Alpha-crystallin protected axons from optic nerve degeneration after crushing in rats

J Mol Neurosci. 2008 Jul;35(3):253-8. doi: 10.1007/s12031-007-9010-1. Epub 2008 Jun 14.

Abstract

In mature mammals, optic nerve injury results in apoptosis of retinal ganglion cells. The literature confirms that lens injury enhances retinal ganglion cells survival, but the mechanism is not very clear. Using silver staining method and computer image analysis techniques, the effect of alpha-crystallin, a major component of the lens in the survival of retinal ganglion cell axons, was investigated in vivo after intravitreal injections. The results showed that enhanced survival of axotomized axons was observed beyond the crush site after a single intravitreal administration of alpha-crystallin at the time of axotomy. Axonal density of the retinal ganglion cell was significantly greater than in the untreated controls until 2 weeks after injection. This effect declined by 4 weeks after injection but survival of axons remained greater than controls. These findings indicate that alpha-crystallin plays a key role in protecting axons after optic nerve injury.

MeSH terms

  • Animals
  • Axons / drug effects
  • Axons / metabolism*
  • Axons / pathology
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Cytoprotection / drug effects
  • Cytoprotection / physiology*
  • Disease Models, Animal
  • Nerve Crush
  • Nerve Growth Factors / metabolism
  • Nerve Growth Factors / pharmacology
  • Nerve Regeneration / drug effects
  • Nerve Regeneration / physiology
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / pharmacology
  • Optic Nerve Injuries / drug therapy
  • Optic Nerve Injuries / metabolism*
  • Optic Nerve Injuries / physiopathology
  • Rats
  • Rats, Long-Evans
  • Retinal Ganglion Cells / drug effects
  • Retinal Ganglion Cells / metabolism*
  • Retinal Ganglion Cells / pathology
  • Treatment Outcome
  • Wallerian Degeneration / drug therapy
  • Wallerian Degeneration / metabolism*
  • Wallerian Degeneration / physiopathology
  • alpha-Crystallins / metabolism*
  • alpha-Crystallins / pharmacology

Substances

  • Nerve Growth Factors
  • Neuroprotective Agents
  • alpha-Crystallins