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波形蛋白通过增强自噬抑制脊髓损伤后的神经元凋亡。

Vimentin Inhibits Neuronal Apoptosis After Spinal Cord Injury by Enhancing Autophagy.

作者信息

Zhao Jie, Chen Kangzhen, Wang Tao, Qiu Xianxiu, Zhang Xiaomin, He Tao, Chen Liji, Chen Jiahong, Cui Xiaojun, Wu Hongfu

机构信息

Dongguan Key Laboratory of Stem Cell and Regenerative Tissue Engineering, the First Dongguan Affiliated Hospital, School of Basic Medical Sciences, Guangdong Medical University, Dongguan, China.

Department of Venereal Diseases and Integrated Chinese and Western Medicine and Bone Paralysis, Longjiang Hospital of Shunde District, Foshan, China.

出版信息

CNS Neurosci Ther. 2025 Jan;31(1):e70200. doi: 10.1111/cns.70200.

DOI:10.1111/cns.70200
PMID:39753767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11702385/
Abstract

AIMS

Neuron death is caused primarily by apoptosis after spinal cord injury (SCI). Autophagy, as a cellular response, can maintain cellular homeostasis to reduce apoptosis. We aimed to investigate the effect and the mechanism of vimentin knockdown on autophagy and neural recovery after SCI.

METHODS

The SD rats with T10 complete transection as SCI model were used. The vimentin RNAi adenovirus was constructed and transplanted into T10 rats with total transection injury of the spinal cord, and the recovery of neurological and motor functions after SCI was evaluated by BBB score, footprint analysis, electrophysiological tests, and immunofluorescence staining. Protein and gene expression were assessed by Western blotting, CO-IP, q-PCR, and immunofluorescence. In addition, neuron-like PC12 cells were infected with adenovirus to further elucidate the effect of vimentin on autophagy and the molecular mechanism of neuronal apoptosis after SCI.

RESULTS

Inhibition of SCI induced-vimentin upregulation improved motor function, enhanced the recovery of autophagy flux, and reduced neuronal apoptosis. Notably, this may be related to the formation of vimentin-14-3-3-Beclin1 complex and PI3K class III complex.

CONCLUSION

Our results suggest that inhibition of vimentin expression may enhance autophagy and anti-apoptosis in neurons after SCI by affecting the formation of the vimentin-14-3-3-Beclin1 complex, thereby promoting neuronal recovery.

摘要

目的

脊髓损伤（SCI）后神经元死亡主要由凋亡引起。自噬作为一种细胞反应，可维持细胞内稳态以减少凋亡。我们旨在研究波形蛋白敲低对SCI后自噬和神经恢复的影响及机制。

方法

采用T10完全横断的SD大鼠作为SCI模型。构建波形蛋白RNA干扰腺病毒并将其移植到T10脊髓完全横断损伤的大鼠中，通过BBB评分、足迹分析、电生理测试和免疫荧光染色评估SCI后神经和运动功能的恢复情况。通过蛋白质印迹法、免疫共沉淀、q-PCR和免疫荧光评估蛋白质和基因表达。此外，用腺病毒感染神经元样PC12细胞以进一步阐明波形蛋白对自噬的影响及SCI后神经元凋亡的分子机制。

结果

抑制SCI诱导的波形蛋白上调可改善运动功能，增强自噬通量的恢复，并减少神经元凋亡。值得注意的是，这可能与波形蛋白-14-3-3-贝克林1复合物和III类磷脂酰肌醇3-激酶复合物的形成有关。

结论

我们的结果表明，抑制波形蛋白表达可能通过影响波形蛋白-14-3-3-贝克林1复合物的形成来增强SCI后神经元的自噬和抗凋亡能力，从而促进神经元恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/7e451f64ce7d/CNS-31-e70200-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/6244c4db2e9f/CNS-31-e70200-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/a36babd229d5/CNS-31-e70200-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/34acefa258cc/CNS-31-e70200-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/82046f3bb19c/CNS-31-e70200-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/a5b75333d04c/CNS-31-e70200-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/314bd07149e5/CNS-31-e70200-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/7e451f64ce7d/CNS-31-e70200-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/6244c4db2e9f/CNS-31-e70200-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/a36babd229d5/CNS-31-e70200-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/34acefa258cc/CNS-31-e70200-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/82046f3bb19c/CNS-31-e70200-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/a5b75333d04c/CNS-31-e70200-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/314bd07149e5/CNS-31-e70200-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f90/11702385/7e451f64ce7d/CNS-31-e70200-g008.jpg

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本文引用的文献

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Impairment of autophagy after spinal cord injury potentiates neuroinflammation and motor function deficit in mice.脊髓损伤后自噬的损伤会加剧小鼠的神经炎症和运动功能缺陷。
Theranostics. 2022 Jul 11;12(12):5364-5388. doi: 10.7150/thno.72713. eCollection 2022.
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The PI3K/AKT signalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities.创伤性脊髓损伤后炎症、细胞死亡和神经胶质瘢痕形成中的 PI3K/AKT 信号通路：机制和治疗机会。
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Inhibition of Autophagy Flux Promotes Secretion of Chondroitin Sulfate Proteoglycans in Primary Rat Astrocytes.
自噬通量的抑制促进原代大鼠星形胶质细胞中硫酸软骨素蛋白聚糖的分泌。
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Systemic Administration of Fibroblast Growth Factor 21 Improves the Recovery of Spinal Cord Injury (SCI) in Rats and Attenuates SCI-Induced Autophagy.全身给予成纤维细胞生长因子21可改善大鼠脊髓损伤（SCI）的恢复并减轻SCI诱导的自噬。
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Vimentin Intermediate Filaments as Potential Target for Cancer Treatment.波形蛋白中间丝作为癌症治疗的潜在靶点
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High glucose: activating autophagy and affecting the biological behavior of human lens epithelial cells.高糖：激活自噬并影响人晶状体上皮细胞的生物学行为。
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