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Updated: Jul 19, 2026

Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion
09:14

Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion

Published on: April 5, 2016

Axon regeneration through scars and into sites of chronic spinal cord injury

Paul Lu1, Leonard L Jones, Mark H Tuszynski

  • 1Department of Neurosciences-0626, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

Experimental Neurology
|October 4, 2006
PubMed

Insights

Bone marrow stromal cells (MSCs) promote axon regeneration after spinal cord injury (SCI). Even in the presence of inhibitory scar tissue, MSCs and neurotrophin-3 (NT-3) facilitate significant axonal regrowth, challenging previous notions of SCI barriers.

Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Spinal Cord Injury Research

Background:

  • Chronic spinal cord injury (SCI) creates an inhibitory environment due to astrocytosis and extracellular matrix (ECM) molecules, hindering axon regeneration.
  • The chronic

Purpose of the Study:

  • To investigate if autologous bone marrow stromal cells (MSCs), with or without neurotrophin-3 (NT-3) expression, can promote axonal regeneration within the inhibitory environment of a chronic SCI scar.
  • To determine if axonal regeneration can occur without surgical resection of the chronic scar tissue.

Main Methods:

  • Grafting of autologous bone marrow stromal cells (MSCs) into chronic SCI sites in adult rats 6 weeks post-injury.
  • Some MSC grafts were genetically modified to express neurotrophin-3 (NT-3).
  • Anatomical analysis was performed 3 months post-grafting to assess axonal regeneration and the lesion environment.

Main Results:

  • Axons successfully penetrated the chronic scar tissue despite the presence of inhibitory molecules like NG2 and extensive astrocytosis.
  • Significant axonal regeneration was observed into lesion cavities expressing NT-3.
  • Regenerating axons were found to associate with Schwann cells expressing both inhibitory (NG2) and permissive (L1, NCAM) substrates.

Conclusions:

  • Inhibitory factors in chronic SCI scars do not form absolute barriers to axonal regeneration.
  • Local and diffusible signals, such as those provided by MSCs and NT-3, can overcome scar-mediated inhibition.
  • Robust axonal growth is achievable even in chronic SCI without scar resection, highlighting potential therapeutic strategies.

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