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Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
Published on: May 12, 2011
Retinal ganglion cell death is delayed by activation of retinal intrinsic cell survival program
1Department of Ophthalmology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-ku, Seoul 137-701, South Korea.
Abstract:
Neuronal cells undergo apoptosis when deprived of neurotrophic factors due to injury, trauma, or neurodegenerative disease. This study examined cell death in the retina after chronic elevation of intraocular pressure (IOP) in an experimental rat model of human glaucomatous disease. Three episcleral veins on the ocular surface of rats were cauterized. Activation of several cell death programs represented by Fas ligand, FADD (Fas Associated Death Domain/Mort1) and the caspase cascade (caspase-8 and -3) and survival programs represented by phosphorylated protein kinase B (PKB/Akt), Bcl-2 associated death domain (BAD), and cAMP responsive element binding protein (CREB) were examined using immunohistochemistry and Western blotting. Following injury, two major events occurred simultaneously in the retina: activation of programmed cell death pathways and activation of survival mechanisms to maintain the cellular homeostasis of the retina. At the later stage of injury, markers of an activated cell death program appeared to be concentrated in the retinal ganglion cells. In conclusion, we suggest that endogenous cell survival factors triggered at the early stage of injury play a critical role in control of the death or survival of retinal ganglion cells and that the manipulation of this decision phase is one of the therapeutic targets for glaucoma.
Insights
In glaucoma models, retinal ganglion cells activate both cell death and survival pathways after injury. Early survival factor activation influences cell fate, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Neuronal cells, including retinal ganglion cells, undergo apoptosis when deprived of neurotrophic factors.
- Glaucoma is characterized by elevated intraocular pressure (IOP) and subsequent retinal cell death.
Purpose of the Study:
- To investigate the activation of cell death and survival pathways in the retina following chronic IOP elevation in a rat glaucoma model.
- To determine the role of endogenous survival factors in regulating retinal ganglion cell fate.
Main Methods:
- Experimental rat model with elevated intraocular pressure induced by episcleral vein cauterization.
- Immunohistochemistry and Western blotting to examine the expression of key proteins in apoptosis (Fas ligand, FADD, caspases) and survival (PKB/Akt, BAD, CREB) pathways.
- Analysis of protein markers in retinal tissue at different stages of injury.
Main Results:
- Simultaneous activation of programmed cell death and survival mechanisms was observed in the retina post-injury.
- Markers of programmed cell death were predominantly found in retinal ganglion cells at later injury stages.
- Early activation of survival pathways appears to influence the balance between cell death and survival.
Conclusions:
- Endogenous cell survival factors play a critical role in controlling retinal ganglion cell death or survival following injury.
- Manipulating the early phase of survival pathway activation presents a potential therapeutic strategy for glaucoma.
