Molecular evidence of repair and plasticity following spinal cord injury

Neuroreport. 2004 Apr 9;15(5):837-9. doi: 10.1097/00001756-200404090-00020.

Abstract

Investigations into the genetic basis of neuronal damage following spinal cord injury have thus far been limited to the acute phase after the injury. Using microarray analysis, the present study compared the spinal-cord-injury-induced gene expression changes in adult rats at the epicenter and rostral segments of spinal cord at acute (12 h) and delayed (42 days) time points. We have previously reported that the acute response to spinal cord injury involves alterations in genes responsible for inflammation, cell cycle alteration, and altered receptor function. In contrast, the delayed response includes changes in the expression of HSP27, MAG, MAP-2, IGF-1 and ApoE. The alteration in expression of these genes suggests an ongoing repair process in animals whose functional recovery has reached a plateau.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Apolipoproteins E / genetics
  • Apolipoproteins E / metabolism
  • Gene Expression Regulation
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Male
  • Microtubule-Associated Proteins / genetics
  • Microtubule-Associated Proteins / metabolism
  • Myelin-Associated Glycoprotein / genetics
  • Myelin-Associated Glycoprotein / metabolism
  • Neuronal Plasticity / genetics
  • Neuronal Plasticity / physiology*
  • Oligonucleotide Array Sequence Analysis / methods
  • Rats
  • Rats, Long-Evans
  • Spinal Cord Injuries / genetics
  • Spinal Cord Injuries / pathology
  • Spinal Cord Injuries / physiopathology*
  • Time Factors
  • Wound Healing / genetics
  • Wound Healing / physiology*

Substances

  • Apolipoproteins E
  • Microtubule-Associated Proteins
  • Myelin-Associated Glycoprotein
  • Insulin-Like Growth Factor I