, Hannover, Germany.
J Mol Neurosci. 2019 Mar;67(3):484-493. doi: 10.1007/s12031-019-1258-8. Epub 2019 Jan 25.
Growth factors play a crucial role during de- and remyelination of the central nervous system (CNS) due to their neurotrophic functions. We have previously shown that the growth factors neuregulin-1 (Nrg-1) and glial cell-derived neurotrophic factor (Gdnf) are upregulated during the first 2 weeks after induction of toxic demyelination in the CNS. Nevertheless, the factors responsible for Nrg-1/Gdnf upregulation and their effects on glia cells are unknown. We investigated the effect on Nrg-1 and Gdnf expressions after stimulation of primary mouse microglia or astrocytes with various pro- and anti-inflammatory factors. Additionally, primary cells were incubated with NRG-1 and/or GDNF followed by determining the gene expression level of their receptors, chemokines, and other growth factors. We demonstrate that inflammatory stimuli have a distinct impact on the expression of Gdnf, Nrg-1, and their receptors in astrocytes and microglia. In microglia, LPS or simultaneous treatment with IFNγ plus TNFα led to downregulation of Nrg-1, whereas LPS treatment slightly increased Nrg-1 expression in astrocytes. Furthermore, Gdnf was slightly upregulated after TFG-β treatment in microglia, while Gdnf was significantly upregulated after LPS treatment in astrocytes. In contrast, treatment with GDNF or/and NRG-1 did not alter any measured gene expression in microglia or astrocytes. Taken together, our in vitro studies show that Nrg-1, Gdnf, and their receptors are differently regulated in astrocytes and microglia upon inflammatory stimuli. The lack of response of astrocytes and microglia to NRG-1 and GDNF suggests that both factors exert their effects directly on neurons.
生长因子在中枢神经系统(CNS)的脱髓鞘和再髓鞘过程中发挥着关键作用,这要归因于它们的神经营养功能。我们之前已经表明,在诱导 CNS 毒性脱髓鞘后的前 2 周内,神经调节蛋白-1(Nrg-1)和胶质细胞衍生的神经营养因子(Gdnf)上调。尽管如此,上调 Nrg-1/Gdnf 的因素及其对神经胶质细胞的影响仍不清楚。我们研究了各种促炎和抗炎因子刺激原代小鼠小胶质细胞或星形胶质细胞后对 Nrg-1 和 Gdnf 表达的影响。此外,原代细胞用 NRG-1 和/或 GDNF 孵育,然后测定其受体、趋化因子和其他生长因子的基因表达水平。我们证明,炎症刺激对星形胶质细胞和小胶质细胞中 Gdnf、Nrg-1 及其受体的表达有明显影响。在小胶质细胞中,LPS 或 IFNγ 加 TNFα 同时处理导致 Nrg-1 下调,而 LPS 处理在星形胶质细胞中轻微增加 Nrg-1 表达。此外,在小胶质细胞中,TFG-β 处理后 Gdnf 略有上调,而在星形胶质细胞中 LPS 处理后 Gdnf 显著上调。相反,用 GDNF 或/和 NRG-1 处理不会改变小胶质细胞或星形胶质细胞中任何测量的基因表达。总之,我们的体外研究表明,在炎症刺激下,Nrg-1、Gdnf 及其受体在星形胶质细胞和小胶质细胞中受到不同的调节。星形胶质细胞和小胶质细胞对 NRG-1 和 GDNF 没有反应表明这两种因子直接作用于神经元。