April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Role of BCL-XL in Photoreceptor Survival Under Diabetes and Hypoxic Stress
Author Affiliations & Notes
  • J. Guo
    Medicine and Harold Hamm Oklahoma Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
  • Y.-Z. 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  J. Guo, None; Y.-Z. Le, None.
  • Footnotes
    Support  NIH grants RR17703 and EY12190, ADA grant 1-06-RA-76, AHAF grant M2008-059, FFB grant BR-CMM-0808-0453-UOK and unrestricted grants from Hope for Visiion and Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 16. doi:https://doi.org/
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    • Get Citation

      J. Guo, Y.-Z. Le; Role of BCL-XL in Photoreceptor Survival Under Diabetes and Hypoxic Stress. Invest. Ophthalmol. Vis. Sci. 2009;50(13):16. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : BCL-XL is an anti-apoptotic member of the BCL-2 family proteins and a cell death/survival checkpoint regulator. Our laboratory previously demonstrated that BCL-XL was a photoreceptor survival factor in rod photoreceptors under light-induced stress (IOVS, 2006 47:5583). To determine the role of BCL-XL in photoreceptor survival under diabetic and hypoxic stress and generate a mouse model of diabetes and/or hypoxia-induced photoreceptor damage, we tested the effect of BCL-XL loss in rod-specific Bcl-x knockout (KO) mice subjected to diabetic or hypoxic stress.

Methods: : Streptozotocin (STZ) and cobalt chloride (CC) were used to induce diabetes or chemical hypoxia in rod photoreceptor-specific Bcl-x KO mice. Apoptosis was assessed by Western blot analysis of cell death/survival pathway-related proteins. Photoreceptor function was assessed with electroretinography (ERG). Retinal morphology was assessed by examination of H & E stained retina sections.

Results: : Loss of BCL-XL caused an up-regulation of caspase-3 and BAX in the retina of rod-specific Bcl-x KO mice subjected to hypoxia. Loss of BCL-XL caused accelerated reduction of rod photoreceptor function in diabetic rod-specific Bcl-x KO mice, which was correlated with a decrease in the thickness of photoreceptor inner nuclear layer. A detailed analysis is in progress.

Conclusions: : Rod photoreceptor is more susceptible to diabetic stress.Therefore, BCL-XL may act as a survival factor for rod photoreceptors by suppression of caspase-related apoptotic pathway under hypoxia and diabetes.

Keywords: diabetes • photoreceptors • cell survival 
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