中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (4): 845-853.doi: 10.4103/1673-5374.322474

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

杆状病毒凋亡抑制蛋白重复序列包含蛋白3可延缓坐骨神经损伤早期的Wallerian变性

  

  • 出版日期:2022-04-15 发布日期:2021-10-18

Baculoviral inhibitor of apoptosis protein repeat-containing protein 3 delays early Wallerian degeneration after sciatic nerve injury

Min Cai1, 2, #, Jian Shao2, #, Bryant Yung2, Yi Wang2, Nan-Nan Gao2, Xi Xu3, Huan-Huan Zhang2, Yu-Mei Feng2, Deng-Bing Yao1, 2, *   

  1. 1Nantong University Medical School, Nantong, Jiangsu Province, China; 2School of Life Sciences, Jiangsu Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China; 3Department of Hand Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China
  • Online:2022-04-15 Published:2021-10-18
  • Contact: Deng-Bing Yao, MD, PhD, yaodb@ntu.edu.cn.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 31971277, 31950410551; Scientific Research Foundation for Returned Scholars, Ministry of Education of China; Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD); and the Postgraduate Research & Practice Innovation Program of Jiangsu Province of China, No. KYCX 19-2050 (all to DBY).

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摘要：

Wallerian变性是神经损伤后发生的一个复杂的生物学过程，涉及神经的变性和再生。其中许旺细胞在周围神经系统Wallerian变性中细胞和分子事件发挥重要作用；然而Wallerian变性调节神经损伤和修复的机制仍不清楚，尤其在早期阶段。作者既往研究发现了一些在Wallerian变性中调控基因表达和信号通路的关键因子，其中杆状病毒凋亡抑制蛋白重复序列包含蛋白3（BIRC3）是调节凋亡抑制蛋白的重要因子之一。实验建立了右侧坐骨神经损伤大鼠体内模型以及许旺细胞体外模型，并以基因转染抑制和过表达BIRC3。结果表明，BIRC3在大鼠坐骨神经损伤后表达显著上调，且其上调和下调都会影响许旺细胞的迁移、增殖和凋亡，并通过激活c-fos和ERK信号通路影响相关因子的表达。而抑制BIRC3则可能通过抑制神经损伤后许旺细胞的凋亡而延缓早期Wallerian变性。结果提示BIRC3在周围神经损伤修复与再生过程中具有重要作用。实验于2019年3月1日经南通大学机构动物伦理委员会批准（批准号2019-nsfc004）。

https://orcid.org/0000-0002-4573-0870 (Min Cai); https://orcid.org/0000-0002-5177-0318 (Deng-Bing Yao)

关键词: 沃勒氏变性, 大鼠, 坐骨神经损伤, 杆状病毒凋亡抑制蛋白重复序列蛋白3, 神经再生, 雪旺细胞, 神经变性, 凋亡, 信号通路

Abstract: Wallerian degeneration is a complex biological process that occurs after nerve injury, and involves nerve degeneration and regeneration. Schwann cells play a crucial role in the cellular and molecular events of Wallerian degeneration of the peripheral nervous system. However, Wallerian degeneration regulating nerve injury and repair remains largely unknown, especially the early response. We have previously reported some key regulators of Wallerian degeneration after sciatic nerve injury. Baculoviral inhibitor of apoptosis protein repeat-containing protein 3 (BIRC3) is an important factor that regulates apoptosis-inhibiting protein. In this study, we established rat models of right sciatic nerve injury. In vitro Schwann cell models were also established and subjected to gene transfection to inhibit and overexpress BIRC3. The data indicated that BIRC3 expression was significantly up-regulated after sciatic nerve injury. Both BIRC3 upregulation and downregulation affected the migration, proliferation and apoptosis of Schwan cells and affected the expression of related factors through activating c-fos and ERK signal pathway. Inhibition of BIRC3 delayed early Wallerian degeneration through inhibiting the apoptosis of Schwann cells after sciatic nerve injury. These findings suggest that BIRC3 plays an important role in peripheral nerve injury repair and regeneration. The study was approved by the Institutional Animal Care and Use Committee of Nantong University, China (approval No. 2019-nsfc004) on March 1, 2019. 

Key words: apoptosis, baculoviral inhibitor of apoptosis protein repeat-containing protein 3, nerve degeneration, rat, Schwann cell, sciatic nerve injury, signal pathway, Wallerian degeneration

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