Schwann cells-derived exosomes promote functional recovery after spinal cord injury by promoting angiogenesis

Exosomes are small vesicles that contain diverse miRNA, mRNA, and proteins that are secreted by multiple cells, and play a vital function in cell-cell communication. Numerous exosomes produced by cells have been demonstrated to be protective against spinal cord injury (SCI). This study aims to investigate the neuroprotective effect of Schwann cells-derived exosomes (SCs-Exos) on spinal cord injury. We found that SCs-Exos can be taken directly by brain-derived endothelial cells.3 (bEnd.3 cells) and promoted to proliferate, migrate, and form bEnd.3 tube. Additionally, our results showed that the pro-angiogenesis molecules, Integrin-beta 1, were highly expressed in SCs-Exos. Moreover, we used special shRNA technology to investigate the role of Integrin-beta 1 in mediating the effect of SCs-Exos-induced angiogenesis on bEnd.3 cells. We observed that the pro-angiogenic effect of SCs-Exos on bEnd.3 cells was suppressed by inhibiting the expression of integrin-beta 1 in SCs-Exos. In the SCI model, we found that SCs-Exos attenuated tissue damage and improved functional recovery after SCI. Using immunofluorescence staining, we observed that SCs-Exos treatment promoted angiogenesis in SCI, and integrin-beta 1 was required to promote angiogenesis. In conclusion, our results indicate that SCs-Exos promote angiogenesis by delivering integrin-beta 1 and may serve as a promising novel therapeutic agent for enhancing neurological functional recovery after SCI.

Automated summary

This study demonstrates that Schwann cells-derived exosomes (SCs-Exos) can promote proliferation, migration, and tube formation of brain-derived endothelial cells (bEnd.3 cells). It is found that SCs-Exos express high levels of the pro-angiogenesis molecules, Integrin-beta 1. The angiogenic effect of SCs-Exos on bEnd.3 cells is dependent on Integrin-beta 1 expression. In an spinal cord injury (SCI) model, treatment with SCs-Exos attenuates tissue damage and enhances functional recovery by promoting angiogenesis, which requires the involvement of Integrin-beta 1.