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Ke Shi, Yun-Zheng Le; Cone Photoreceptors Are Vulnerable To Diabetes-induced Rod Photoreceptor Death. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2590.
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Diabetic retinopathy (DR) is a leading cause of blindness in the United States and is considered as a microvascular complication in diabetic retina. However, emerging evidences suggest that the loss of retinal neuron function and the death of retinal neurons are involved in DR. To determine whether the diabetes-induced rod photoreceptor death affects cone photoreceptor survival in DR, we used rod-specific Bcl-x knockout (KO) mice that had been shown to have impaired stress-induced survival previously and determined the effect of accelerated rod death on cone survival in diabetic conditional Bcl-x KO mice.
Diabetes was induced with streptozotocin. Retinal function was measured with electroretinography (ERG) and retinal morphology was assessed with hematoxylin & eosin (H&E) stained sections. Cone density was evaluated with immunohistochemistry.
Thirty two weeks after inducing diabetes, rod-specific Bcl-x KO mice demonstrated accelerated loss of outer nuclear layer (ONL) thickness and rod photoreceptor function, compared with that of wildtype animals. Interestingly, cone photoreceptor function, as measured by photopic ERG, was significantly reduced, compared with wildtype controls. Immunohistochemical analysis of S-opsin and M-opsin, markers of cone photoreceptors, showed that cone density was also significantly reduced in diabetic rod-specific Bcl-x KO mice, compared with wildtype animals. Investigating the underlying mechanism for our observation is in progress.
Our data showed that BCL-xL, a PI3K-AKT survival pathway downstream target, is involved in rod photoreceptor protection under diabetic condition. Our results also suggest that cone photoreceptors are vulnerable to diabetes-induced rod photoreceptor death.
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