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M. C. Lai, I. S. Ali Rahman, C. Li, N. Vagaja, E. P. Rakoczy; A Non-Invasive in vivo Assessment of the Akimba Mouse Eye. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3663.
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© ARVO (1962-2015); The Authors (2016-present)
Imaging the mouse eye in vivo in experimental mouse models of retinal diseases is of great interest for tracking disease progression. We recently generated the Akimba mouse by crossing the hyperglycemic Akita mouse with the VEGF-driven retinal neovascularisation Kimba mouse. Our purpose is to assess the disease processes in Akimba mouse eyes in vivo.
We examined all 3 mouse genotypes and control C57Bl/6J mice at monthly intervals from 4-24 weeks postnatal. Mice were anesthetized, their pupils dilated, and then injected intraperitoneally with sodium fluorescein. A contact lens was placed on the eye to prevent dehydration of the cornea during imaging using the combined confocal scanning laser ophthalmoscope and spectral domain optical coherence tomograph (OCT) imaging device, Spectralis HRA+OCT, with the 488 nm laser exciter. Images acquired using the Automatic Real-Time Mode to track eye movements in real-time and stabilize the OCT scans on the retina were analyzed on the Heidelberg Eye Explorer Software. Volume scans and thickness profiles were assessed.
From fluorescein angiograms, the retinal vasculature of control and Akita mice was normal; the vessels were patent and the capillary network was dense. In contrast, fluorescein leakage was present in all Akimba and Kimba mouse eyes, with more foci of fluorescein leakage in younger mice. The capillary network was sparse in most Akimba and Kimba mouse eyes and was almost missing in some older mice. On detail analysis, we observed changes such as vessel dilatation, tortuosity, venous beading, microaneurysms, capillary dropout and areas of capillary non-perfusion. From thickness profiles and OCT scans, the retinae of Akimba and Kimba mice were uneven, with the average thickness ranging from 65% to 90% of that in C57Bl/6J mice. From OCT scans, we also found new vessels, edema and loss of photoreceptors in Akimba and Kimba mice. Overall, the retinal damage was more severe in Akimba mice.
Although vascular changes in Akimba mice did not arise from hyperglycemia, they closely mimicked human diabetic retinopathy and were more severe than those in Kimba mice. The Akimba mice could serve as a good model for studying the interplay between hyperglycemia and VEGF-driven retinal damage. In addition, the imaging device allowed the disease processes to be tracked over time.
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