ArticleNPJ Regenerative medicine2025
Circulating beta-2-microglobulin promotes revascularization via TGFBR2 after spinal cord injury.
Article in NPJ Regenerative medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Construction of a prediction model for retinopathy of prematurity based on placenta-derived genes and clinical variables.Translational pediatrics · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
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.
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