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Celsr2 基因敲除减轻抑制性突触去除，并有益于臂丛根性撕脱伤后运动神经元存活和轴突再生。

Celsr2 Knockout Alleviates Inhibitory Synaptic Stripping and Benefits Motoneuron Survival and Axon Regeneration After Branchial Plexus Avulsion.

机构信息

Guangdong-Hongkong-Macau CNS Regeneration Institute of Jinan University, Key Laboratory of CNS Regeneration (Jinan University)-Ministry of Education, Guangzhou, 510632, People's Republic of China.

Department of Neurology and Stroke Center, The First Affiliated Hospital & Clinical Neuroscience Institute of Jinan University, Guangzhou, 510632, People's Republic of China.

出版信息

Mol Neurobiol. 2023 Apr;60(4):1884-1900. doi: 10.1007/s12035-022-03198-3. Epub 2023 Jan 3.

DOI:10.1007/s12035-022-03198-3
PMID:36593433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9984348/
Abstract

Axotomy-induced synaptic stripping modulates survival and axon regeneration of injured motoneurons. Celsr2 is supposed to mediate homophilic interactions of neighboring cells during development, and its role in synaptic stripping remains unknow. In a model of brachial plexus avulsion, Celsr2 knockout improved functional recovery, motoneuron survival, and axon regeneration. Celsr2 was indicated to express in spinal motoneurons, excitatory and inhibitory interneurons, astrocytes, and a subset of oligodendrocytes using Celsr2 mice. Double immunostaining showed that the coverage of inhibitory and excitatory vesicles on injured motoneurons were remarkably reduced after injury, whereas more inhibitory vesicles were maintained in Celsr2 mutants than control mice. In the ultrastructure, the density of inhibitory F-boutons on injured motoneurons was higher in Celsr2 mutants than controls. Conditional knockout of Celsr2 in astrocytes or oligodendrocytes showed the similar axotomy-induced synaptic withdrawal to the control. RNAseq of injured spinal samples identified 12 MHC I molecules with significant changes between Celsr2 and control mice. After injury, expression of MHC I surrounding injured motoneurons was increased, particularly high in Celsr2 mutants. In conclusion, Celsr2 knockout enhances MHC I signaling, alleviates inhibitory synaptic stripping cell-autonomously, and contributes to motoneuron survival and regeneration, and Celsr2 is a potential target for neural repair.

摘要

轴突切断诱导的突触去除调节损伤运动神经元的存活和轴突再生。Cadherin 相关富含表皮生长因子样结构域受体 2（Celsr2）被认为在发育过程中介导相邻细胞的同源相互作用，但其在突触去除中的作用尚不清楚。在臂丛神经根撕脱模型中，Celsr2 基因敲除可改善运动神经元存活和轴突再生，并促进功能恢复。使用 Celsr2 基因敲除小鼠表明 Celsr2 表达于脊髓运动神经元、兴奋性和抑制性中间神经元、星形胶质细胞和少突胶质细胞亚群。双重免疫染色显示，损伤后运动神经元上抑制性和兴奋性囊泡的覆盖率显著降低，而 Celsr2 突变体中的抑制性囊泡比对照组保留更多。在超微结构中，Celsr2 突变体损伤运动神经元上抑制性 F-末梢的密度高于对照组。星形胶质细胞或少突胶质细胞中 Celsr2 的条件性敲除显示出与对照组相似的轴突切断诱导的突触退缩。受伤脊髓样本的 RNAseq 鉴定出 12 种 MHC I 分子在 Celsr2 和对照组之间有显著变化。损伤后，损伤运动神经元周围 MHC I 的表达增加，在 Celsr2 突变体中尤其高。总之，Celsr2 基因敲除增强了 MHC I 信号，自主减轻抑制性突触去除，有助于运动神经元的存活和再生，Celsr2 是神经修复的潜在靶点。

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