• Tianjun Chen, Zhiwan Chen, Ping Wu, Jianxian Luo, Qiuling Liu, Hua Yang, Cheng Peng, Guowei Zhang, Hongsheng Lin, and Zhisheng Ji.
• Department of Orthopedics, The First Affiliated Hospital of Jinan University, Guangdong Province, Guangzhou 510630, People's Republic of China.
• Neuroscience. 2024 Apr 19; 544: 758775-87.

AbstractThe cytoskeleton must be remodeled during neurite outgrowth, and Superior Cervical Ganglion 10 (SCG10) plays a critical role in this process by depolymerizing Microtubules (MTs), conferring highly dynamic properties to the MTs. However, the precise mechanism of action of SCG10 in the repair of injured neurons remains largely uncertain. Using transcriptomic identification, we discovered that SCG10 expression was downregulated in neurons after Spinal Cord Injury (SCI). Additionally, through mass spectrometry identification, immunoprecipitation, and pull-down assays, we established that SCG10 could interact with Adenosine Kinase (ADK). Furthermore, we developed an excitotoxicity-induced neural injury model and discovered that ADK suppressed injured neurite re-growth, whereas, through overexpression and small molecule interference experiments, SCG10 enhanced it. Moreover, we discovered ADK to be the upstream of SCG10. More importantly, the application of the ADK inhibitor called 5-Iodotubercidin (5-ITu) was found to significantly enhance the recovery of motor function in mice with SCI. Consequently, our findings suggest that ADK plays a negative regulatory role in the repair of injured neurons. Herein, we propose a molecular interaction model of the SCG10-ADK axis to regulate neuronal recovery.Copyright © 2024. Published by Elsevier Inc.

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