Abstract
Purpose:To characterize histopathologic and electroretinographic (ERG) changes in the retina of pigmented rats injected with sodium iodate in order to establish a model of retinal degeneration for future cell therapy studies.Methods:In 50 male pigmented rats weighing 250-300 grams, NaIO3 was injected into the left orbital venous plexus at 40 and 60 mg/kg doses (25 eyes in each group). Fourteen rats received phosphate buffered saline (PBS) injection in their left orbital plexus and were considered as the sham-control group. Histopathologic and ERG studies were performed at baseline and on days 1, 7, 14 and 28 after the injections.Results:Progressive retinal pigment epithelial (RPE) changes were observed from the first day of injection in both the 40 and 60 mg/kg study groups in a dose dependent manner. These changes manifested as loss of melanin pigment and accumulation of lipofuscin in RPE cells with subsequent cell death and patchy loss of RPE cells (in flat mounts), as well as thinning of the outer nuclear layer and later the inner nuclear layer in the succeeding days. ERG showed a progressive and significant decrease in a- and b- wave amplitudes in both case groups relative to baseline values and the controls (P < 0.05).Conclusion:NaIO3 injection into the retrobulbar venous plexus of pigmented rats can result in significant and progressive damage to the RPE and subsequently to the neuroretina of the injected eye, and may serve as a model of retinal degeneration.
Highlights
At one‐day post‐injection in animals treated with 40 mg/kg sodium iodate there was reduction of melanin granules along with accumulation of lipofuscin in retinal pigment epithelium (RPE) cells [Figure 1b]
The amount of lipofuscin granules increased in the animals which were sacrificed 28 days after injection, and the specimens showed patchy loss of RPE cells [Figure 1c]
Cross sections of the retinas stained with hematoxylin and eosin are presented in Figure 2a‐f, which show progressive reduction in the outer nuclear layer (ONL) and inner nuclear layer (INL) cell counts, and reduction in thickness; the reduction was more prominent with the higher dose (60 mg/kg) in the animals sacrificed 28 days post‐injection [Figure 2f]
Summary
Among individuals older than 65 years of age, AMD is regarded as the leading cause of blindness in the industrialized world.[6] The drusen develop as small and hard deposits that gradually increase with age.[7,8] Enlargement of these deposits may be associated with regional RPE loss and eventually degeneration of the overlying photoreceptors These changes are funduscopically visible and their progression is used to classify lesions along the continuum of early to late dry AMD.[9] Another retinal dystrophic condition which involves RPE cells with subsequent photoreceptor loss is retinitis pigmentosa (RP). A well characterized and cost effective animal model of retinal RPE and photoreceptor cell degeneration is very helpful to design studies on cell therapies
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