Induction of Eph B3 after spinal cord injury

Jorge D. Miranda, Linda A. White, Alexander Marcillo, Christopher A. Willson, Jonathan Jagid, Scott R. Whittemore

Research output: Contribution to journalArticle

122 Citations (Scopus)

Abstract

Spinal cord injury (SCI) in adult rats initiates a cascade of events producing a nonpermissive environment for axonal regeneration. This nonfavorable environment could be due to the expression of repulsive factors. The Eph receptor protein tyrosine kinases and their respective ligands (ephrins) are families of molecules that play a major role in axonal pathfinding and target recognition during central nervous system (CNS) development. Their mechanism of action is mediated by repellent forces between receptor and ligand. The possible role that these molecules play after CNS trauma is unknown. We hypothesized that an increase in the expression of Eph proteins and/or ephrins may be one of the molecular cues that restrict axonal regeneration after SCI. Rats received a contusive SCI at T10 and in situ hybridization studies 7 days posttrauma demonstrated: (i) a marked up-regulation of Eph B3 mRNA in cells located in the white matter at the lesion epicenter, but not rostral or caudal to the injury site, and (ii) an increase in Eph B3 mRNA in neurons in the ventral horn and intermediate zone of the gray matter, rostral and caudal to the lesion. Immunohistochemical analyses localizing Eph B3 protein were consistent with the mRNA results. Colocalization studies performed in injured animals demonstrated increased Eph B3 expression in white matter astrocytes and motor neurons of the gray matter. These results suggest that Eph B3 may contribute to the unfavorable environment for axonal regeneration after SCI.

Original languageEnglish
Pages (from-to)218-222
Number of pages5
JournalExperimental Neurology
Volume156
Issue number1
DOIs
StatePublished - Mar 1 1999

Fingerprint

Spinal Cord Injuries
Ephrins
Regeneration
Messenger RNA
Central Nervous System
Eph Family Receptors
Anterior Horn Cells
Ligands
Nervous System Trauma
Motor Neurons
Astrocytes
Protein-Tyrosine Kinases
In Situ Hybridization
Cues
Proteins
Up-Regulation
Wounds and Injuries
Gray Matter
White Matter

Keywords

  • Astrocytes
  • Eph receptors
  • Gray matter
  • In situ hybridization
  • MRNA
  • Protein expression
  • Spinal cord injury
  • White matter

ASJC Scopus subject areas

  • Neurology
  • Neuroscience(all)

Cite this

Miranda, J. D., White, L. A., Marcillo, A., Willson, C. A., Jagid, J., & Whittemore, S. R. (1999). Induction of Eph B3 after spinal cord injury. Experimental Neurology, 156(1), 218-222. https://doi.org/10.1006/exnr.1998.7012

Induction of Eph B3 after spinal cord injury. / Miranda, Jorge D.; White, Linda A.; Marcillo, Alexander; Willson, Christopher A.; Jagid, Jonathan; Whittemore, Scott R.

In: Experimental Neurology, Vol. 156, No. 1, 01.03.1999, p. 218-222.

Research output: Contribution to journalArticle

Miranda, JD, White, LA, Marcillo, A, Willson, CA, Jagid, J & Whittemore, SR 1999, 'Induction of Eph B3 after spinal cord injury', Experimental Neurology, vol. 156, no. 1, pp. 218-222. https://doi.org/10.1006/exnr.1998.7012
Miranda JD, White LA, Marcillo A, Willson CA, Jagid J, Whittemore SR. Induction of Eph B3 after spinal cord injury. Experimental Neurology. 1999 Mar 1;156(1):218-222. https://doi.org/10.1006/exnr.1998.7012
Miranda, Jorge D. ; White, Linda A. ; Marcillo, Alexander ; Willson, Christopher A. ; Jagid, Jonathan ; Whittemore, Scott R. / Induction of Eph B3 after spinal cord injury. In: Experimental Neurology. 1999 ; Vol. 156, No. 1. pp. 218-222.
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