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ERK1/2 and AKT are vital factors in regulation of the migration of rat Schwann cells. | LitMetric

AI Article Synopsis

  • Wallerian degeneration occurs after nerve injury, leading to changes in Schwann cells that support nerve regeneration.
  • Elevated levels of phosphorylated ERK1/2 are linked to Schwann cell migration, influenced by nerve degeneration and a specific growth factor.
  • Inhibiting both ERK1/2 and AKT pathways significantly reduces Schwann cell motility, suggesting these signals are key to their migration and essential for nerve regeneration.

Article Abstract

After peripheral nerve injury, Wallerian degeneration (WD) occurs in the distal nerve segment. During the process of degeneration, Schwann cells (SCs) dedifferentiate, proliferate and migrate to align in "bands of Büngner", providing structural guidance and growth-promoting substrates to regenerating axons. The molecular signals that trigger SCs migration remain unclear. Here, we explored the molecular characteristics of the migration of cultured SCs prepared from rat sciatic nerves that had degenerated. The results revealed that elevated p-ERK1/2 was coupled with the migration of SCs, activated either by nerve degeneration or the addition of placenta growth factor. However, the inhibition of ERK1/2 activity, which activated the PI3K pathway, did not show a significant negative effect on SC migratory potential. Combined inhibition of ERK1/2 and AKT activity resulted in a significant decrease in SCs motility. These molecular characteristics suggest that both the ERK1/2 and AKT signals are involved in the migratory potential of SCs. It may be helpful to understand the process of nerve regeneration and perspective on promoting peripheral nerve regeneration.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427743PMC
http://dx.doi.org/10.1292/jvms.14-0555DOI Listing

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