HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Sema-3A indirectly disrupts the regeneration process of goldfish optic nerve after controlled injury.

AbstractBACKGROUND:
Neurons of adult mammalian CNS are prevented from regenerating injured axons due to formation of a non-permissive environment. The retinal ganglion cells (RGC), which are part of the CNS, share this characteristic. In sharp contrast, the RGC of lower vertebrates, such as fish, are capable of re-growing injured optic nerve axons, and achieve, through a complex multi-factorial process, functional vision after injury. Semaphorin-3A (sema-3A), a member of the class 3 semaphorins known for its repellent and apoptotic activities, has previously been shown to play a key role in the formation of a non-permissive environment after CNS injury in mammalians.
METHODS:
The expression of sema-3A and its effect on regenerative processes in injured gold fish retina and optic nerve were investigated in this study. Unilateral optic nerve axotomy or crush was induced in goldfish. 2 microl sema-3A was injected intraviterally 48 hours post injury. Neuronal viability was measured using the lipophilic neurotracer dye 4-Di-10-Asp. Axonal regeneration was initiated using the anterograde dye dextran. Retinas and optic nerves were collected at intervals of 2, 3, 7, 14 and 28 days after the procedure. Using Western blot and immunohistochemical analysis, the expression levels of semaphorin-3A, axonal regeneration, the removal of myelin debris and macrophage invasion were studied.
RESULTS:
We found a decrease in sema-3A levels in the retina at an early stage after optic nerve injury, but no change in sema-3A levels in the injured optic nerve. Intravitreal injection of sema-3A to goldfish eye, shortly after optic nerve injury, led to destructive effects on several pathways of the regenerative processes, including the survival of retinal ganglion cells, axonal growth, and clearance of myelin debris from the lesion site by macrophages.
CONCLUSIONS:
Exogenous administration of sema-3A in fish indirectly interferes with the regeneration process of the optic nerve. The findings corroborate our previous findings in mammals, and further validate sema-3A as a key factor in the generation of a non-permissive environment after transection of the optic nerve.
AuthorsShira Rosenzweig, Dorit Raz-Prag, Anat Nitzan, Ronit Galron, Ma'ayan Paz, Gunnar Jeserich, Gera Neufeld, Ari Barzilai, Arieh S Solomon
JournalGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie (Graefes Arch Clin Exp Ophthalmol) Vol. 248 Issue 10 Pg. 1423-35 (Oct 2010) ISSN: 1435-702X [Electronic] Germany
PMID20449604 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Semaphorin-3A
Topics
  • Animals
  • Axons (physiology)
  • Axotomy
  • Blotting, Western
  • Cell Count
  • Cell Survival
  • Fluorescent Antibody Technique, Indirect
  • Goldfish
  • Injections
  • Macrophages (physiology)
  • Nerve Crush
  • Nerve Regeneration (drug effects, physiology)
  • Optic Nerve (physiology)
  • Retinal Ganglion Cells (physiology)
  • Semaphorin-3A (pharmacology, physiology)
  • Vitreous Body

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: