March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Müller Cell Is A Major Cellular Source Of Survival Signals For Photoreceptors In Diabetes
Author Affiliations & Notes
  • Shuhua Fu
    Medicine and Cell Biology and Harold Hamm Oklahoma Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Ophthalmology, The Second Affiliated Hospital of Nanchang University, Nanchang, China
  • Shuqian Dong
    Medicine and Cell Biology and Harold Hamm Oklahoma Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Ophthalmology, Xiangya Hospital, Central South University, Changsha city, 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 City, Oklahoma
  • Footnotes
    Commercial Relationships  Shuhua Fu, None; Shuqian Dong, 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, 2004. doi:
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      Shuhua Fu, Shuqian Dong, Yun-Zheng Le; Müller Cell Is A Major Cellular Source Of Survival Signals For Photoreceptors In Diabetes. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2004.

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

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Abstract

Purpose: : Diabetic retinopathy (DR) is traditionally considered as a microvascular complication in diabetic retinas . However, emerging evidences suggest that the loss of retinal neuron function and the death of retinal neurons are involved in DR. To determine whether Müller cell is a major cellular source of survival signals for photoreceptors in DR, we generated a mouse model of Müller cell-specific knockout for vascular endothelial growth factor receptor-2 (VEGFR2) . We then determined the effect of loss of VEGF signaling in Müller cells on their own survival and the survival of photoreceptors.

Methods: : Diabetes was induced with streptozotocin. Retinal function was measured with electroretinography (ERG). Retinal morphology was assessed with hematoxylin & eosin (H&E) stained sections. The density of Müller cells and cone photoreceptors was evaluated with immunohistochemistry. Gene expression was analyzed with immunoblotting.

Results: : While loss of VEGF signaling in Müller cells did not cause any apparent alteration in the retina under normal conditions, the conditional VEGFR2 knockout mice exhibited a significant loss of Müller cells, cones and rods, as well as both scotopic and photopic ERG amplitudes under diabetic conditions. Mechanistic studies regarding the diabetes-induced loss of photoreceptors are in progress.

Conclusions: : Our results suggest that VEGF signaling is required for Müller cell survival and Müller cell is a major cellular source of survival signals for photoreceptors in DR.

Keywords: diabetic retinopathy • Muller cells • photoreceptors 
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