Skip to main content
construction release_alert
Scholars@Duke will be undergoing maintenance April 11-15. Some features may be unavailable during this time.
cancel

Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system.

Publication ,  Journal Article
Bukhari, N; Torres, L; Robinson, JK; Tsirka, SE
Published in: J Neurosci
October 19, 2011

Spinal cord injury (SCI) causes permanent debilitation due to the inability of axons to grow through established scars. Both the sugar chains and core proteins of chondroitin sulfate proteoglycans (CSPGs) are inhibitory for neurite regrowth. Chondroitinase ABC (ChABC) degrades the sugar chains and allows for synaptic plasticity, suggesting that after the sugar chain cleavage additional steps occur promoting a permissive microenvironment in the glial scar region. We report that the clearance of the core protein by the tissue plasminogen activator (tPA)/plasmin proteolytic system partially contributes to ChABC-promoted plasticity. tPA and plasmin are upregulated after SCI and degrade the deglycosylated CSPG proteins. Mice lacking tPA (tPA(-/-)) exhibit attenuated neurite outgrowth and blunted sensory and motor recovery despite ChABC treatment. Coadministration of ChABC and plasmin enhanced the tPA(-/-) phenotype and supported recovery in WT SCI mice. Collectively, these findings show that the tPA/plasmin cascade may act downstream of ChABC to allow for synergistic sensory and motor improvement compared with each treatment alone and suggest a potential new approach to enhance functional recovery after SCI.

Duke Scholars

Altmetric Attention Stats
Dimensions Citation Stats

Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

October 19, 2011

Volume

31

Issue

42

Start / End Page

14931 / 14943

Location

United States

Related Subject Headings

  • Tissue Plasminogen Activator
  • Spinal Cord Injuries
  • Rotarod Performance Test
  • Recovery of Function
  • Proteoglycans
  • Neurology & Neurosurgery
  • Motor Activity
  • Microfilament Proteins
  • Mice, Knockout
  • Mice, Inbred C57BL
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Bukhari, N., Torres, L., Robinson, J. K., & Tsirka, S. E. (2011). Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system. J Neurosci, 31(42), 14931–14943. https://doi.org/10.1523/JNEUROSCI.3339-11.2011
Bukhari, Noreen, Luisa Torres, John K. Robinson, and Stella E. Tsirka. “Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system.J Neurosci 31, no. 42 (October 19, 2011): 14931–43. https://doi.org/10.1523/JNEUROSCI.3339-11.2011.
Bukhari N, Torres L, Robinson JK, Tsirka SE. Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system. J Neurosci. 2011 Oct 19;31(42):14931–43.
Bukhari, Noreen, et al. “Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system.J Neurosci, vol. 31, no. 42, Oct. 2011, pp. 14931–43. Pubmed, doi:10.1523/JNEUROSCI.3339-11.2011.
Bukhari N, Torres L, Robinson JK, Tsirka SE. Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system. J Neurosci. 2011 Oct 19;31(42):14931–14943.

Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

October 19, 2011

Volume

31

Issue

42

Start / End Page

14931 / 14943

Location

United States

Related Subject Headings

  • Tissue Plasminogen Activator
  • Spinal Cord Injuries
  • Rotarod Performance Test
  • Recovery of Function
  • Proteoglycans
  • Neurology & Neurosurgery
  • Motor Activity
  • Microfilament Proteins
  • Mice, Knockout
  • Mice, Inbred C57BL