John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, E.D. Adrian Building, Forvie Site, Robinson Way, Cambridge, CB2 0PY, UK.
Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.
Nat Commun. 2017 Oct 27;8(1):1164. doi: 10.1038/s41467-017-01283-z.
Astrocyte responses to neuronal injury may be beneficial or detrimental to neuronal recovery, but the mechanisms that determine these different responses are poorly understood. Here we show that ephrin type-B receptor 1 (EphB1) is upregulated in injured motor neurons, which in turn can activate astrocytes through ephrin-B1-mediated stimulation of signal transducer and activator of transcription-3 (STAT3). Transcriptional analysis shows that EphB1 induces a protective and anti-inflammatory signature in astrocytes, partially linked to the STAT3 network. This is distinct from the response evoked by interleukin (IL)-6 that is known to induce both pro inflammatory and anti-inflammatory processes. Finally, we demonstrate that the EphB1-ephrin-B1 pathway is disrupted in human stem cell derived astrocyte and mouse models of amyotrophic lateral sclerosis (ALS). Our work identifies an early neuronal help-me signal that activates a neuroprotective astrocytic response, which fails in ALS, and therefore represents an attractive therapeutic target.
星形胶质细胞对神经元损伤的反应可能对神经元的恢复有益或有害,但决定这些不同反应的机制还知之甚少。在这里,我们表明,脑源性神经营养因子受体 1(EphB1)在受损的运动神经元中上调,反过来,EphB1 通过信号转导和转录激活因子 3(STAT3)介导的刺激可以激活星形胶质细胞。转录分析表明,EphB1 在星形胶质细胞中诱导一种保护性和抗炎特征,部分与 STAT3 网络有关。这与白细胞介素(IL)-6 引发的反应不同,后者已知可诱导促炎和抗炎过程。最后,我们证明在人类干细胞衍生的星形胶质细胞和肌萎缩侧索硬化症(ALS)的小鼠模型中,EphB1-ephrin-B1 途径被破坏。我们的工作确定了一种早期的神经元帮助信号,它激活了一种神经保护性的星形胶质细胞反应,而在 ALS 中这种反应失败了,因此代表了一个有吸引力的治疗靶点。