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<p>Vascular network disruption caused by spinal cord injury (SCI) exacerbates secondary neuronal damage. Although vascular barrier disruption naturally restores over time, its underlying mechanism is not fully clarified. Here, we found that blood factors promote the proliferation of endothelial cells (ECs), which are essential for revascularization in the repair process after SCI. In vivo, endogenous IgG leakage into the spinal cord initiates EC proliferation at the lesion after injury. In vitro, adult mouse serum promotes mouse ECs proliferation through beta-2-microglobulin (B2M) via transforming growth factor beta receptor 2 (TGFBR2). Under EC-specific knockdown of Tgfbr2 in vivo, we observed exacerbated blood extravasation and increased inflammatory cell infiltration compared to controls. Additionally, suppression of endothelial Tgfbr2 impaired motor function recovery, axon regrowth, and regeneration in injured mice. These findings suggest that targeting the B2M-TGFBR2 axis could be a potential therapeutic approach to promoting functional recovery against vascular disruption after SCI.</p>

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Circulating beta-2-microglobulin promotes revascularization via TGFBR2 after spinal cord injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月29日

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  • Hiroshi Yamagishi,
  • Akiko Uyeda,
  • Lili Quan,
  • Hidemi Misawa,
  • Rieko Muramatsu

摘要

Vascular network disruption caused by spinal cord injury (SCI) exacerbates secondary neuronal damage. Although vascular barrier disruption naturally restores over time, its underlying mechanism is not fully clarified. Here, we found that blood factors promote the proliferation of endothelial cells (ECs), which are essential for revascularization in the repair process after SCI. In vivo, endogenous IgG leakage into the spinal cord initiates EC proliferation at the lesion after injury. In vitro, adult mouse serum promotes mouse ECs proliferation through beta-2-microglobulin (B2M) via transforming growth factor beta receptor 2 (TGFBR2). Under EC-specific knockdown of Tgfbr2 in vivo, we observed exacerbated blood extravasation and increased inflammatory cell infiltration compared to controls. Additionally, suppression of endothelial Tgfbr2 impaired motor function recovery, axon regrowth, and regeneration in injured mice. These findings suggest that targeting the B2M-TGFBR2 axis could be a potential therapeutic approach to promoting functional recovery against vascular disruption after SCI.