Abstract
Schwann cell incredible plasticity is a hallmark of the utmost importance following nerve damage or in demyelinating neuropathies. After injury, Schwann cells undergo dedifferentiation before redifferentiating to promote nerve regeneration and complete functional recovery. This review updates and discusses the molecular mechanisms involved in the negative regulation of myelination as well as in the reprogramming of Schwann cells taking place early following nerve lesion to support repair. Significant advance has been made on signaling pathways and molecular components that regulate SC regenerative properties. These include for instance transcriptional regulators such as c-Jun or Notch, the MAPK and the Nrg1/ErbB2/3 pathways. This comprehensive overview ends with some therapeutical applications targeting factors that control Schwann cell plasticity and highlights the need to carefully modulate and balance this capacity to drive nerve repair.
Highlights
The peripheral nervous system (PNS) shows a surprising capacity of regeneration compared to the central nervous system (CNS)
Parkinson and colleagues showed that overexpressing the mitogen activated protein kinase (MAPK) kinase 7 (MKK7), a protein upstream of jun N-terminal kinase (JNK), in Schwann cells (SCs) primary cultures, inhibits myelin gene expression by elevating c-Jun, suggesting a role for JNK signaling in SC plasticity (Parkinson et al, 2008)
This study identified DNA damage-inducible transcript 4 protein (DDIT4) as a sustained negative regulator of myelination
Summary
Angélique Boerboom 1, Valérie Dion 1, Alain Chariot 2, 3 and Rachelle Franzen 1*. Reviewed by: Xavier Navarro, Autonomous University of Barcelona, Spain Melissa R. This review updates and discusses the molecular mechanisms involved in the negative regulation of myelination as well as in the reprogramming of Schwann cells taking place early following nerve lesion to support repair. Significant advance has been made on signaling pathways and molecular components that regulate SC regenerative properties. These include for instance transcriptional regulators such as c-Jun or Notch, the MAPK and the Nrg1/ErbB2/3 pathways. This comprehensive overview ends with some therapeutical applications targeting factors that control Schwann cell plasticity and highlights the need to carefully modulate and balance this capacity to drive nerve repair
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