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首页> 外文期刊>Cell death & disease. >Critical role of astrocytic interleukin-17?A in post-stroke survival and neuronal differentiation of neural precursor cells in adult mice
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Critical role of astrocytic interleukin-17?A in post-stroke survival and neuronal differentiation of neural precursor cells in adult mice

机译：星形细胞白细胞介素17？A在成年小鼠中风后存活和神经前体细胞神经元分化中的关键作用

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The brain and the immune system interact in complex ways after ischemic stroke, and the long-term effects of immune response associated with stroke remain controversial. As a linkage between innate and adaptive immunity, interleukin-17?A (IL-17?A) secreted from gamma delta (γδ) T cells has detrimental roles in the pathogenesis of acute ischemic stroke. However, to date, the long-term actions of IL-17?A after stroke have not been investigated. Here, we found that IL-17?A showed two distinct peaks of expression in the ischemic hemisphere: the first occurring within 3 days and the second on day 28 after stroke. Our data also showed that astrocyte was the major cellular source of IL-17?A that maintained and augmented subventricular zone (SVZ) neural precursor cells (NPCs) survival, neuronal differentiation, and subsequent synaptogenesis and functional recovery after stroke. IL-17?A also promoted neuronal differentiation in cultured NPCs from the ischemic SVZ. Furthermore, our in vitro data revealed that in primary astrocyte cultures activated astrocytes released IL-17?A via p38 mitogen-activated protein kinase (MAPK). Culture media from reactive astrocytes increased neuronal differentiation of NSCs in vitro . Blockade of IL-17?A with neutralizing antibody prevented this effect. In addition, after screening for multiple signaling pathways, we revealed that the p38 MAPK/calpain 1 signaling pathway was involved in IL-17?A-mediated neurogenesis in vivo and in vitro . Thus, our results reveal a previously uncharacterized property of astrocytic IL-17?A in the maintenance and augment of survival and neuronal differentiation of NPCs, and subsequent synaptogenesis and spontaneous recovery after ischemic stroke.
机译：缺血性中风后，大脑和免疫系统以复杂的方式相互作用，与中风相关的免疫反应的长期影响仍存在争议。作为先天性免疫和适应性免疫之间的联系，从γ-δ（γδ）T细胞分泌的白介素-17？A（IL-17？A）在急性缺血性中风的发病机理中具有有害作用。然而，迄今为止，尚未研究中风后IL-17？A的长期作用。在这里，我们发现IL-17？A在缺血半球中显示了两个不同的表达峰：第一个出现在中风后3天内，第二个出现在中风后28天。我们的数据还表明，星形胶质细胞是维持和增强脑室下区（SVZ）神经前体细胞（NPC）存活，神经元分化以及中风后突触发生和功能恢复的IL-17？A的主要细胞来源。 IL-17αA还促进了来自缺血性SVZ的培养NPC的神经元分化。此外，我们的体外数据显示，在原代星形胶质细胞培养物中，活化的星形胶质细胞通过p38丝裂原活化的蛋白激酶（MAPK）释放IL-17？A。反应性星形胶质细胞的培养基增加了神经干细胞的神经元分化。用中和抗体阻断IL-17αA可防止这种作用。此外，在筛选了多种信号通路后，我们发现p38 MAPK / calpain 1信号通路在体内和体外均参与IL-17？A介导的神经发生。因此，我们的结果揭示了星形细胞IL-17ΔA以前未表征的特性，可以维持和增加NPC的存活和神经元分化，以及随后的突触形成和缺血性中风后的自发恢复。

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