Protein post-translational modifications after spinal cord injury

Spinal cord injury (SCI) often results in deficits due to limited neuronal capacity, lack of growth support, and inhibitory molecules that hinder axonal growth. Treatment strategies aim to counter these inhibitory factors or boost supportive ones. Post-translational modifications (PTMs) of proteins have been identified as having significant implications for axonal growth after SCI. These modifications, including tyrosination, acetylation, and phosphorylation, can affect axonal growth, functional recovery, and neuropathic pain. PTMs are seen as promising therapeutic targets for SCI because they are more easily regulated and reversible compared to gene transcription and translation. Targeting PTMs could offer a more accurate and economic approach to slowing or stopping the progression of SCI.

• 1
  PTMs like phosphorylation, acetylation, detyrosination, and polyglutamylation modify tubulin, influencing microtubule functions essential for neurite outgrowth and growth cone guidance during nerve regeneration after SCI.
• 2
  The expression level of the Rho signaling pathway increases after SCI, and its activation triggers growth cone collapse, hindering axon regeneration. Inhibiting CRMP2 phosphorylation promotes axonal regeneration and reduces inflammatory cell infiltration.
• 3
  Glycosylation of MMPs improves their binding with the extracellular matrix, influencing the proteolytic process essential for wound healing and matrix remodeling after SCI. Phosphorylation also regulates MMP activity, affecting regeneration.