Autophagy induced by Schwann cell-derived exosomes promotes recovery after spinal cord injury in rats.
Dayu PanShibo ZhuWeixin ZhangZhijian WeiFuhan YangZhenglong GuoGuangzhi NingShi-Qing FengPublished in: Biotechnology letters (2021)
Spinal cord injury (SCI) is catastrophic to humans and society. However, there is currently no effective treatment for SCI. Autophagy is known to serve critical roles in both the physiological and pathological processes of the body, but its facilitatory and/or deleterious effects in SCI are yet to be completely elucidated. This study aimed to use primary Schwann cell-derived exosomes (SCDEs) to treat rats after SCI. In the present study, SCDEs were purified and their efficacy in ameliorating the components of SCI was examined. Using both in vivo and in vitro experiments, it was demonstrated that SCDEs increased autophagy and decreased apoptosis after SCI, which promoted axonal protection and the recovery of motor function. Furthermore, it was discovered that an increased number of SCDEs resulted in a decreased expression level of EGFR, which subsequently inhibited the Akt/mTOR signaling pathway, which upregulated the level of autophagy to ultimately induce microtubule acetylation and polymerization. Collectively, the present study identified that SCDEs could induce axonal protection after SCI by increasing autophagy and decreasing apoptosis, and it was suggested that this may involve the EGFR/Akt/mTOR signaling pathway.
Keyphrases
- spinal cord injury
- signaling pathway
- endoplasmic reticulum stress
- cell death
- oxidative stress
- spinal cord
- neuropathic pain
- pi k akt
- induced apoptosis
- small cell lung cancer
- cell proliferation
- tyrosine kinase
- epidermal growth factor receptor
- stem cells
- epithelial mesenchymal transition
- mesenchymal stem cells
- long non coding rna
- histone deacetylase