Integrin signalling and traffic during axon growth and regeneration

Abstract

Adult corticospinal tract axons do not regenerate because they have low intrinsic growth ability, and are exposed to inhibitory molecules after injury. PNS axons have a better regenerative capacity, mediated in part by integrins (extracellular matrix receptors). These are subject to complex regulation by signalling and trafficking. Recent studies have found that integrin mediated axon growth relies on signalling via focal adhesion molecules, and that integrins are inactivated by inhibitory molecules in the CNS. Forced activation of integrins can overcome inhibition and increase axon regeneration, however integrins are not transported into some CNS axons. Studies of PNS integrin traffic have identified molecules that can be manipulated to increase axonal integrin expression, suggesting strategies for repairing the injured spinal cord.