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

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Tianqi Jiang, Aitao Wang, Guangyu Wen, Hao Qi, Yuntao Gu, Wenhai Tang, Chunzhao Xu, Shanwu Ren, Shunli Zhang, Shengxing Liu, Yongxiong He
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Abstract

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.

Abstract Image

萼萼素能通过抑制 PTPRS 促进轴突生长,缓解脊髓损伤。
我们以前的研究发现了萼胝体素(CA)对脊髓损伤(SCI)的缓解作用。本研究的目的是从促进轴突生长的角度探讨萼萼素对脊髓损伤的影响。通过脊髓压迫构建SCI动物模型,进行大鼠初级皮层神经元分离,并通过硫酸软骨素蛋白多糖(CSPG)处理建立轴突生长受限细胞模型。通过免疫荧光染色和 Western 印迹检测轴突再生标记物的表达,并用银染色检测 CA 的直接靶标。最后,用 Western 印迹法评估了蛋白酪氨酸磷酸酶受体 S 型(PTPRS)的表达。CA处理增加了SCI模型大鼠和CSPG处理的原发性皮层神经元的神经元过程生长和轴突再生标记物的表达,如神经丝蛋白H(NF-H)、谷氨酸转运体1(vGlut1)和突触素(Syn),并且PTPRS水平在SCI诱导后升高。此外,PTPRS 是 CA 的直接靶标,根据体内研究结果,暴露于 CA 会降低 PTPRS 的含量。此外,PTPRS的过表达抑制了CA对轴突再生标记物含量和神经元轴突长度的增强作用。CA通过调节PTPRS的表达来增加轴突的发育,从而改善SCI。
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来源期刊
Journal of Molecular Neuroscience
Journal of Molecular Neuroscience 医学-神经科学
CiteScore
6.60
自引率
3.20%
发文量
142
审稿时长
1 months
期刊介绍: The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellence, originality, and relevance to the field of molecular neuroscience. Manuscripts with clinical relevance are especially encouraged since the journal seeks to provide a means for accelerating the progression of basic research findings toward clinical utilization. All experiments described in the Journal of Molecular Neuroscience that involve the use of animal or human subjects must have been approved by the appropriate institutional review committee and conform to accepted ethical standards.
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