June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Protective role of AIBP in glaucomatous retinal ganglion cells and their axons
Author Affiliations & Notes
  • Wonkyu Ju
    Ophthalmology, University of California San Diego, La Jolla, California, United States
  • Footnotes
    Commercial Relationships   Wonkyu Ju None
  • Footnotes
    Support  NIH grants EY031697 (WKJ) and P30 EY022589 (Vision Research Core Grant)
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 1617 – A0440. doi:
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      Wonkyu Ju; Protective role of AIBP in glaucomatous retinal ganglion cells and their axons. Invest. Ophthalmol. Vis. Sci. 2022;63(7):1617 – A0440.

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

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Purpose : The goal of this study is to investigate the effect of Apolipoprotein A-I binding protein (AIBP; gene name APOAIBP) on retinal ganglion cell survival and central visual pathway preservation in a mouse model of glaucoma

Methods : Human retina tissues sections were obtained from a normal human donor or patients with glaucoma. Five mo-old Pre-glaucomatous DBA/2J (D2) mice eyes were intravitreally transduced with recombinant adeno-associated virus serotype 2 (AAV2) constructs including AAV2-Null or AIBP for 5 months. Each of the 10-mo-old D2 mice used in this study had a single IOP measurement. RGC survival and its axon preservation were assessed by cell counting and RBPMS or NF68 immunohistochemistry. The microglial alteration was measured by IBA1 immunohistochemistry. The preservation of the central visual pathway was assessed in the superior colliculus (SC) by labeling with cholera toxin submit B (CTB).

Results : We found that RGC soma and axons were the primary sites of AIBP expression in the normal retina from a human donor. In contrast, AIBP immunoreactivity was significantly decreased in the RGC somas in glaucomatous human retinas. In 10-mo-old glaucomatous D2 mice, we found that cholesterol content was significantly elevated in the inner retinal layer, and expression of AIBP and ABCA1 was significantly decreased – by half – compared to age-matched control D2-Gpnmb+ mice. Based on these data, we overexpressed AIBP in the retina by in vivo delivery of AAV-AIBP. Our results demonstrated that overexpression of AIBP significantly protected RGCs in the middle and peripheral retinas and preserved their axons in the glial lamina of 10-mo-old glaucomatous D2 mice. We also found that overexpression of AIBP significantly increased microglial branch length and the number of endpoints in the middle area of the retina in 10-mo-old glaucomatous D2 mice. However, there were no changes in soma size and number of IBA1-positive microglia. Using CTB labeling, we found that 10-mo-old glaucomatous D2 mice had decreased CTB density in the SC. Surprisingly, we also found that overexpression of AIBP significantly increased CTB density in the SC of 10-mo-old glaucomatous D2 mice.

Conclusions : These findings suggest the possibility that AIBP has a therapeutic potential to treat glaucoma and other optic neuropathies

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.


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