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Yanzhao Wang, Louvenia D Carter-Dawson, Nimesh Bhikhu Patel, Ronald S Harwerth, Laura J Frishman; Altered distribution of AQP4 in retinal glia in eyes with experimental glaucoma. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2455.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the distribution of aquaporin 4 (AQP4) water channels in Müller cells and astrocytes in a nonhuman primate model of unilateral experimental glaucoma.
Posterior segments from monkeys experimental and fellow control eyes, were fixed in 4% paraformaldehyde with phosphate buffer. Retina samples were taken from several nerve fiber rich regions within 5 mm of the optic nerve head. Vibratome sections were subjected to antigen retrieval and exposed to polyclonal antibody to AQP4, and monoclonal antibody to glutamine synthetase (a marker for Müller cells), and an antibody to GFAP, a marker for astrocytes. Antibody binding in retina was visualized with the appropriate secondary antibody conjugate of fluorescein, Cy3 and Cy5. Images of immunolabeled retina were captured by confocal microscopy and converted to 3D-projections using Image J software.
In the retinas of control eyes, AQP4 was prominent in blood vessel walls and in Müller cells in the outer plexiform layer, their somas in the inner nuclear layer (INL), and processes surrounding the nerve fiber bundles. AQP4 immunoreactivity generally did not co-localize with the GFAP positive astrocytes of the nerve fiber layer. However, in eyes with experimental glaucoma and retinal nerve fiber loss, AQP4 was greatly reduced in Müller cells, whereas strikingly strong immunoreactivity was detected in GFAP positive astrocytes. AQP4 positive astrocyte processes aggregated in the region typically occupied by retinal nerve fiber bundles and remained surrounded by Müller cell processes.
In control eyes, AQP4 in the retina shows a regional distribution similar to that described in rodents. The reduction of AQP4 in Müller cells of eyes with experimental glaucoma is likely to cause a major deficit in water flux, particularly in inner retina. The expression of AQP4 in astrocytes of experimental eyes is a pathophysiological alteration that might reflect a compensation for the loss of AQP4 mediated water movement, or other changes in neighboring Müller cells and degenerating nerve fibers.
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