April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Upregulated GLAST Levels by GDNF May Help Ameliorate Retinal Damages in STZ-induced Diabetic Rats
Author Affiliations & Notes
  • Jun Yu
    Institute of Neurobiology, Fudan University, Shanghai, China
  • Lu Wang
    Institute of Neurobiology, Fudan University, Shanghai, China
  • Xiong-Li Yang
    Institute of Neurobiology, Fudan University, Shanghai, China
  • Yong-Mei Zhong
    Institute of Neurobiology, Fudan University, Shanghai, China
  • Footnotes
    Commercial Relationships  Jun Yu, None; Lu Wang, None; Xiong-Li Yang, None; Yong-Mei Zhong, None
  • Footnotes
    Support  National Program of Basic Research sponsored by the Ministry of Science and Technology of China (2007cb512205), The National Science Foundation of China(30770698)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3558. doi:
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      Jun Yu, Lu Wang, Xiong-Li Yang, Yong-Mei Zhong; Upregulated GLAST Levels by GDNF May Help Ameliorate Retinal Damages in STZ-induced Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3558.

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

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Abstract

Purpose: : Elevated level of glutamate in vitreous and/or retinas of patients and animal models of diabetes is believed to be implicated in the pathophysiology of neuronal loss in diabetic retinopathy. The purpose of this work was to examine possible association of morphological changes with the expression of GLAST, a prominent glutamate-aspartate transporter, and possible ameliorative effects of glial cell line-derived neurotrophic factor (GDNF) administration on changed retinal morphology and cell apoptosis.

Methods: : Experiments were conducted in 4-week streptozotocin (STZ)-diabetic rats or age-matched normal rats (control). GDNF, for a total of three times, was given every 3 days, beginning 2 weeks after the intraperitoneal injection of STZ, by intraocular injection into vitreous space of one eye chosen at random. Changes in GLAST protein levels were detected by Western blot analysis. Pathophysiology impairments of retinas were evaluated by TUNEL analysis and HE staining.

Results: : Western blot analysis showed that GLAST levels were considerably decreased by 61.11% in STZ-treated rat retinas, compared to control (P<0.05). Morphometric analysis of STZ-treated rat retinas revealed that the inner plexiform layer (IPL) was significantly reduced in thickness (P<0.01) and more TUNEL-positive cells were found (P<0.05) in the outer nuclear layer (ONL). GDNF administration remarkably increased GLAST levels by 124.90%, as compared to the vehicle-treated group (P<0.01). Additionally, the number of TUNEL-positive cells in the ONL became much lower (P<0.05) and the IPL was rather well preserved in the GDNF-treated group (P<0.05). These results suggest a possibility that upregulated GLAST levels by GDNF may help ameliorate retinal damages in diabetic rats. To further explore the above possibility, we are now examining whether the retinal damages in STZ-treated rats could be ameliorated while the increase in GLAST levels by GDNF delivery is prevented by RNA interference.

Conclusions: : Intraocular administration of GDNF effectively ameliorates retinal damages in STZ-induced diabetic rats, which could be in part due to upregulation of GLAST expression by GDNF.

Keywords: diabetic retinopathy • neuroprotection • apoptosis/cell death 
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