March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Cone Photoreceptors Are Vulnerable To Diabetes-induced Rod Photoreceptor Death
Author Affiliations & Notes
  • Ke Shi
    Medicine and Harold Hamm Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Ophthalmology,The Second Affiliated Hospital, Nanchang University, Nanchang, China
  • Yun-Zheng Le
    Medicine and Cell Biology and Harold Hamm Oklahoma Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Dean A. McGee Eye Institute, Oklahoma City, Oklahoma
  • Footnotes
    Commercial Relationships  Ke Shi, None; Yun-Zheng Le, None
  • Footnotes
    Support  NIH grants R01EY020900 and P20RR024215, ADA grant 1-10-BS-94, OCAST contract HR09-058
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2590. doi:
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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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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : 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.

Methods: : 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.

Results: : 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.

Conclusions: : 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.

Keywords: diabetic retinopathy • retinal degenerations: cell biology • photoreceptors 

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