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The p75 receptor mediates axon growth inhibition through an association with PIR-B

Y Fujita1, R Takashima, S Endo

  • 1Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.

Cell Death & Disease
|September 2, 2011
PubMed

Insights

The p75 receptor is crucial for inhibiting axon growth by interacting with paired immunoglobulin-like receptor B (PIR-B) and myelin-associated glycoprotein (MAG). Blocking p75 promotes axonal regeneration after nerve injury.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Nogo receptor and paired immunoglobulin-like receptor B (PIR-B) mediate axon growth inhibition by myelin-derived factors.
  • Myelin-associated glycoprotein (MAG) is a key inhibitor of axonal regeneration.

Purpose of the Study:

  • To investigate the role of the p75 receptor in the signaling pathways of PIR-B and MAG.
  • To determine if p75 receptor signaling contributes to axon growth inhibition.

Main Methods:

  • Investigated the interaction between p75 and PIR-B upon ligand binding.
  • Assessed the requirement of p75 for Src homology 2-containing protein tyrosine phosphatase (SHP) activation.
  • Examined axonal regeneration in mice with a mutated p75 gene after optic nerve injury.

Main Results:

  • p75 receptor interacts with PIR-B following ligand binding.
  • p75 receptor is necessary for MAG-induced activation of SHP.
  • Mice lacking functional p75 receptor exhibit enhanced axonal regeneration post-optic nerve injury.

Conclusions:

  • p75 receptor is essential for signal transduction initiated by PIR-B and MAG.
  • p75 receptor plays a critical role in inhibiting axon growth in specific neuronal pathways.
  • Targeting the p75 receptor may promote axonal regeneration.

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