Abstract
Schwann cells play a crucial role in successful peripheral nerve repair and regeneration by supporting both axonal growth and myelination. Schwann cells are therefore a feasible option for cell therapy treatment of peripheral nerve injury. However, sourcing human Schwann cells at quantities required for development beyond research is challenging. Due to their availability, rapid in vitro expansion, survival, and integration within the host tissue, stem cells have attracted considerable attention as candidate cell therapies. Among them, induced pluripotent stem cells (iPSCs) with the associated prospects for personalized treatment are a promising therapy to take the leap from bench to bedside. In this critical review, we firstly focus on the current knowledge of the Schwann cell phenotype in regard to peripheral nerve injury, including crosstalk with the immune system during peripheral nerve regeneration. Then, we review iPSC to Schwann cell derivation protocols and the results from recent in vitro and in vivo studies. We finally conclude with some prospects for the use of iPSCs in clinical settings.
Highlights
Schwann cells (SCs) develop from the neural crest [1] and are important for peripheral nerve development, function, and repair after injury
This review is the first to focus on differentiation of SCs from induced pluripotent stem cells, and what this implies for the field of peripheral nerve regenerative medicine
Schwann cells play a critical role in peripheral nerve repair through axon guidance and promoting the establishment of a pro-regenerative environment in the nerve bridge
Summary
Schwann cells (SCs) develop from the neural crest [1] and are important for peripheral nerve development, function, and repair after injury. This review is the first to focus on differentiation of SCs from induced pluripotent stem cells (iPSCs), and what this implies for the field of peripheral nerve regenerative medicine During development, they become associated with developing axons through a process of radial sorting [2,3]; SCs wrap around larger developing axons and produce myelin as they mature [2]. Upon losing contact with the collapsed axon, SCs begin to upregulate the transcription factor c-Jun which initiates their transformation to repair SCs [7] These cells undergo myelinophagy (autophagy of myelin and myelin debris), become proliferative, and elongate to form tracts called bands of Büngner [5,6,8,9]. What is upregulated in repair SCs is the expression of proteins contributing to a pro-regenerative environment for regenerative axon growth [8], e.g., nerve growth factor (NGF) and glial cell-derived neurotrophic factor (GDNF)
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