Microglia and macrophages promote corralling, wound compaction and recovery after spinal cord injury via Plexin-B2.,Nature Neuroscience

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Microglia and macrophages promote corralling, wound compaction and recovery after spinal cord injury via Plexin-B2.
Nature Neuroscience ( IF 21.2 ) Pub Date : 2020-03-01 , DOI: 10.1038/s41593-020-0597-7
Xiang Zhou _{1,

2} , Shalaka Wahane ₁ , Marie-Sophie Friedl ₃ , Michael Kluge ₃ , Caroline C Friedel ₃ , Kleopatra Avrampou ₁ , Venetia Zachariou _{1,

4} , Lei Guo ₅ , Bin Zhang ₅ , Xijing He _{2,

6} , Roland H Friedel _{1,

7} , Hongyan Zou _{1,

7}

Affiliation

Tissue repair after spinal cord injury requires the mobilization of immune and glial cells to form a protective barrier that seals the wound and facilitates debris clearing, inflammatory containment and matrix compaction. This process involves corralling, wherein phagocytic immune cells become confined to the necrotic core, which is surrounded by an astrocytic border. Here we elucidate a temporally distinct gene signature in injury-activated microglia and macrophages (IAMs) that engages axon guidance pathways. Plexin-B2 is upregulated in IAMs and is required for motor sensory recovery after spinal cord injury. Plexin-B2 deletion in myeloid cells impairs corralling, leading to diffuse tissue damage, inflammatory spillover and hampered axon regeneration. Corralling begins early and requires Plexin-B2 in both microglia and macrophages. Mechanistically, Plexin-B2 promotes microglia motility, steers IAMs away from colliding cells and facilitates matrix compaction. Our data therefore establish Plexin-B2 as an important link that integrates biochemical cues and physical interactions of IAMs with the injury microenvironment during wound healing.

中文翻译：

小胶质细胞和巨噬细胞通过 Plexin-B2 促进脊髓损伤后的聚集、伤口压实和恢复。

脊髓损伤后的组织修复需要动员免疫细胞和神经胶质细胞形成保护屏障，密封伤口并促进碎片清除、炎症抑制和基质压实。这个过程涉及聚集，其中吞噬免疫细胞被限制在被星形细胞边界包围的坏死核心中。在这里，我们阐明了损伤激活的小胶质细胞和巨噬细胞（IAM）中参与轴突引导通路的时间上不同的基因特征。 Plexin-B2 在 IAM 中表达上调，是脊髓损伤后运动感觉恢复所必需的。骨髓细胞中的 Plexin-B2 缺失会损害聚集，导致弥漫性组织损伤、炎症溢出并阻碍轴突再生。聚集很早就开始，并且需要小胶质细胞和巨噬细胞中的 Plexin-B2。从机制上讲，Plexin-B2 促进小胶质细胞运动，引导 IAM 远离碰撞细胞并促进基质压实。因此，我们的数据表明 Plexin-B2 是一个重要的环节，它将 IAM 的生化线索和物理相互作用与伤口愈合过程中的损伤微环境结合起来。

更新日期：2020-02-28

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