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B.J. Winn, J. Wong, R.B. Bhisitkul; Determining The Mechanism Of Retinal Damage Induced By Subretinal Hemorrhage In A Rabbit Model Of Macular Degeneration: Does Apoptosis Play A Role? . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2095.
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© ARVO (1962-2015); The Authors (2016-present)
Subretinal hemorrhage (SRH) is a complication of exudative age–related macular degeneration (AMD) causing irreversible retinal damage. In order to assess potential neuroprotective therapies, a more thorough understanding of the mechanism of SRH related retinal injury is essential. Apoptosis is postulated to be a part of this mechanism as it has been shown to play a role in oxidative stress related neuronal injury in the brain.(1,2) A rabbit model of SRH is used to determine if apoptosis is involved in SRH retinopathy via the labeling of DNA strand breaks (TUNEL technology).(3)
New Zealand white adult rabbits were anesthetized with 3–5% isfluorane in oxygen. Autologous whole blood was injected into the subretinal space of both eyes. At 24 and 48 hours after injections, the eyes were enucleated, fixed, embedded in parafin, sectioned at 5 microns, and stained using a FragEL DNA Fragmentation Detection Kit (Calbiochem) with positive and negative controls. Morphometric analysis was performed with light and fluorescence microscopy.
Autologous subretinal blood was found on histology to produce neuronal toxicity confined to the photoreceptor outer segments and the outer nuclear layer overlying the SRH at 48 hours. Using both positive and negative TUNEL staining controls, the presence of apoptotic cells preceded histologically evident photoreceptor dysmorphia in areas of retina overlying SRH at 24 and 48 hours, while areas of retina outside the region of SRH were TUNEL negative.
Subretinal hemorrhage produces retinal photoreceptor cell death within 48 hours. Through the use of TUNEL staining, apoptosis is identified as at least a component of the mechanism of SRH retinopathy. Neoroprotective therapies for subretiual hemorrhage especially those with antiapoptosis properties warrant further study as adjuncts to antiangiogenic agents. 1 Bastianetto S, et al. Brain Res. Molec. Brain Res. 1999;66:35–41.
2 Kaasik A, et al. Neuroscience. 2001;102(2):427–32.
3 Gavrieli G, et al. J. Cell Biol. 1992;119:493–501.
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