June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Increased astrogliosis and aquaporin 4 in retinal hypoxia
Author Affiliations & Notes
  • Barbara da Silva
    Ophthalmology , Stanford University, Menlo park, California, United States
  • Louise Alessandra Mesentier-Louro
    Ophthalmology , Stanford University, Menlo park, California, United States
  • Ali Shariati
    Ophthalmology , Stanford University, Menlo park, California, United States
  • Roopa Dalal
    Ophthalmology , Stanford University, Menlo park, California, United States
  • Abinaya Nathan
    Department of Pulmonary Medicine, Stanford University, Palo Alto, California, United States
  • Vinicio De Jesus Perez
    Department of Pulmonary Medicine, Stanford University, Palo Alto, California, United States
  • Yaping Joyce Liao
    Ophthalmology , Stanford University, Menlo park, California, United States
    Neurology, Stanford University, Palo Alto, California, United States
  • Footnotes
    Commercial Relationships   Barbara da Silva, None; Louise Mesentier-Louro, None; Ali Shariati, None; Roopa Dalal, None; Abinaya Nathan, None; Vinicio De Jesus Perez, None; Yaping Liao, None
  • Footnotes
    Support  This project was supported by North American Neuro-Ophthalmology Society Pilot Grant, Stanford Vice Provost for Undergraduate Education Grant, Stanford Diabetes Research Center Pilot Grant, National Eye Institute (P30-026877) and Research to Prevent Blindness, Inc. L.A.M.L was supported by Stanford TRAM Pilot Grant.
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 1268. doi:
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    • Get Citation

      Barbara da Silva, Louise Alessandra Mesentier-Louro, Ali Shariati, Roopa Dalal, Abinaya Nathan, Vinicio De Jesus Perez, Yaping Joyce Liao; Increased astrogliosis and aquaporin 4 in retinal hypoxia. Invest. Ophthalmol. Vis. Sci. 2020;61(7):1268.

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

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Abstract

Purpose : Hypoxia is a common cause of vision loss in systemic diseases, and injury via hypoxic-ischemic mechanisms also plays a key role in blinding diseases such as diabetic retinopathy, glaucoma, and high-altitude retinopathy.In this study, we investigated the impact of hypoxia on retinal glial cells, which are important in ion- and osmo-homeostasis in the retina.

Methods : We induced systemic hypoxia in adult (6-8 weeks old) C57BL/6 mice using a hypoxia chamber at 10% oxygen for one week. The retinae were dissected and immunolabeled with antibodies against glial fibrillary acidic protein (GFAP) and the water channel aquaporin-4 (AQP-4), a protein that is highly expressed at the perivascular glial cells.

Results : Systemic hypoxia for one week led to significant increase in the number of GFAP+ Muller cell processes in the retina compared with controls (control: 10.2±2.5 processes/0.5mm, n=5; hypoxia:45.1±10.9 processes/0.5mm, n=5;p=0.04, one-way ANOVA with Tukey’s post hoc test). However, there was no change in the total retinal GFAP immunoreactivity. One week hypoxia also led to a significant increase in the AQP-4 immunoreactivityin the retina(control: 1066±157.5 n=4; hypoxia: 2009±55.5 gray value, n=5; p=0.0005) and in the ganglion cell layer (control: 1065±163.6, n=4; hypoxia: 1801±23.4 gray value, n=5, p=0.001) compared with controls. In contrast to retinal glial cells, one week hypoxia had little effect on retinal neurons. There was no change in the number of Brn3a+ retinal ganglion cells in the ganglion cell layer and only rare number of TUNEL+ cells in the inner nuclear layer.

Conclusions : Systemic hypoxia for one week led to retinal Muller cell activation and increase in AQP-4 expression without substantial neuronal loss. These glial changes likely contribute to hypoxia-induced breakdown in blood retina barrier and increased retinal edema.

This is a 2020 ARVO Annual Meeting abstract.

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