中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (7): 1440-1441.doi: 10.4103/1673-5374.301014

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

神经修复的分子特征:人类再现啮齿动物

  

  • 出版日期:2021-07-15 发布日期:2021-01-07

The molecular profile of nerve repair: humans mirror rodents

Matthew B. Wilcox, Kristjan R. Jessen, Tom J. Quick, James B. Phillips*   

  1. Peripheral Nerve Injury Research Unit, Royal National Orthopaedic Hospital, Stanmore, UK (Wilcox MB, Quick TJ)
    Department of Pharmacology, UCL School of Pharmacy, University College London, London WC1N 1AX, UK (Wilcox MB, Phillips JB) 
    UCL Centre for Nerve Engineering, University College London, London, UK (Wilcox MB, 
    Jessen KR, Quick TJ, Phillips JB) 
    Department of Cell and Developmental Biology, University College London, London, UK (Jessen KR)
  • Online:2021-07-15 Published:2021-01-07
  • Contact: James B. Phillips, jb.phillips@ucl.ac.uk.
  • Supported by:
    The present work was funded by the Royal National Orthopaedic Hospital Charitable Trust, England Golf Trust, Engineering and Physical Sciences Research Council (EP/R004463/1) and a UCL Graduate Research Scholarship (to MBW).

摘要: https://orcid.org/0000-0001-8117-3074
(James B. Phillips) 

Abstract: Peripheral nerve injuries (PNI) are common following blunt or penetrating trauma and can lead to disability and chronic pain in affected individuals, with limited options available to promote regeneration and functional recovery. From animal models, it is known that the regenerative capacity of the peripheral nervous system (PNS) is heavily dependent upon the remarkable ability of Schwann cells to undergo a phenotypic shift from a supportive/myelinating/maintaining phenotype to one that encourages neural regeneration. In rodents, a great deal is known about the molecular signals that control this process or mark the cells and cellular changes involved (Boerboom et al., 2017; Jessen and Mirsky, 2019). Effective translation of the wealth of animal model data into a human paradigm of nerve injury would be of great benefit in the development of improved clinical treatments. However, progress has been limited by ethical and practical challenges associated with studying human nerve injury (Hewitt et al., 2008; Wilcox et al., 2019). Moreover, the intricate anatomy and diverse range of injuries make PNI a heterogeneous pathology to study. To address this issue, in our recent article entitled Characterizing cellular and molecular features of human peripheral nerve degeneration, we analyzed nerve tissue retrieved from patients undergoing reconstructive nerve procedures (Wilcox et al., 2020). Since the patients had a range of differing time intervals between injury and surgery, it was possible to construct an impression of the phenotypic changes of Schwann cells within a population over acute and chronic time points of denervation. The findings reveal novel information about the cellular and molecular features that underpin human nerve degeneration. The patterns of changes seen in the human nerve samples were similar to those previously reported in rodent models of neural degeneration. Schwann cells adopted a repair phenotype in acutely injured nerve samples which faded over time with chronic denervation. This finding may assist clinicians to optimize the timing of surgical nerve repair, to understand how pharmacological interventions might be used to improve clinical outcomes following surgery, or perhaps to ensure that surgery is not necessary.