Calycosin promotes axon growth by inhibiting PTPRS and alleviates spinal cord injury

• Published in: Journal of molecular neuroscience 2024-06, Vol.74 (3), p.60, Article 60
• Main Authors: Jiang, Tianqi, Wang, Aitao, Wen, Guangyu, Qi, Hao, Gu, Yuntao, Tang, Wenhai, Xu, Chunzhao, Ren, Shanwu, Zhang, Shunli, Liu, Shengxing, He, Yongxiong
• Format: Article
• Language: English
• Subjects: Animal models; Animals; Axonogenesis; Axons - drug effects; Axons - metabolism; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cells, Cultured; Cerebral Cortex - cytology; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Chondroitin sulfate; Chondroitin Sulfate Proteoglycans - metabolism; Female; Glutamic acid transporter; Isoflavones - pharmacology; Isoflavones - therapeutic use; Male; Neurochemistry; Neurofilament Proteins - metabolism; Neurofilaments; Neurology; Neuronal Outgrowth - drug effects; Neurons - drug effects; Neurons - metabolism; Neurosciences; Protein-tyrosine-phosphatase; Proteoglycans; Proteomics; Rats; Rats, Sprague-Dawley; Receptor-Like Protein Tyrosine Phosphatases, Class 2 - genetics; Receptor-Like Protein Tyrosine Phosphatases, Class 2 - metabolism; Regeneration; Spinal cord injuries; Spinal Cord Injuries - drug therapy; Spinal Cord Injuries - metabolism; Staining; Synaptophysin; Synaptophysin - genetics; Synaptophysin - metabolism; Tyrosine; Vesicular Glutamate Transport Protein 1 - genetics; Vesicular Glutamate Transport Protein 1 - metabolism; Vesicular Glutamate Transport Protein 2
• ISSN: 1559-1166; 0895-8696; 1559-1166
• DOI: 10.1007/s12031-024-02235-1

Our former studies have identified the alleviating effect of Calycosin (CA) on spinal cord injury (SCI). In this study, our purpose is to explore the influence of CA on SCI from the perspective of promoting axon growth. The SCI animal model was constructed by spinal cord compression, wherein rat primary cortex neuronal isolation was performed, and the axonal growth restriction cell model was established via chondroitin sulfate proteoglycan (CSPG) treatment. The expressions of axon regeneration markers were measured via immunofluorescent staining and western blot, and the direct target of CA was examined using silver staining. Finally, the expression of the protein tyrosine phosphatase receptor type S (PTPRS) was assessed using western blot. CA treatment increased neuronal process outgrowth and the expressions of axon regeneration markers, such as neurofilament H (NF-H), vesicular glutamate transporter 1 (vGlut1), and synaptophysin (Syn) in both SCI model rats and CSPG-treated primary cortical neurons, and PTPRS levels were elevated after SCI induction. In addition, PTPRS was the direct target of CA, and according to in vivo findings, exposure to CA reduced the PTPRS content. Furthermore, PTPRS overexpression inhibited CA’s enhancement of axon regeneration marker content and neuronal axon lengths. CA improves SCI by increasing axon development through regulating PTPRS expression.