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神经的TRPV1-CGRP轴通过ERK/HIF-1信号通路调节外围神经的再生

Huiling Che^1,2, Yu Du^1,2, Yixuan Jiang¹

¹State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Journal of neurochemistry

|January 10, 2025

概括

激活神经元TRPV1-CGRP通路通过增强施万细胞功能和轴突再生来促进外围神经的修复. 抑制这种途径会延迟恢复,突出其治疗神经损伤的治疗潜力.

科学领域:

神经科学是一个神经科学.
再生医学是一种再生医学.
分子生物学分子生物学

背景情况:

外周神经损伤是一个重大的临床挑战.
素基因相关 (CGRP) 在神经修复中起作用.
神经短暂受体潜在化物1型 (TRPV1) 是CGRP的潜在调节者.

研究的目的:

研究神经元TRPV1-CGRP轴在坐骨神经 (SN) 修复中的作用.
探索TRPV1-CGRP激活对施万细胞 (SC) 功能的影响.
阐明涉及ERK/HIF-1信号的潜在分子机制.

主要方法:

建立了SN压伤的小鼠模型.
使用素 (Cap) 激活素 (Cpz) 抑制TRPV1-CGRP轴.
使用了神经元和老鼠SC线 (RSC96) 的体外间接共同培养模型.
评估了SC的扩散,迁移,髓化蛋白表达和神经营养分泌.
测量了细胞外信号调节激酶1/2 (ERK1/2) 酸化和缺氧诱导因子1α (HIF-1α) 积累.

主要成果:

内囊素激活了TRPV1-CGRP轴,并促进了SN修复.
西平抑制了TRPV1-CGRP轴,并延迟了SN修复.
神经元TRPV1的激活与增强的SC增殖,迁移和功能正相关.
TRPV1-CGRP轴上调了ERK1/2酸化和SC中的HIF-1α积累,促进了它们的增殖和迁移.
在受伤部位进行局部CGRP恢复,改善了神经的修复.

结论:

神经元的TRPV1-CGRP轴是施万细胞生物行为的关键调节者,并在外围神经受伤后进行轴突再生.
激活TRPV1-CGRP轴通过ERK/HIF-1信号通路促进神经修复.
这一轴代表了治疗神经损伤和开发再生生物材料的新型治疗点.

关键词:

这是CGRP的CGRP.在HIF-1信号通道上.施万的细胞是什么?在 TRPV1 中.神经再生的神经再生

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