Department of Spine Surgery, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, 130033, People's Republic of China.
Department of Orthopedics, Jilin Province People's Hospital, Changchun, 130021, People's Republic of China.
Mol Neurobiol. 2024 Feb;61(2):646-661. doi: 10.1007/s12035-023-03548-9. Epub 2023 Sep 1.
This study aimed to investigate the molecular mechanisms underlying spinal cord ischemia-reperfusion (SCI/R) injury. Through RNA-Seq high-throughput sequencing and bioinformatics analysis, we found that EGFR was downregulated in the spinal cord of SCI/R mice and may function via mediating the JAK2/STAT3 signaling pathway. In vitro cell experiments indicated that overexpression of EGFR activated the JAK2/STAT3 signaling pathway and reduced neuronal apoptosis levels. In vivo animal experiments further confirmed this conclusion, suggesting that EGFR inhibits SCI/R-induced neuronal apoptosis by activating the JAK2/STAT3 signaling pathway, thereby improving SCI/R-induced spinal cord injury in mice. This study revealed the molecular mechanisms of SCI/R injury and provided new therapeutic strategies for treating neuronal apoptosis.
本研究旨在探讨脊髓缺血再灌注（SCI/R）损伤的分子机制。通过 RNA-Seq 高通量测序和生物信息学分析，我们发现 EGFR 在 SCI/R 小鼠脊髓中下调，可能通过介导 JAK2/STAT3 信号通路发挥作用。体外细胞实验表明，EGFR 的过表达激活了 JAK2/STAT3 信号通路，降低了神经元凋亡水平。体内动物实验进一步证实了这一结论，表明 EGFR 通过激活 JAK2/STAT3 信号通路抑制 SCI/R 诱导的神经元凋亡，从而改善 SCI/R 诱导的小鼠脊髓损伤。本研究揭示了 SCI/R 损伤的分子机制，为治疗神经元凋亡提供了新的治疗策略。
