ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2006
Cortisol promotes survival and regeneration of axotomised retinal ganglion cells and enhances effects of aurintricarboxylic acid.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 26 citations in OpenAlex.
- Multiple cytokine analysis of aqueous humor in uveitis with or without secondary glaucoma.BMC ophthalmology · 2024Article
- Lipofuscin-dependent stimulation of microglial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- The effect of glial fibrillary acidic protein expression on neurite outgrowth from retinal explants in a permissive environment.BMC research notes · 2012Article
- Hydrocortisone stimulates neurite outgrowth from mouse retinal explants by modulating macroglial activity.Investigative ophthalmology & visual science · 2012Article
- RGMA and neogenin protein expression are influenced by lens injury following optic nerve crush in the rat retina.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2012Article
- Impediments to eye transplantation: ocular viability following optic-nerve transection or enucleation.The British journal of ophthalmology · 2009Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroprotection is essential for repair processes after a traumatic insult in the central nervous system. We have demonstrated previously significant neuroprotective properties of the anti-apoptotic drug aurintricarboxylic acid in the model of axotomised retinal ganglion cells. Glucocorticoids are widely used to treat injuries of the nervous system. Due to the anti-inflammatory and microglia-inhibiting properties of glucocorticoids, we studied the neuroprotective effects of intravitreally administered cortisol after an optic nerve cut.
methodsNinety-eight adult Sprague-Dawley rats were used in this study. The optic nerve was cut intra-orbitally. Either vehicle or compound solution was injected intravitreally. Fluorescent dye was put onto the optic nerve stump to label retinal ganglion cells retrogradely. Retinal whole mounts were prepared 2 weeks after axotomy, and surviving retinal ganglion cells were counted.
resultsTwo weeks after axotomy, up to 50+/-7% of all retinal ganglion cells survived if cortisol was injected into the eye compared with 17+/-5% survival if only vehicle solution was injected. The neuroprotective effects of aurintricarboxylic acid (43+/-5% survival) could be further enhanced if combined with cortisol (up to 61+/-5% survival). Regeneration of cut retinal ganglion cell axons into a peripheral nerve graft could also be enhanced by an intravitreal injection of cortisol (169+/-42 regenerating retinal ganglion cells per mm2 vs. 73+/-12 cells per mm2 after vehicle injection). The increase was not as high as with aurintricarboxylic acid (192+/-40 cells per mm2), although more retinal ganglion cells survived with cortisol. This indicates that neuronal survival alone is not sufficient for subsequent axonal regeneration. Nevertheless, regeneration could be markedly increased if aurintricarboxylic acid and cortisol were combined (308+/-72 cells per mm2).
conclusionsWhereas aurintricarboxylic acid seems to act directly on lesioned retinal ganglion cells, cortisol seems to act on the glial environment, as indicated by microglial cell morphology and enhanced glial fibrillary acidic protein expression. The results show that both neuroprotection and regeneration can be enhanced by the combination of two simple compounds acting on different sites.
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