中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (8): 1732-1733.doi: 10.4103/1673-5374.363195

• 观点:周围神经损伤修复保护与再生 • 上一篇    下一篇

新的神经元–许旺细胞共培养模型研究周围神经变性和再生

  

  • 出版日期:2023-08-15 发布日期:2023-02-23

Novel neuron-Schwann cell co-culture models to study peripheral nerve degeneration and regeneration

Kazunori Sango*   

  1. Diabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
  • Online:2023-08-15 Published:2023-02-23
  • Contact: Kazunori Sango, MD, PhD, sango-kz@igakuken.or.jp.

摘要: https://orcid.org/0000-0002-9750-9596 (Kazunori Sango)

Abstract: Schwann cells are glial cells in the peripheral nervous system that provide trophic support for the growth and maintenance of sensory, motor, and autonomic neurons and ensheath their axons in either a myelinating or an unmyelinating form. Myelinating Schwann cells wrap around large-diameter axons to form multilayered myelin structures essential for the rapid action potential propagation from one node of Ranvier to the next node (saltatory conduction). In contrast, non-myelinating Schwann cells surround several small-diameter axons to form Remak bundles. Following peripheral nerve injury, Schwann cells lose axonal contact and change their phenotype in favor of axonal regeneration and functional restoration. These “de-differentiated” Schwann cells migrate into the site distal to the injury and phagocytose axonal and myelin debris together with macrophages (Wallerian degeneration). Subsequently, they proliferate to constitute the bands of Büngner which act as guideposts for regenerating axons and provide various neurotrophic factors and chemokines that help axonal reinnervation toward target tissues and protect injured neurons from degeneration and cell death. At the final regeneration stage, the “re-differentiated” Schwann cells remyelinate growing large diameter axons or ensheath small diameter axons forming Remak bundles (Sango et al., 2017). Schwann cell abnormalities and/or their crosstalk with neurons lead to demyelinating neuropathy (myelinopathy) development and progression. These deviations are also involved in the manifestations of axons (axonopathy) and neuronal cell bodies (neuronopathy) (Niimi et al., 2019).