September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Experimental Anterior Ischemic Optic Neuropathy in Diabetic Mice Exhibited Severe Retinal Swelling and Subretinal Fluid Accumulation Acutely and More Severe Thinning Chronically
Author Affiliations & Notes
  • Ming-Hui Sun
    Byers Eye Institute Stanford University, Palo Alto, California, United States
    Ophthalmology, Chang Gung Memorial Hospital, Taoyuan, Taiwan
  • Ali Shariati
    Byers Eye Institute Stanford University, Palo Alto, California, United States
  • Yaping Joyce Liao
    Byers Eye Institute Stanford University, Palo Alto, California, United States
  • Footnotes
    Commercial Relationships   Ming-Hui Sun, None; Ali Shariati, None; Yaping Liao, None
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5445. doi:
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      Ming-Hui Sun, Ali Shariati, Yaping Joyce Liao; Experimental Anterior Ischemic Optic Neuropathy in Diabetic Mice Exhibited Severe Retinal Swelling and Subretinal Fluid Accumulation Acutely and More Severe Thinning Chronically. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5445.

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

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Abstract

Purpose : Non-arteritic ischemic optic neuropathy (AION) is the most common acute optic neuropathy in those older than 50 and is associated with post-ischemic inflammation and oligodendrocyte dysfunction and degeneration. Diabetes mellitus (DM) is one of the most common vascular risk factors and leads to vascular changes, inflammation, and neuron loss. We studied the contribution of elevated glucose in experimental AION and assessed retinal and inflammatory changes.

Methods : We induced photochemical thrombosis model of AION in STZ-induced chronically diabetic C57BL/6 mice (N = 43) and performed optical coherence tomography (OCT), fluorescence angiography (FA), and immunohistochemical and morphometric analyses of anti-Iba-1 antibody stain (activated microglia). Statistical analysis was performed using SPSS.

Results : We measured post-ischemic swelling one-day after AION using OCT and found there was significant swelling of the ganglion cell complex (GCC: RNFL+GCL+IPL) and increased total retinal thickness (P < 0.01) in animals with or without DM, which was associated with increased Iba-1+ staining at the optic nerve head and microglial activation. There was more subretinal fluid accumulation in the DM-AION eyes compared with non-DM AION eyes (DM vs. non-DM: 38.5% vs. 12.5%, P = 0.081). There was no correlation between serum glucose level and the severity of swelling. There was greater GCC thinning in DM mice at week-1 (DM: 79.2 ± 1.2 µm, non-DM: 97.6 ± 11.2 µm, P = 0.096) and at week-4 (DM: 66.6 ± 2.9 µm, non-DM: 74.7 ± 3.5 µm, P = 0.2) as well as greater decrease in total retina thickness 4 weeks after ischemia (DM: -16.0 ± 5.4 µm, non-DM: -3.0 ± 3.6 µm, P = 0.088).

Conclusions : After AION, there was post-ischemic inflammation and microglial activation in DM and non-DM mice, but diabetes was associated with greater swelling and subretinal fluid one day after ischemia and greater thinning four weeks later. Our findings suggested that diabetes may be a risk factor associated with greater optic neuropathy and loss of retinal ganglion cells after AION.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

 

Subretinal fluid shown in optical coherence tomography (OCT) 1 day after induction of anterior ischemic optic neuropathy (AION).

Subretinal fluid shown in optical coherence tomography (OCT) 1 day after induction of anterior ischemic optic neuropathy (AION).

 

Activation of microglial cells around optic disc 1 day after induction of anterior ischemic optic neuropathy (AION) in diabetic and non-diabetic mice.

Activation of microglial cells around optic disc 1 day after induction of anterior ischemic optic neuropathy (AION) in diabetic and non-diabetic mice.

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